66
Penyakit penting pada unggas akibat infeksi virus Sri Murtini
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Penyakit penting pada unggas akibat infeksi virus
Sri Murtini
Beberapa penyakit viral penting dalamindustri peternakan diIndonesia
bull Avian reovirus
bull Infectious Bronchitis
bull Infectious Laryngotracheitis
bull Eggs Drops Syndrom
bull Pox virus
Infeksi Avian Reovirus
Agent Reoviridae ----------Orthoreovirus
bull Avian Reoviruses are ubiquitous viruses in nature and are commonly isloated from a variety of tissues in poultry affected my multiple disease conditions such as viral arthritistenosynovitis sttunting syndrome respiratory disease enteric disease and malabsorption syndrome
bull 85-90 reovirus non pathogenicHost
broiler breeders (meat type chickens) 7-16 weeks of age
Chicks 2 weeks of age
Malabsorption syndrome
1 RuntingStunting
2 Poor pigmentation
3 Abnormal feathering
4 Skeletal abnormalities
5 Increased mortality
6 Enlarged proventriculus
Clinical SignsGross Lesions
Viral arthritistenosynovitis
1 Lameness
2 Joint swelling
3 Thickenedruptured tendons
Post-mortem Findings
ndash Rupture of the gastrocnemius tendon----------green discoloration of the skin at the join
ndash Erosion articular cartilage
bull Ptechie in synovial membranes
bull clear fluid in capsula-------2nd infection
ndash Rupture digital flexor tendons
ndash Gastrointestinal Distention (fluid and gas) pancreas atrophy proventriculus dilatation
Histopathology
bullEosinophilic intracytoplasmic inclusion bodies in
liver
bullThickening of the tendon oedema hypertrophy and
hyperplasia of the synoviocytes
bullVillous proliferation and invasion imflamatory cells
of the synovial membranes
bull PathogenicityReoviruses have been identified as the etiology of other disease
conditions such as
1 Arthritistenosynovitis
2 Runtingstunting
3Pericarditismyocarditishydropericardium
4 Hepatitis
5 Bursal and thymus atrophy
Prevention Strategies
1 Good Husbandry Programs
2 Biosecurity Programs
3 Vaccination Programs
Vaccination (Broiler Breeders)
Purpose
1 Prevent VA in the breeders
2 Prevent egg transmission to progeny
3 Produce maternal antibodies for the progeny
Vaccination Strategies (Broiler Breeders)
Program 1 1st Live 1-2 Wks SQWater
1st2nd Live 3-8 W SQWaterWingweb
2nd3rd Live 8-16 Wks SQWaterWingweb
Program 2 1st Live 1 week SQWater
2nd Live 3-4 Wks SQWater
2nd3rd Live 6-8 Wks SQWingwebWater
1st Killed 10-14 Wks SQIM
2nd Killed 14-20 Wks SQIM
Prevention
Select birds that are leukosis virus negative using serologic
methods to prevent spread of the disease
Treatment
None
Special note
It is immunosuppressive and a major cause of condemnation
in adult broiler breeders and layers Tumors are a common
cause of condemnation in layer processing plants
PoxviridaeOrthopoxvirus (image)
bull Largest and most complex of all viruses
bull Brick shaped
bull 250 x 200 x 200 nm in size
bull Parapoxviridae are OVOID 260 x 160 nm
bull Virions are complex
bull Core
bull Lateral bodies
bull Outer membrane
bull + - envelope
bull Core ndashDumbbell shaped Contains viral DNA viral proteins
bull Lateral bodies ndash unknown nature
bull + - Envelope
bull Genome is linear and double stranded
bull Largest genome of any animal virus
bull Encodes all transcription and replication enzymes needed for viral genome
Poxviridae ndash Subfamilies and Generabull Orthopoxvirus ndash vaccinia
bull Parapoxvirus ndash pseudocowpox virus
bull Avipoxvirus ndash fowlpox virus
bull Capripoxvirus ndash sheeppox virus
bull Leporipoxvirus ndash Leooripoxvirus
bull Suiposvirus ndash Swinepox virus
bull Molluscipoxvirus ndash Myxoma virus
bull Yabapoxvirus ndash Yaba monkey tumor virus
bull Subfamily Entomopoxvirinae ndash contains viruses of insects
bull Viral replication ndash cytoplasm
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Beberapa penyakit viral penting dalamindustri peternakan diIndonesia
bull Avian reovirus
bull Infectious Bronchitis
bull Infectious Laryngotracheitis
bull Eggs Drops Syndrom
bull Pox virus
Infeksi Avian Reovirus
Agent Reoviridae ----------Orthoreovirus
bull Avian Reoviruses are ubiquitous viruses in nature and are commonly isloated from a variety of tissues in poultry affected my multiple disease conditions such as viral arthritistenosynovitis sttunting syndrome respiratory disease enteric disease and malabsorption syndrome
bull 85-90 reovirus non pathogenicHost
broiler breeders (meat type chickens) 7-16 weeks of age
Chicks 2 weeks of age
Malabsorption syndrome
1 RuntingStunting
2 Poor pigmentation
3 Abnormal feathering
4 Skeletal abnormalities
5 Increased mortality
6 Enlarged proventriculus
Clinical SignsGross Lesions
Viral arthritistenosynovitis
1 Lameness
2 Joint swelling
3 Thickenedruptured tendons
Post-mortem Findings
ndash Rupture of the gastrocnemius tendon----------green discoloration of the skin at the join
ndash Erosion articular cartilage
bull Ptechie in synovial membranes
bull clear fluid in capsula-------2nd infection
ndash Rupture digital flexor tendons
ndash Gastrointestinal Distention (fluid and gas) pancreas atrophy proventriculus dilatation
Histopathology
bullEosinophilic intracytoplasmic inclusion bodies in
liver
bullThickening of the tendon oedema hypertrophy and
hyperplasia of the synoviocytes
bullVillous proliferation and invasion imflamatory cells
of the synovial membranes
bull PathogenicityReoviruses have been identified as the etiology of other disease
conditions such as
1 Arthritistenosynovitis
2 Runtingstunting
3Pericarditismyocarditishydropericardium
4 Hepatitis
5 Bursal and thymus atrophy
Prevention Strategies
1 Good Husbandry Programs
2 Biosecurity Programs
3 Vaccination Programs
Vaccination (Broiler Breeders)
Purpose
1 Prevent VA in the breeders
2 Prevent egg transmission to progeny
3 Produce maternal antibodies for the progeny
Vaccination Strategies (Broiler Breeders)
Program 1 1st Live 1-2 Wks SQWater
1st2nd Live 3-8 W SQWaterWingweb
2nd3rd Live 8-16 Wks SQWaterWingweb
Program 2 1st Live 1 week SQWater
2nd Live 3-4 Wks SQWater
2nd3rd Live 6-8 Wks SQWingwebWater
1st Killed 10-14 Wks SQIM
2nd Killed 14-20 Wks SQIM
Prevention
Select birds that are leukosis virus negative using serologic
methods to prevent spread of the disease
Treatment
None
Special note
It is immunosuppressive and a major cause of condemnation
in adult broiler breeders and layers Tumors are a common
cause of condemnation in layer processing plants
PoxviridaeOrthopoxvirus (image)
bull Largest and most complex of all viruses
bull Brick shaped
bull 250 x 200 x 200 nm in size
bull Parapoxviridae are OVOID 260 x 160 nm
bull Virions are complex
bull Core
bull Lateral bodies
bull Outer membrane
bull + - envelope
bull Core ndashDumbbell shaped Contains viral DNA viral proteins
bull Lateral bodies ndash unknown nature
bull + - Envelope
bull Genome is linear and double stranded
bull Largest genome of any animal virus
bull Encodes all transcription and replication enzymes needed for viral genome
Poxviridae ndash Subfamilies and Generabull Orthopoxvirus ndash vaccinia
bull Parapoxvirus ndash pseudocowpox virus
bull Avipoxvirus ndash fowlpox virus
bull Capripoxvirus ndash sheeppox virus
bull Leporipoxvirus ndash Leooripoxvirus
bull Suiposvirus ndash Swinepox virus
bull Molluscipoxvirus ndash Myxoma virus
bull Yabapoxvirus ndash Yaba monkey tumor virus
bull Subfamily Entomopoxvirinae ndash contains viruses of insects
bull Viral replication ndash cytoplasm
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Infeksi Avian Reovirus
Agent Reoviridae ----------Orthoreovirus
bull Avian Reoviruses are ubiquitous viruses in nature and are commonly isloated from a variety of tissues in poultry affected my multiple disease conditions such as viral arthritistenosynovitis sttunting syndrome respiratory disease enteric disease and malabsorption syndrome
bull 85-90 reovirus non pathogenicHost
broiler breeders (meat type chickens) 7-16 weeks of age
Chicks 2 weeks of age
Malabsorption syndrome
1 RuntingStunting
2 Poor pigmentation
3 Abnormal feathering
4 Skeletal abnormalities
5 Increased mortality
6 Enlarged proventriculus
Clinical SignsGross Lesions
Viral arthritistenosynovitis
1 Lameness
2 Joint swelling
3 Thickenedruptured tendons
Post-mortem Findings
ndash Rupture of the gastrocnemius tendon----------green discoloration of the skin at the join
ndash Erosion articular cartilage
bull Ptechie in synovial membranes
bull clear fluid in capsula-------2nd infection
ndash Rupture digital flexor tendons
ndash Gastrointestinal Distention (fluid and gas) pancreas atrophy proventriculus dilatation
Histopathology
bullEosinophilic intracytoplasmic inclusion bodies in
liver
bullThickening of the tendon oedema hypertrophy and
hyperplasia of the synoviocytes
bullVillous proliferation and invasion imflamatory cells
of the synovial membranes
bull PathogenicityReoviruses have been identified as the etiology of other disease
conditions such as
1 Arthritistenosynovitis
2 Runtingstunting
3Pericarditismyocarditishydropericardium
4 Hepatitis
5 Bursal and thymus atrophy
Prevention Strategies
1 Good Husbandry Programs
2 Biosecurity Programs
3 Vaccination Programs
Vaccination (Broiler Breeders)
Purpose
1 Prevent VA in the breeders
2 Prevent egg transmission to progeny
3 Produce maternal antibodies for the progeny
Vaccination Strategies (Broiler Breeders)
Program 1 1st Live 1-2 Wks SQWater
1st2nd Live 3-8 W SQWaterWingweb
2nd3rd Live 8-16 Wks SQWaterWingweb
Program 2 1st Live 1 week SQWater
2nd Live 3-4 Wks SQWater
2nd3rd Live 6-8 Wks SQWingwebWater
1st Killed 10-14 Wks SQIM
2nd Killed 14-20 Wks SQIM
Prevention
Select birds that are leukosis virus negative using serologic
methods to prevent spread of the disease
Treatment
None
Special note
It is immunosuppressive and a major cause of condemnation
in adult broiler breeders and layers Tumors are a common
cause of condemnation in layer processing plants
PoxviridaeOrthopoxvirus (image)
bull Largest and most complex of all viruses
bull Brick shaped
bull 250 x 200 x 200 nm in size
bull Parapoxviridae are OVOID 260 x 160 nm
bull Virions are complex
bull Core
bull Lateral bodies
bull Outer membrane
bull + - envelope
bull Core ndashDumbbell shaped Contains viral DNA viral proteins
bull Lateral bodies ndash unknown nature
bull + - Envelope
bull Genome is linear and double stranded
bull Largest genome of any animal virus
bull Encodes all transcription and replication enzymes needed for viral genome
Poxviridae ndash Subfamilies and Generabull Orthopoxvirus ndash vaccinia
bull Parapoxvirus ndash pseudocowpox virus
bull Avipoxvirus ndash fowlpox virus
bull Capripoxvirus ndash sheeppox virus
bull Leporipoxvirus ndash Leooripoxvirus
bull Suiposvirus ndash Swinepox virus
bull Molluscipoxvirus ndash Myxoma virus
bull Yabapoxvirus ndash Yaba monkey tumor virus
bull Subfamily Entomopoxvirinae ndash contains viruses of insects
bull Viral replication ndash cytoplasm
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Malabsorption syndrome
1 RuntingStunting
2 Poor pigmentation
3 Abnormal feathering
4 Skeletal abnormalities
5 Increased mortality
6 Enlarged proventriculus
Clinical SignsGross Lesions
Viral arthritistenosynovitis
1 Lameness
2 Joint swelling
3 Thickenedruptured tendons
Post-mortem Findings
ndash Rupture of the gastrocnemius tendon----------green discoloration of the skin at the join
ndash Erosion articular cartilage
bull Ptechie in synovial membranes
bull clear fluid in capsula-------2nd infection
ndash Rupture digital flexor tendons
ndash Gastrointestinal Distention (fluid and gas) pancreas atrophy proventriculus dilatation
Histopathology
bullEosinophilic intracytoplasmic inclusion bodies in
liver
bullThickening of the tendon oedema hypertrophy and
hyperplasia of the synoviocytes
bullVillous proliferation and invasion imflamatory cells
of the synovial membranes
bull PathogenicityReoviruses have been identified as the etiology of other disease
conditions such as
1 Arthritistenosynovitis
2 Runtingstunting
3Pericarditismyocarditishydropericardium
4 Hepatitis
5 Bursal and thymus atrophy
Prevention Strategies
1 Good Husbandry Programs
2 Biosecurity Programs
3 Vaccination Programs
Vaccination (Broiler Breeders)
Purpose
1 Prevent VA in the breeders
2 Prevent egg transmission to progeny
3 Produce maternal antibodies for the progeny
Vaccination Strategies (Broiler Breeders)
Program 1 1st Live 1-2 Wks SQWater
1st2nd Live 3-8 W SQWaterWingweb
2nd3rd Live 8-16 Wks SQWaterWingweb
Program 2 1st Live 1 week SQWater
2nd Live 3-4 Wks SQWater
2nd3rd Live 6-8 Wks SQWingwebWater
1st Killed 10-14 Wks SQIM
2nd Killed 14-20 Wks SQIM
Prevention
Select birds that are leukosis virus negative using serologic
methods to prevent spread of the disease
Treatment
None
Special note
It is immunosuppressive and a major cause of condemnation
in adult broiler breeders and layers Tumors are a common
cause of condemnation in layer processing plants
PoxviridaeOrthopoxvirus (image)
bull Largest and most complex of all viruses
bull Brick shaped
bull 250 x 200 x 200 nm in size
bull Parapoxviridae are OVOID 260 x 160 nm
bull Virions are complex
bull Core
bull Lateral bodies
bull Outer membrane
bull + - envelope
bull Core ndashDumbbell shaped Contains viral DNA viral proteins
bull Lateral bodies ndash unknown nature
bull + - Envelope
bull Genome is linear and double stranded
bull Largest genome of any animal virus
bull Encodes all transcription and replication enzymes needed for viral genome
Poxviridae ndash Subfamilies and Generabull Orthopoxvirus ndash vaccinia
bull Parapoxvirus ndash pseudocowpox virus
bull Avipoxvirus ndash fowlpox virus
bull Capripoxvirus ndash sheeppox virus
bull Leporipoxvirus ndash Leooripoxvirus
bull Suiposvirus ndash Swinepox virus
bull Molluscipoxvirus ndash Myxoma virus
bull Yabapoxvirus ndash Yaba monkey tumor virus
bull Subfamily Entomopoxvirinae ndash contains viruses of insects
bull Viral replication ndash cytoplasm
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Clinical SignsGross Lesions
Viral arthritistenosynovitis
1 Lameness
2 Joint swelling
3 Thickenedruptured tendons
Post-mortem Findings
ndash Rupture of the gastrocnemius tendon----------green discoloration of the skin at the join
ndash Erosion articular cartilage
bull Ptechie in synovial membranes
bull clear fluid in capsula-------2nd infection
ndash Rupture digital flexor tendons
ndash Gastrointestinal Distention (fluid and gas) pancreas atrophy proventriculus dilatation
Histopathology
bullEosinophilic intracytoplasmic inclusion bodies in
liver
bullThickening of the tendon oedema hypertrophy and
hyperplasia of the synoviocytes
bullVillous proliferation and invasion imflamatory cells
of the synovial membranes
bull PathogenicityReoviruses have been identified as the etiology of other disease
conditions such as
1 Arthritistenosynovitis
2 Runtingstunting
3Pericarditismyocarditishydropericardium
4 Hepatitis
5 Bursal and thymus atrophy
Prevention Strategies
1 Good Husbandry Programs
2 Biosecurity Programs
3 Vaccination Programs
Vaccination (Broiler Breeders)
Purpose
1 Prevent VA in the breeders
2 Prevent egg transmission to progeny
3 Produce maternal antibodies for the progeny
Vaccination Strategies (Broiler Breeders)
Program 1 1st Live 1-2 Wks SQWater
1st2nd Live 3-8 W SQWaterWingweb
2nd3rd Live 8-16 Wks SQWaterWingweb
Program 2 1st Live 1 week SQWater
2nd Live 3-4 Wks SQWater
2nd3rd Live 6-8 Wks SQWingwebWater
1st Killed 10-14 Wks SQIM
2nd Killed 14-20 Wks SQIM
Prevention
Select birds that are leukosis virus negative using serologic
methods to prevent spread of the disease
Treatment
None
Special note
It is immunosuppressive and a major cause of condemnation
in adult broiler breeders and layers Tumors are a common
cause of condemnation in layer processing plants
PoxviridaeOrthopoxvirus (image)
bull Largest and most complex of all viruses
bull Brick shaped
bull 250 x 200 x 200 nm in size
bull Parapoxviridae are OVOID 260 x 160 nm
bull Virions are complex
bull Core
bull Lateral bodies
bull Outer membrane
bull + - envelope
bull Core ndashDumbbell shaped Contains viral DNA viral proteins
bull Lateral bodies ndash unknown nature
bull + - Envelope
bull Genome is linear and double stranded
bull Largest genome of any animal virus
bull Encodes all transcription and replication enzymes needed for viral genome
Poxviridae ndash Subfamilies and Generabull Orthopoxvirus ndash vaccinia
bull Parapoxvirus ndash pseudocowpox virus
bull Avipoxvirus ndash fowlpox virus
bull Capripoxvirus ndash sheeppox virus
bull Leporipoxvirus ndash Leooripoxvirus
bull Suiposvirus ndash Swinepox virus
bull Molluscipoxvirus ndash Myxoma virus
bull Yabapoxvirus ndash Yaba monkey tumor virus
bull Subfamily Entomopoxvirinae ndash contains viruses of insects
bull Viral replication ndash cytoplasm
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Post-mortem Findings
ndash Rupture of the gastrocnemius tendon----------green discoloration of the skin at the join
ndash Erosion articular cartilage
bull Ptechie in synovial membranes
bull clear fluid in capsula-------2nd infection
ndash Rupture digital flexor tendons
ndash Gastrointestinal Distention (fluid and gas) pancreas atrophy proventriculus dilatation
Histopathology
bullEosinophilic intracytoplasmic inclusion bodies in
liver
bullThickening of the tendon oedema hypertrophy and
hyperplasia of the synoviocytes
bullVillous proliferation and invasion imflamatory cells
of the synovial membranes
bull PathogenicityReoviruses have been identified as the etiology of other disease
conditions such as
1 Arthritistenosynovitis
2 Runtingstunting
3Pericarditismyocarditishydropericardium
4 Hepatitis
5 Bursal and thymus atrophy
Prevention Strategies
1 Good Husbandry Programs
2 Biosecurity Programs
3 Vaccination Programs
Vaccination (Broiler Breeders)
Purpose
1 Prevent VA in the breeders
2 Prevent egg transmission to progeny
3 Produce maternal antibodies for the progeny
Vaccination Strategies (Broiler Breeders)
Program 1 1st Live 1-2 Wks SQWater
1st2nd Live 3-8 W SQWaterWingweb
2nd3rd Live 8-16 Wks SQWaterWingweb
Program 2 1st Live 1 week SQWater
2nd Live 3-4 Wks SQWater
2nd3rd Live 6-8 Wks SQWingwebWater
1st Killed 10-14 Wks SQIM
2nd Killed 14-20 Wks SQIM
Prevention
Select birds that are leukosis virus negative using serologic
methods to prevent spread of the disease
Treatment
None
Special note
It is immunosuppressive and a major cause of condemnation
in adult broiler breeders and layers Tumors are a common
cause of condemnation in layer processing plants
PoxviridaeOrthopoxvirus (image)
bull Largest and most complex of all viruses
bull Brick shaped
bull 250 x 200 x 200 nm in size
bull Parapoxviridae are OVOID 260 x 160 nm
bull Virions are complex
bull Core
bull Lateral bodies
bull Outer membrane
bull + - envelope
bull Core ndashDumbbell shaped Contains viral DNA viral proteins
bull Lateral bodies ndash unknown nature
bull + - Envelope
bull Genome is linear and double stranded
bull Largest genome of any animal virus
bull Encodes all transcription and replication enzymes needed for viral genome
Poxviridae ndash Subfamilies and Generabull Orthopoxvirus ndash vaccinia
bull Parapoxvirus ndash pseudocowpox virus
bull Avipoxvirus ndash fowlpox virus
bull Capripoxvirus ndash sheeppox virus
bull Leporipoxvirus ndash Leooripoxvirus
bull Suiposvirus ndash Swinepox virus
bull Molluscipoxvirus ndash Myxoma virus
bull Yabapoxvirus ndash Yaba monkey tumor virus
bull Subfamily Entomopoxvirinae ndash contains viruses of insects
bull Viral replication ndash cytoplasm
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Histopathology
bullEosinophilic intracytoplasmic inclusion bodies in
liver
bullThickening of the tendon oedema hypertrophy and
hyperplasia of the synoviocytes
bullVillous proliferation and invasion imflamatory cells
of the synovial membranes
bull PathogenicityReoviruses have been identified as the etiology of other disease
conditions such as
1 Arthritistenosynovitis
2 Runtingstunting
3Pericarditismyocarditishydropericardium
4 Hepatitis
5 Bursal and thymus atrophy
Prevention Strategies
1 Good Husbandry Programs
2 Biosecurity Programs
3 Vaccination Programs
Vaccination (Broiler Breeders)
Purpose
1 Prevent VA in the breeders
2 Prevent egg transmission to progeny
3 Produce maternal antibodies for the progeny
Vaccination Strategies (Broiler Breeders)
Program 1 1st Live 1-2 Wks SQWater
1st2nd Live 3-8 W SQWaterWingweb
2nd3rd Live 8-16 Wks SQWaterWingweb
Program 2 1st Live 1 week SQWater
2nd Live 3-4 Wks SQWater
2nd3rd Live 6-8 Wks SQWingwebWater
1st Killed 10-14 Wks SQIM
2nd Killed 14-20 Wks SQIM
Prevention
Select birds that are leukosis virus negative using serologic
methods to prevent spread of the disease
Treatment
None
Special note
It is immunosuppressive and a major cause of condemnation
in adult broiler breeders and layers Tumors are a common
cause of condemnation in layer processing plants
PoxviridaeOrthopoxvirus (image)
bull Largest and most complex of all viruses
bull Brick shaped
bull 250 x 200 x 200 nm in size
bull Parapoxviridae are OVOID 260 x 160 nm
bull Virions are complex
bull Core
bull Lateral bodies
bull Outer membrane
bull + - envelope
bull Core ndashDumbbell shaped Contains viral DNA viral proteins
bull Lateral bodies ndash unknown nature
bull + - Envelope
bull Genome is linear and double stranded
bull Largest genome of any animal virus
bull Encodes all transcription and replication enzymes needed for viral genome
Poxviridae ndash Subfamilies and Generabull Orthopoxvirus ndash vaccinia
bull Parapoxvirus ndash pseudocowpox virus
bull Avipoxvirus ndash fowlpox virus
bull Capripoxvirus ndash sheeppox virus
bull Leporipoxvirus ndash Leooripoxvirus
bull Suiposvirus ndash Swinepox virus
bull Molluscipoxvirus ndash Myxoma virus
bull Yabapoxvirus ndash Yaba monkey tumor virus
bull Subfamily Entomopoxvirinae ndash contains viruses of insects
bull Viral replication ndash cytoplasm
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
bull PathogenicityReoviruses have been identified as the etiology of other disease
conditions such as
1 Arthritistenosynovitis
2 Runtingstunting
3Pericarditismyocarditishydropericardium
4 Hepatitis
5 Bursal and thymus atrophy
Prevention Strategies
1 Good Husbandry Programs
2 Biosecurity Programs
3 Vaccination Programs
Vaccination (Broiler Breeders)
Purpose
1 Prevent VA in the breeders
2 Prevent egg transmission to progeny
3 Produce maternal antibodies for the progeny
Vaccination Strategies (Broiler Breeders)
Program 1 1st Live 1-2 Wks SQWater
1st2nd Live 3-8 W SQWaterWingweb
2nd3rd Live 8-16 Wks SQWaterWingweb
Program 2 1st Live 1 week SQWater
2nd Live 3-4 Wks SQWater
2nd3rd Live 6-8 Wks SQWingwebWater
1st Killed 10-14 Wks SQIM
2nd Killed 14-20 Wks SQIM
Prevention
Select birds that are leukosis virus negative using serologic
methods to prevent spread of the disease
Treatment
None
Special note
It is immunosuppressive and a major cause of condemnation
in adult broiler breeders and layers Tumors are a common
cause of condemnation in layer processing plants
PoxviridaeOrthopoxvirus (image)
bull Largest and most complex of all viruses
bull Brick shaped
bull 250 x 200 x 200 nm in size
bull Parapoxviridae are OVOID 260 x 160 nm
bull Virions are complex
bull Core
bull Lateral bodies
bull Outer membrane
bull + - envelope
bull Core ndashDumbbell shaped Contains viral DNA viral proteins
bull Lateral bodies ndash unknown nature
bull + - Envelope
bull Genome is linear and double stranded
bull Largest genome of any animal virus
bull Encodes all transcription and replication enzymes needed for viral genome
Poxviridae ndash Subfamilies and Generabull Orthopoxvirus ndash vaccinia
bull Parapoxvirus ndash pseudocowpox virus
bull Avipoxvirus ndash fowlpox virus
bull Capripoxvirus ndash sheeppox virus
bull Leporipoxvirus ndash Leooripoxvirus
bull Suiposvirus ndash Swinepox virus
bull Molluscipoxvirus ndash Myxoma virus
bull Yabapoxvirus ndash Yaba monkey tumor virus
bull Subfamily Entomopoxvirinae ndash contains viruses of insects
bull Viral replication ndash cytoplasm
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Prevention Strategies
1 Good Husbandry Programs
2 Biosecurity Programs
3 Vaccination Programs
Vaccination (Broiler Breeders)
Purpose
1 Prevent VA in the breeders
2 Prevent egg transmission to progeny
3 Produce maternal antibodies for the progeny
Vaccination Strategies (Broiler Breeders)
Program 1 1st Live 1-2 Wks SQWater
1st2nd Live 3-8 W SQWaterWingweb
2nd3rd Live 8-16 Wks SQWaterWingweb
Program 2 1st Live 1 week SQWater
2nd Live 3-4 Wks SQWater
2nd3rd Live 6-8 Wks SQWingwebWater
1st Killed 10-14 Wks SQIM
2nd Killed 14-20 Wks SQIM
Prevention
Select birds that are leukosis virus negative using serologic
methods to prevent spread of the disease
Treatment
None
Special note
It is immunosuppressive and a major cause of condemnation
in adult broiler breeders and layers Tumors are a common
cause of condemnation in layer processing plants
PoxviridaeOrthopoxvirus (image)
bull Largest and most complex of all viruses
bull Brick shaped
bull 250 x 200 x 200 nm in size
bull Parapoxviridae are OVOID 260 x 160 nm
bull Virions are complex
bull Core
bull Lateral bodies
bull Outer membrane
bull + - envelope
bull Core ndashDumbbell shaped Contains viral DNA viral proteins
bull Lateral bodies ndash unknown nature
bull + - Envelope
bull Genome is linear and double stranded
bull Largest genome of any animal virus
bull Encodes all transcription and replication enzymes needed for viral genome
Poxviridae ndash Subfamilies and Generabull Orthopoxvirus ndash vaccinia
bull Parapoxvirus ndash pseudocowpox virus
bull Avipoxvirus ndash fowlpox virus
bull Capripoxvirus ndash sheeppox virus
bull Leporipoxvirus ndash Leooripoxvirus
bull Suiposvirus ndash Swinepox virus
bull Molluscipoxvirus ndash Myxoma virus
bull Yabapoxvirus ndash Yaba monkey tumor virus
bull Subfamily Entomopoxvirinae ndash contains viruses of insects
bull Viral replication ndash cytoplasm
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Prevention
Select birds that are leukosis virus negative using serologic
methods to prevent spread of the disease
Treatment
None
Special note
It is immunosuppressive and a major cause of condemnation
in adult broiler breeders and layers Tumors are a common
cause of condemnation in layer processing plants
PoxviridaeOrthopoxvirus (image)
bull Largest and most complex of all viruses
bull Brick shaped
bull 250 x 200 x 200 nm in size
bull Parapoxviridae are OVOID 260 x 160 nm
bull Virions are complex
bull Core
bull Lateral bodies
bull Outer membrane
bull + - envelope
bull Core ndashDumbbell shaped Contains viral DNA viral proteins
bull Lateral bodies ndash unknown nature
bull + - Envelope
bull Genome is linear and double stranded
bull Largest genome of any animal virus
bull Encodes all transcription and replication enzymes needed for viral genome
Poxviridae ndash Subfamilies and Generabull Orthopoxvirus ndash vaccinia
bull Parapoxvirus ndash pseudocowpox virus
bull Avipoxvirus ndash fowlpox virus
bull Capripoxvirus ndash sheeppox virus
bull Leporipoxvirus ndash Leooripoxvirus
bull Suiposvirus ndash Swinepox virus
bull Molluscipoxvirus ndash Myxoma virus
bull Yabapoxvirus ndash Yaba monkey tumor virus
bull Subfamily Entomopoxvirinae ndash contains viruses of insects
bull Viral replication ndash cytoplasm
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
PoxviridaeOrthopoxvirus (image)
bull Largest and most complex of all viruses
bull Brick shaped
bull 250 x 200 x 200 nm in size
bull Parapoxviridae are OVOID 260 x 160 nm
bull Virions are complex
bull Core
bull Lateral bodies
bull Outer membrane
bull + - envelope
bull Core ndashDumbbell shaped Contains viral DNA viral proteins
bull Lateral bodies ndash unknown nature
bull + - Envelope
bull Genome is linear and double stranded
bull Largest genome of any animal virus
bull Encodes all transcription and replication enzymes needed for viral genome
Poxviridae ndash Subfamilies and Generabull Orthopoxvirus ndash vaccinia
bull Parapoxvirus ndash pseudocowpox virus
bull Avipoxvirus ndash fowlpox virus
bull Capripoxvirus ndash sheeppox virus
bull Leporipoxvirus ndash Leooripoxvirus
bull Suiposvirus ndash Swinepox virus
bull Molluscipoxvirus ndash Myxoma virus
bull Yabapoxvirus ndash Yaba monkey tumor virus
bull Subfamily Entomopoxvirinae ndash contains viruses of insects
bull Viral replication ndash cytoplasm
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Poxviridae ndash Subfamilies and Generabull Orthopoxvirus ndash vaccinia
bull Parapoxvirus ndash pseudocowpox virus
bull Avipoxvirus ndash fowlpox virus
bull Capripoxvirus ndash sheeppox virus
bull Leporipoxvirus ndash Leooripoxvirus
bull Suiposvirus ndash Swinepox virus
bull Molluscipoxvirus ndash Myxoma virus
bull Yabapoxvirus ndash Yaba monkey tumor virus
bull Subfamily Entomopoxvirinae ndash contains viruses of insects
bull Viral replication ndash cytoplasm
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Avian Pox
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Morbidity + Mortality
bull Avipoxvirus
bull WW all ages
bull Break in skin allows virus in infected scabs can contaminate the environment
bull Cutaneous formndash Papule Vesicle Pustule Scab
bull Diptheritic formndash Space occupying plaque in upper GI
and Resp
ndash May cause suffocation
bull Cutaneous form- 1-2 mort
bull Diptheritic form- up to 40 mort
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Poxviridae Avipoxvirus ndash Fowlpox virus
bull Causes disease in chickens turkeys guinea fowl peacocks pheasants and other avian species
bull Exact relationship between the poxviruses of the different avian species is not certain but it has been shown experimentally that the virus causing one type of pox can give rise to disease in other species and that infection with one may stimulate protection against another
bull Eg milk maids
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
PoxviridaeAvipoxirus ndash Fowlpox virus
bull Distribution ndash worldwide
bull Hosts ndash chickens turkeys pigeons pheasants etc
bull Etiologic agent ndash Avipoxvirus extremely resistant to dessication and can survive in exfoliated scabs for prolonged periods
bull Inclusions bodies ndash Bollinger Bodies ndash large intracytoplasmic inclusions ndash Borrel bodies ndashelementary bodies occur inside the Bollinger bodies
bull Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies
bull Transmission ndash occurs through small abrasions in the mouth or through injuries to the comb wattle as a result of fighting pecking or other injuries
bull Mechanical transmission by mosquitoes ticks biting flies and lice
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Avian Pox Continued
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Intracytoplasmic eosinophilic inclusion bodies viral isolation ELISA viral material will produce lesions in fertile chicken eggs
bull Recovery gives long immunity live vax eliminate cannibalism with beak trimming
bull No treatment
bull Live vax
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Poxviridae ndash Epidemiology Pathogenesis and Immunity
bull Epidemiology bull Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabsbull Poxviruses are transmitted between animals by skin abrasions aerosol to the
URT mechanical transmission by arthropods
bull Pathogenesis and Immunity bull Highly epitheliotropic ndash causing cutaneous and systemic disease in birds and
wild and domestic mammalsbull Many are host specific but orthopoxviruses infect a wide range of hostsbull After cutaneous introduction or inhalation ndash the virus gains access to the
systemic circulation through the lymphatics bull Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia bull Secondary viremia disseminates the virus back to the skin and other target
organs
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
PoxviridaePathogenesis Immunity
bull Poxviruses induce lesions by a variety of mechanisms
bull Degenerative changes in the epithelium
bull Lesions start as erytheamatous macules become papular and then vesicular
bull Vesicles develop into umbilicated pustules ndash POCK LESION
bull Pustules rupture and for a crustscab
bull Lesions heal and leave a scar
bull Rupture of the pustule can lead to secondary bacterial infection
bull Proliferative lesions
bull Poxviruses replicating in epidermis may result in virus induced (encoded epidermal growth factor) cellular hyperplasia
bull Poxviruses encode proteins which may counteract host defenses
bull Immunity ndash varies from short lived like in parapoxvirus infections to prolonged in others
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
PoxviridaeDiagnosis
bull Virus isolation
bull Scrapings from skin lesions vesicular lesions and crusts
bull Chorioallantoic membrane
bull Pock lesions ndash not parapoxviruses ndash DO NOT replicate in embryonated eggs
bull Cell culture
bull Poxviruse grow in a variety of cell cultures
bull Virus identification
bull Negative stain electron microscopy ndash FAT etc
bull Histopathology
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Infectious Laryngotracheitis
bull Penyebab Herpesvirus
bull Sensitivity mild (halogen-detergents + iodophors heating freezing (-18deg -25deg C )
bull Acute respiratory disease
bull ConjunctivitisLaryngitisTracheitis(Histopathology intranuclear inclusion body in epithelial cells by 3 day PI)
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Avian infectious laryngotracheitis virus
bull Acute disease of chicken pheasants (3-9 month)
bull Respiration problems bloody mucous secretion
bull Conjunctivitis - panophtalmitis
bull Mild - peracute disease
bull Antigenic uniformity strains differ in virulence
bull Impact of environment (iritation of resptract low
temperature concurrent infections)
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Laryngs(left - normal) (medium - hyperemic) (right - fibrin)
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Avian infectious laryngotracheitis virus
bull Virus latency ndash in infected and vaccinated animals
bull Rezidual pathogenicity of vaccine strains
bull Cell immunity ndash non-transmissible to the newborns
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Avian infectious laryngotracheitis virus
Samples 4-6 living animals
trachea larynx - chilled not frozen
Diagnostics
bull IN inklusions - trachea
bull IF test ndash trachea
bull Izolation on EE (CAM) IFA identification
bull Differentiation of vaccine and field strains by REA
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Laryngotracheitis
bull Synonyms infectious laryngotracheitis (ILT)avian diphtheria
History
bull First described 1925
bull Perhaps observed earlier
bull Isolated (1930)
bull Named by AVMA (1931)
bull Caused by filterable virus (Beaudette 1937)
bull First major effective avian virus vaccine
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
REPLIKASI VIRUS PROSES REPLIKASI TERJADI DI NUCLEUS Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-
independent endocytosis Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang DNA virus tersebut ditranskripsi menjadi mRNAs virus mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein yang akanmemproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untukproses trankripsi dan replikasib) akan dibungkus oleh kapsid protein dan meghasilkan virus baru virus tersebut dilepaskan dari sel melalui budding
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Laryngotracheitis ndashIncidence and Distribution
bull Worldwide distributionbull Intensive rearingbull Controlbull Layers and breedersbull Typically well vaccinatedcontrolledbull Broilersbull Short life cycle often not vaccinated unless regionalbull problemsbull NicheFanciersbull May be endemic in some flocks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Laryngotracheitis ndashHosts
bull Primarily in chickens
bull Usually older birds
bull Respiratory tract viremia unlikely
bull Pheasants amp pheasant crosses (sporadic)
bull Peafowl (rare isolate)
bull Turkeys (experimental)
bull Other birds resistant (ducks pigeons doves
sparrows crows starlings guinea fowl) May still carry virus mechanically
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Laryngotracheitis ndashEconomic Significance
bull Not determinedbull Estimated millions of $$$ in USbull Mortalitybull Decreased productionbull Meat eggs breeder potential increased down timebull Uniformity feed conversionbull Processing issuesbull Vaccination (vaccines labor)bull Waste disposal amp storagebull Labor (service responsibilities transport cleaning and
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Laryngotracheitis ndash Etiology
bull Alphaherpesvirusbull Morphologycompositionbull Similar to other Alphaherpes virusesbull Double stranded DNA (155kb)bull Envelopedbull Glycoprotein spikes (humoral and cell mediated
immunity)bull Shape Icosahedralbull Size 195-250 nmbull Similar to MDV
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Laryngotracheitis ndash Strain classification
bull Importance differentiation of wild-type field strains vs modified live vaccine strain
bull Antigenically homogenous Differ in pathogenicity
Laryngotracheitis ndash PhysicalChemical Susceptibilitybull Susceptible to heatbull 100F (48 hours)bull 155F (15min )bull Susceptible to many chemicalsbull Chloroform ether iodophors cresols lyebull Hydrogen peroxide mistfumigant (5)
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Laryngotracheitis ndash Pathogenesis
bull Portal of entry Upper respiratoryocularIngestion rarr nasal epithelium
bull Horizontal transmissionbull Aerosolization of virusbull Birds feed waterbull Contaminated litterbull Fomites (equipment boots clothes tires)bull Moves slowly through flockbull No vertical or egg transmission known
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Laryngotracheitis ndash Pathogenesis
bull Virus present in trachea for 6-10 days PIbull Inflammation and necrosis (tracheal cores)bull Necrotic cells blood inflammatory debrisbull High virus shed during infectionbull Leads to Death (asphyxiation)Latent carriersbull Latent carriers Trigeminal ganglion + tracheal epitheliumPersistent infection amp intermittent shedding
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
bull Laryngotracheitis ndash Pathogenesis
bull Spread to trigeminal ganglion 4-7 days PI
bull Found to be latent for up to 15 months
bull Stress may cause virus to recrudesce
Movement reproduction etc
Carriers in flock for 16 months
bull racheal swabs ~ 2
bull Organ cultures ~ 50
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
bull Laryngotracheitis ndashClinical SignsAcute respiratory diseasebull 1048708 Conjunctivitis ndash almond eye (often first signs)bull 1048708 Nasal dischargebull 1048708 Moist rales coughing gaspingbull 1048708 Dyspneabull 1048708 Expectoration of blood (only in severe infections)bull 1048708 Decreased productionbull 1048708 Egg production 5-15 no problems with shell qualitybull 1048708 Unthrifty birdsbull 1048708 Recovery in ~7-28 days (usually 10-14 days)bull 1048708 Duration ~2-6 weeks in flockbull
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Laryngotracheitis ndash Clinical Signs
bull Incubation 6-12 days post infection (PI)
bull 2-4 days experimentally
bull Severe
bull 90-100 morbidity
bull 5-70 mortality (usually 10-20)
Mild (lsquosilent LTrsquo)
bull As low as 5 morbidity and 01 mortality
bull Males slightly more susceptible
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
38
Adenoviruses aden = gland (Greek)
Key Features
1 Icosahedral capsid (80 nm)
2 Larger dsDNA genome (35 kbp) 30-40 genes
3 Encodes own DNA polymerase and factors that regulate cellular processes
4 Many animals are infected by multiple serotypes
5 Mainly associated with mild respiratory disease
6 Highly immunogenic Fairly resistant
Adenoviruses
first isolated from adenoid tissue
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
39
Adenoviruses
Adenovirus Structure
hexon
pentonfibre
terminal protein
DNA
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
40
Adenoviruses
Importance of Adenoviral capsid
1 Fibre and penton bind to proteins on the cell surface- determine tissueinfectivity
2 Adenoviruses can cause red blood cells to clump (haemagglutination)Mediated by the fibre Used for diagnosis- haemagglutination-inhibition(HI) test
3 Hexon is the most abundant capsid protein and the major target for theinfected animalrsquos immune system Immunity is long-lasting
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Egg Drop Syndrome lsquo76
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs + Lesions
bull Diagnosis
bull Vaccine
bull Adenovirus Infection Type 3
bull Chicken layers + ducks
bull Pharynx and feces
bull Loss of color in pigmented eggs drop in egg production thin to shell less eggs rough shell inactive and atrophied oviducts edema in uterus
bull Viral Isolation
bull Inactivated vax 14-16wk pullets
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
42
Adenoviruses
Avian Adenoviruses
1 Egg drop syndrome(EDS76)- first reported in1976 Infects pouch shellgland with soft-shelled andshell-less eggs producedwith no clinical signsEffectively eradicated frommost countries
2 Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marblespleen disease of pheasants Also causes immunosuppression Controlledby vaccination
3 Avian adenovirus 1- causes bronchitis in quails Control by isolation anddecontamination
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
43
INFECTIOUS BRONCHITIS
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
44
SIFAT VIRUS IB
bullVIRUS CORONA
bullLABIL MUDAH MATI
bullMUDAH BERMUTASI
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
45
SIFAT VIRUS IB
bull AYAM YANG SEMBUH MASIH MENGELUARKAN VIRUS HINGGA BEBERAPA MINGGU
bull SERANGAN SAAT MUDA MENYEBABKAN AYAM CACAT PERMANEN PADA OVIDUCT
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
46
SIFAT PENYAKIT IB
bull AKUT
bull SANGAT CEPAT MENULAR
bull SELURUH DUNIA TERPAPAR
bull MENYERANG UMUMNYA AYAM MUDA
bull MENYERANG SALURAN REPRODUKSI
bull DAPAT MENYERANG GINJAL
bull MENURUNKAN PRODUKSI TELUR
bull MENURUNKAN KUALITAS TELUR
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
47
2 Infectious Bronchitis (IB)
Gejala klinis pernafasan
Ginjal pembendungan kadang ada endapan asam urat
Ayam masa produksi yang mati ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm keadaan pecah
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
48
Perubahan Patologi
Cangkang telur tipisBentuk telur yang abnormal
Perubahan Bentuk Telur
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
49
ANTIGEN PERMUKAAN
MUDAH BERUBAH
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Avian Infectious Bronchitis
bull Cause
bull Age group affected
bull Transmission
bull Clinical Signs
bull Coronavirus
bull Chickens only all ages
bull Inhalation of virus containing droplets carriers survive up to 4 wks in environment
bull Marked decrease in egg prod soft shelled eggs with watery albimen gasping resp sneezing coughing
Most common URI
in the US
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
AIB continued
bull Lesions
bull Morbidity + Mortality
bull Diagnosis
bull Control + Prevention
bull Treatment
bull Vaccine
bull Cheesy exudate at tracheal bifurcation ocular and nasal discharge in young chicks
bull Morbidity 100 Mortality 50
bull Viral isolation ELISA
bull Vax
bull No effective tx broad spectrum ABrsquos may prevent complications
bull Modified live or killed Vax
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
52
VAKSIN IDEALNYA MAMPU MENCIPTAKAN
ldquoIMUNITAS YANG MENSTERILKANrdquo
BUKAN UNTUK IB ATAU PENYAKIT LAIN YANG HIDUPNYA DI MUKOSA
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
FACTORS INFLUENCING SUSCEPTIBILITY
bull Virusbull Strain
bull Dosage
bull Route of exposure
bull Hostbull Age Common in birds 12-24 weeks of age
bull Sex Female are more susceptible
bull Immune status
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Avian encephalomyelitis
bull Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors) Primarily a viral infection of poultry chickens turkey and pheasants
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Kingdom Virus
Family Picornaviridae
Genus Hepatovirus
Species Avian encephalomyelitis-like virus 1
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Avian encephalomyelitis
bull First reported in 1932 the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens Most prevalent in chickens 1 to 6 weeks of age
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
bull Susceptible chickens more than 5 weeks old will develop antibodies to AE but do not show clinical signs at the time of infection
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
bull AE occurs world wide and occurs in all seasons of the year but most cases are reported from January to June
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
bull Egg-passage transmission from infected hen to chick is the most common mode of spread but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock Indirect spread via fecal contamination of feed and water also occurs The virus can survive at least 4 weeks in droppings
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
Clinical signs
bull Clinical signs appear at 7 to 10 days of age Tremors of the head and neck are presumptive of the disease in the flock hence the name Epidemic tremor Affected chicks first may show a dull expression of the eyes followed by progressive in coordination sitting on hocks tremors of the head and neck and finally paralysis or prostration Muscular tremors are best seen by exercising the bird Affected birds are inactive some may refuse to walk or walk on their hocks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
bull Chickens of all ages are susceptible but clinical signs of encephalitis only develop in those younger than four weeks The disease is similar in turkeys and chickens Following initial dull expression of the eyes the following signs are seen
bull progressive ataxia with the chick losing control of legs sitting on its haunches and falling onto its side
bull tremor of the head and neckbull Ataxia progresses to paralysis and death results from
inability to feed or drink or through being trampled Some birds recover and others may survive with persistent clinical signs In susceptible adult birds infection is usually sub-clinical although there may be a transient drop in egg production
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
bull Diagnosis is confirmed by fluorescent antibody test virus isolation and agar gel precipitin test AE must be differentiated from other encephalitic diseases such as ND EEE MD etc
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
bull There is no treatment for acute outbreaks Control is through prevention Affected birds should be removed killed and incinerated Recovered chicks are unthrifty Prove good nursing during outbreaks will help with mortality Prevention is by selecting hatching eggs from immune breeder flocks Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks
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