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Viral Disease in Ruminant
Sukolrat Boonyayatra
DVM, M.S.
Clinic for Ruminant, FVM. CMU.
Disease topic including:
Bovine Ephemeral Fever Bovine Respiratory Syncytial Virus Parainfluenza-3 Bovine Viral Diarrhea Infectious Bovine Rhinotracheitis Foot and Mouth Disease Bovine Spongioform Encephalopathy Rinderpest Lumpy Skin Disease Papillomavirus Pseudocowpox
BOVINE EPHEMERAL FEVER
(Three-day sickness, Bovine Epizootic Fever, Three-day stiffsickness,
Dragon boat disease)
Definition
a noncontagious epizootic arthropod-borne viral disease
cattle and water buffaloes sudden onset of fever depression stiffness lameness rapid recovery
Etiology
Family Rhabdoviridae1. Genus Vesiculovirus
Type Species vesicular stomatitis Indiana virus
2. Genus LyssavirusType Species rabies virus
3. Genus EphemerovirusType Species Bovine ephemeral fever virus
4. Genus CytorhabdovirusType Species lettuce necrotic yellows virus
5. Genus NucleorhabdovirusType Species potato yellow dwarf virus
Epidemiology
first described in South Africa in 1906 tropical, subtropical, and temperate countries
in Africa, Asia, and Australia Thailand since 1984
Transmission
Insect bite not spread from cow to cow
Culicoides Mosquitoes
Clinical Signs (1)
Depressed High fever (105-107 F) with biphasic or
triphasic fever Serous ocular and nasal discharge Anorexia Decreased milk production Weight loss Stiffness and lameness More severe in high BW animals
Severe case
Muscle stiffness
Drag feet when forced to walk
Lying down, with hide limbs outstretched-
to relieve muscle cramp
Lie down for three days
Clinical Signs (2)
Morbidity may reach to 30% Low mortality Causes of the death
Pneumonia from secondary infection Muscle damaged and inflammation from long
period lying down Pregnancy toxemia (fatty liver syndrome)
Clinical Signs (3)
Gross lesions
the small amounts of fibrin-rich fluid in the pleural, peritoneal, pericardial cavities and joint capsules
the synovial surfaces of the spine may have fibrin plaques.
The lungs may have patchy edema. Lymphadenitis Focal necrosis can be found in major muscle
groups in some cases.
Hematology
an absolute rise in leukocyte numbers a rapid fall in circulating lymphocytes a return to normal levels after 3-4 days The serum fibrinogen level rises to 3-4 times the nor
mal level and returns to normal 1-2 weeks after recovery.
The total serum calcium level falls to 1.8 mmol-1 during the febrile phases and returns to normal on recovery.
This is the biochemical event that causes the reversible early paralysis.
Diagnosis
Clinical signs Sero-conversion: paired serum
SN test ELISA
Gross lesion
Differential Diagnosis
Bluetongue Babesiosis Blackleg
Treatment
Recovery with no treatment In severe cases
Anti-inflammatory drug: NSAIDs Fluid therapy and calcium Broad spectrum ABO
Recovery period 3-4 wks.
Prevention and Control
Vector control Vaccine: Attenuated lived virus vaccine
(Australia)
Bovine Respiratory Syncytial Virus (BRSV)
Bovine respiratory disease complex (BRD) Synergistically infect with bacteria to cause pneumonia
Pasteurella haemolytica P. multocida Haemophillus somnus
1960: The existence of BRSV 1970: Isolation of BRSV from an outbreak (Switzerland) 1974: Isolation of BRSV in USA 1978: An attenuated lived vaccine was available in Europe. 1984: An attenuated lived vaccine (USA) 1988: Inactivated vaccines were commercially available in USA
Etiology
Family Paramyxoviridae Genus Pneumovirus
Human Respiratory Syncytial Virus (HRSV) Bovine Respiratory Syncytial Virus (BRSV) Ovine Respiratory Syncytial Virus (ORSV) Turkey Rhinotracheitis virus
“Single stranded RNA virus that replicate in the cytoplasm and mature by budding from apical cell membrane”
Epidemiology
Worldwide distribution in the cattle population High seropositive ranging from 65-75%
(USA) before vaccine was introduced BRSV was determined to be involved in
14% of respiratory infections in UK 32% of outbreaks of calf pneumonia in North
Ireland 53% of respiratory outbreaks in Belgium 71% of the outbreaks of calf pneumonia in
Minnesota
Clinical signs Initial signs
A decreased appetite Milk depression Nasal and lacrimal discharge (serous to mucoid) Increased respiratory rate
Progress signs Elevated BT (104-108 F) Dyspnea Opened mouth breathing Hyperpnea (abdominal breathing) Cough Increased bronchial and bronchovesicular sounds, and fine crackles Decreased milk production
Duration of disease is variable, lasting from 1-2 weeks Calf :more severe
Postmortem findings
Atypical interstitial pneumonia (AIP) Gross findings:
Initially involves the cranioventral lobes Calves die from severe lung edema and interstitial
pneumonia Lung fail to collapse Subpleural emphysema Bronchial and mediastinal lymphnodes are
enlarged and edema.
Histopathological findings
Vary depending on stage of viral infection and the secondary bacterial infection
Bronchointerstitial pneumonia with severe bronchiolitis in cranioventral part
Alveolar edema and emphysema are diffusely present
Multinucleated syncytial cells (bronchiolar epithelium)
Bacterial pneumonia: suppurative or fibrous bronchopneuminia
Lung. Multinucleated syncytial cell is prominent within the bronchiole and appears to be arising from the epithelial layer. The lumen is packed with neutrophils. A few neutrophils are also transmigrating the bronchiolar wall and are in the adjacent atelectactic parenchyma. 40X
Immunohistochemistry staining
Pathogenesis (1)
Virus infects epithelial cells in the pulmonary airways
Cytopathic changes and necrosis Necrotizing bronchiolotis Alveolar epithelium: interstitial pheumonia Mixed inflammatory cell infiltration with a
predominance of neutrophils
May suppress the immune system Atypical interstitial pneumonia Necrotizing bronchiolitis:
Extensive viral replication at bronchiolar epithelium
Dyspnea and forced expiration Emphysema
Pathogenesis (2)
Immune response to infection Both dies and recovery from clinically severe
have antibody responses to proteins of virus (F and N): may not protective effect
Colostrum IgG-1 do not prevent the infection but make disease less severe
Cell-mediated immune responses may play a protective role
Differential diagnosis
Parainfluenza-3 IBR Mycoplasma spp. Haemophilus somnus etc…
Diagnosis
Clinical signs Necropsy Laboratory Diagnosis
Viral isolation Antigen Detection Enzyme ImmunoassayImmunofluorescent Antibody StainingDetection of Nucleic acids: PCRSerological Diagnosis
Treatment (1)
ABO: Bacterial pneumonia
- Pasteurella haemolytica P. multocida Haemophilus somnus
Anti-inflammatory agents Corticosteroid Antihistamine NSAIDs
Antiviral therapy: Ribivarin: HRSV Immunotherapy: Hyperimmune serum :
HRSV Supportive treatment
Dehydration and electrolyte imbalances Anorectic animals: B-complex vitamins
Treatment (2)
Prevention and Control
Management: Stress, ventilation, maternity pen, calf-rearing
area Immunization
Passive Immunization: Modify severity of disease Vaccination: Modified-lived BRSV vaccine
Inactivated BRSV vaccine
IBR, BRSV, PI-3, BVD killed vaccine + Haemophilus somnus bacterin
Killed vaccine protects against IBR, BVD, PI3 and BRSV, and Pasteurella haemolytica and Haemophilus.
Infectious Agents Identified in the Bovine Respiratory Disease Complex
Infectious Agents Identified in the Bovine Respiratory Disease ComplexViruses
- Bovine herpesvirus type1 (IBR)- Bovine herpesvirus type3 (malignant
catarrhal fever virus)- Bovine herpesvirus type4 (DN-599,
Movar 33/63)- Bovine adenovirus types1 to 8- Bovine parainfluenza virus type3- Bovine respiratory syncytial virus- Bovine viral diarrhea virus- Reovirus types1 to 3- Bovine Rhinovirus types1 and 2- Bovine Enterovirus types1 to 7- Calcivirus- Influenza virus (reported from Russia)
Viruses
- Bovine herpesvirus type1 (IBR)- Bovine herpesvirus type3 (malignant
catarrhal fever virus)- Bovine herpesvirus type4 (DN-599,
Movar 33/63)- Bovine adenovirus types1 to 8- Bovine parainfluenza virus type3- Bovine respiratory syncytial virus- Bovine viral diarrhea virus- Reovirus types1 to 3- Bovine Rhinovirus types1 and 2- Bovine Enterovirus types1 to 7- Calcivirus- Influenza virus (reported from Russia)
Bacteria
- Pasteurella haemolytica- Pasteurella multocida- Haemophilus somnus- Mycoplasma mycoides subspecies
mycoides- Mycoplasma bovis- Mycoplasma dispar- Ureaplasma spp.
Chlamydial agent
- Chlamydia psittaci
Bacteria
- Pasteurella haemolytica- Pasteurella multocida- Haemophilus somnus- Mycoplasma mycoides subspecies
mycoides- Mycoplasma bovis- Mycoplasma dispar- Ureaplasma spp.
Chlamydial agent
- Chlamydia psittaci
Parainfluenza-3 Virus (PI-3)
Enzootic Pneumonia Etiology
Family Paramyxoviridae Genus Paramyxovirus
Pathogenesis
Virus infects ciliated respiratory epithelium of the upper and lower respiratory tracts and also alveolar macrophage.
Reduce alveolar macrophage Facilitate pulmonary bacterial colonization Infection of calves is rarely fatal, producing
mild or subclinical cases.
Epidemiology
World wide distribution Subclinical Stress produce more severe clinical case Disease is commonly seen in calves 2-8
mths. Thailand:
1994- 1,788 of 2,070 bulk milk samples were antibody positive (86.3%)
Transmission
Aerosal Direct contact
Clinical signs
Fever 104-105 F Rhinitis and pneumonia Cough (easily by pinching the trachea) Recovery in few days
Diagnosis
Virus isolation Immunofluorescent or immunoperoxidase
test Serology: Hemagglutination-Inhibition (HI)
Viral Neutralization
Bovine viral diarrhea virus (BVDV)
BVD was first recognised in Canada and the United States in the 1940's.
In 1987, outbreaks of BVD occurred affecting veal calves and older cattle in New York and Pennsylvania.
Beginning in 1992, an outbreak of BVD affected veal calves and dairy herds in Quebec.
Today BVDV infections are seen in all ages of cattle throughout the world and has significant economic impact due to productive and reproductive losses.
Etiology
RNA virus Family Flaviviridae
Pestivirus
2 biotypes: cytopathogenic (cp) or noncytopathogenic (ncp)
Both biotypes of BVDV infect cattle and cause disease, but only ncp BVDV causes persistent infections.
Effect of BVDV infection on cattle Reproductive failure: Embryonic death,
Mummification, Abortions, Stillbirths Repeated breeding syndrome Immunosuppression Congenital defects: Cerebellar hypoplasia, Cataract Persistent infections: Carrier animals Acute BVD Bovine respiratory tract disease Mucosal disease
Transmission
Persistent infected animals Acute infected cattle Semen Embryo transfer Rectal sleeves Contaminated water Biting insect (experimentally)
Effect of Pregnant Cow InfectionDays pregnancy Effect
0-40 Embryonic death40-120 Abortion or
Persistent Infected calf90-160 Abortion or
Congenital defect160-Parturition Abortion or normal calf
Critical concerns
1. Prenatally infected cattle and that are persistently viremic after birth
2. Postnatally infected cattle that are transiently viremic for about 2 to 10 days or possibly longer
Both groups of animal are considered as source of infection in herd.
Prevalence
Prevalence survey in many areas of cattle raising countries: 60-80% of animals antibody positive
1-2% PI animals Variation in cattle population structure and
herd management can account for the difference.
Interspecies transfer
Sheep Wild ruminants
Natural infections (caribou: 40-100%) Transfer (llamas: dead end)
Prevalence of BVDV infections
Seroprevalence Antigen/virus isolation
United Kingdom + +
Germany NK +
Denmark + +
Sweden + +
Norway + NK
United state + +
Thailand +(Bulk milk) NK
NK: Not Known
Thailand
Muaglek area: 4.4% (7/160) of dairy herds were positive for antibodies to BVDV in bulk tank milk samples (Aiumlamai et al, 1992)
And colleague reported 22.8% of bulk tank milk samples (473/2,070) form all over the country; Muaglek and area close by (Livestock area1) had 15.8% (Veerakul et al, 1996)
There are evidences of BVDV infections among pigs in Thailand (Ornveerakul et al, 1994)
158 of 522 bulk milk samples are antibody positive in survey study (Ajariyakhajorn, 1999)
Evidences of natural exposure of BVDV in dairy cattle
Clinical signs (1)
Acute BVDV of young animals, 6-24 months old Fever, ulcers in mouth, throat (esophagus) and intestine,
diarrhea (some bloody), high mortallity
Mild infection: off feed, depressed, mild diarrhea and recovery
Subclinical infection with no visible signs are most common
Colostral antibodies protect most calves until 4-8 months
Acute BVDV in adult cattle (> 2 years) Fever, off feed, decreased milk production,
diarrhea Occasionally ulcers in mouth Outbreaks occur in unvaccinated cattle after
introduction of new animals shedding BVD or in first calf heifers when they enter the milk string
During outbreaks up to 25% of adult cattle may become ill
Clinical signs (2)
Lesion on Nose
Lesion on nose, foamy saliva
Mucosal lesions on tongue and GI tract
Lesion on hard palate
Ataxia resulting from congenital infection
Cerebellar hypoplasia resulting from congenital infection
Fluorescent Antibody test for noncytopathic virus
Figure 1: Choroid plexus, filly: EHV-1 within endothelium and circulating macrophages. Peroxidase immunohistochemistry and hematoxylin.
Figure 2: Lung, calf persistently infected with bovine pestivirus (BVD virus) with bacterial bronchopneumonia. BVDV is contained within the cytoplasm of numerous cells (macrophages, endothelia, alveolar epithelium). Peroxidase immunohistochemistry and hematoxylin.
Diagnosis (1)
Virus Isolation Persistent Infection
Adults — Serum Calves — Serum if pre colostrum or older than 4 months of ag
e. Calves — Whole blood if post colostrum and less than 4 of mo
nths age. Acute Infection
Whole blood. Post Mortem
Spleen, Peyer's patch, lymph nodes. Abortion
Spleen, thymus.
Serology
Virus neutralization
FA
Immunohistochemistry test
ELISA
PCR
Diagnosis (2)
Herd screening
Bulk milk tank (Antibodies or PCR)
Pre immunization antibody titers at 6-12 months of age (serology) (5-10% of unvaccinated calves)
Test all animals Skin Biopsy : Immunoperoxidase (IPX) Blood from <4 mths, serum >4 mths for
Virus isolation Test again in 3 months (isolation + serology)
Prevention and control
Elimination of Carrier Animals Herd testing Test calves at birth
Immunization Modified live or killed vaccines Maximize immunity pre-breeding and early gestation
Biosecurity Closed herd Test all new arrivals Test newborns of new arrivals Quarantine all new arrivals and reintroduced cattle for 21 days
Infectious Bovine Rhinotracheitis (IBR)
Red nose
Etiology
Herpes virus (DNA virus) 3 genotypes
BHV1: IBR BHV2: Infectious pustular vulvovaginitis (IPV)
Infectious balanoposthitis (IBP) BHV3: Neurologic signs
Transmission
Nasal and ocular viral shedding is detected for 10-14 days after infection.
Aerosal Venereal transmission Carrier animals : virus persist in trigeminal
ganglia-reactivated-viremia-shedding
Pathogenesis
In the respiratory disease syndrome, the virus replicates in the nasal cavity and the mucosa of the upper respiratory tract resulting in inflammation of the nasal cavity, larynx and trachea.
The virus may spread to the eyes causing ocular lesions. The virus can become systemic and localize in various tissues in
cluding the placenta that results in fetal infection and abortion.
Localization in the brain leads to encephalitis.
The incubation period can be variable. In feedlot cattle the disease tends to occur 10
-20 days after the introduction of susceptible cattle.
Nasal discharge Inflammation of nostrils (Red nose) Erosion of nasal mucosa
Clinical signs (1)
Clinical signs (2)
Lacrimation Conjunctivitis High fever Inappetance Drop in milk production late abortion (between the 5th and 8ht month
of pregnancy) and placenta retention 10% mortality in severe outbreak
Gross lesions
Swelling and congestion of respiratory mucosal surfaces
Secondary bacterial infections produce mucopurulent nasal discharge
Cervical lymphnode become swallen Conjunctivitis (edema and inflammation) resulting in
excessive lacrimation Clear ocular discharge progresses to mucopurulent
Histopathological lesions
Secondary bronchopneumonia or interstitial emphysema due to labored breathing
Rhinitis Laryngotracheitis Bronchitis
Epidemiology
Infectious Bovine Rhinotracheitis (IBR) was originally recognized as a respiratory disease of feeder cattle in the western United States during the early 1950s.
1990- Survey in central part of Thailand (12 provinces) 558/1,780 (31.3%) serum samples were positive (SN>1:2)
1990- BHV1 was isolated from nasal and vaginal swab of seropositive cow after administration of dexamethazone
1992- 26/40 bulk milk samples were antibody positive (37.3%)
Epidemiology (Thailand)
Diagnosis
Clinical signs Necropsy Laboratory diagnosis
Virus isolation Direct fluorescent antibody test ELIZA (serum and milk) SN (serum) PCR
Vaccination (1)
Replicating IBR Vaccine Modified Live Virus - should not be used in pregnant cows
or in calves nursing pregnant cows. one injection to provide protection. A booster is recommended when an IBR exposure
is anticipated.
Non-Replicating IBR Vaccine Killed Virus and Chemically Altered Virus are safe to use in
all cattle. Requires two doses initially and an annual booster t
o provide adequate protection.
Intra-Nasal IBR Vaccine Intra-nasal IBR Vaccine is safe to use in all age cattle regar
dless of pregnancy status. short-lived Immunity The vaccine of choice to stimulate rapid resistance when a
n outbreak of IBR is occurring or is anticipated. A booster vaccination with a replicating or a non-replicating
form of IBR vaccine is required to provide longer protection.
The basic principle of establishing an immune population before a disease appears is particularly important in the control of IBR, especially the abortion form of IBR.
Vaccination (2)
Prevention and Control
Once introduced it is difficult and expensive to eradicate IBR/IPV especially because as the disease establishes animals tend to become unapparent carriers. Systematic testing and elimination of positives has been successful in some countries.
Bovine Leukosis
Etiology Family Retroviridae (Oncogenic RNA virus)
Genus Bovine leukaemia virus (BLV)
2 forms Enzootic form (Enzootic Bovine Leukosis) Sporadic form
Epidemiology
Worldwide distribution Prevalence increases with age Dairy cattle generally have higher prevalence rate
s than beef cattle Management factors Breed susceptibility differences?
Clinical signs (1)
Enzootic Bovine Leukosis Persistent lymphocytosis (~40% of infected cow) Most infected animals (~70%) do not develop the
disease. Cattle 4-8 years old Weight loss with/with out no appetite
Clinical signs (2)
Anemia Decreased milk yield Enlarged external and enlarged internal
lymph nodes Partial paralysis of the hind legs Abnormal breathing Bulging eyes Diarrhea Constipation
Sporadic form Rarely cases Calve <3 years old 3 forms of pathological lesions
Calf form : animals less than 6 mths old general lymphadenopathy widespread tumour metastasis
Thymic form : animals of 6-8 mths old thymic tumour sometimes extension into the thorax
Skin leucosis : a non fatal form
Young adults develop superficial cutaneous tumour that disappear spontaneously after a few weeks.
Clinical signs (3)
Gross lesions
Firm white tumour masses in any organs and more commonly in lymph nodes.
Organs most frequently involved: abomasum, right auricle of the heart, spleen, intestine, liver, kidney, omasum, lung, and uterus
Diagnosis
Virus isolation PCR Sheep inoculation Serology – can be first detected 3-8 wks after
infection - calves < 6 mths old can be false
positive Agar Gel Immunodiffusion (AGID) Milk ELISA
Transmission
Mechanical transmission Blood suckling insects: Tabanus spp.
Natural transmission Transfer of infected cell Ex. Parturition.
Artificial transmission Blood contaminated needles Surgical equipment Gloves used for rectal examination
Important (1)
Direct Losses Condemnation at slaughter Higher culling rates Decreased reproductive performance Decreased milk yields
Most all economic analyses have failed to distinguish various clinical entities of BLV
Indirect Losses Loss of export market Loss of sales to AI industry Loss of sales to embryo transfer industry Loss of consumer confidence Expenses involved in status testing
Important (2)
Zoonotic Potential BLV will infect human cells No study has linked BLV to human disease
Most not willing to deny potential exists Molecular technology should be able to provide d
efinitive answer
Important (3)
Prevention and Control
Use individual sterile needles for transdermal injection or blood collection.
Disinfect tattoo equipment between animals. Use electric dehorners, or disinfect dehorning equipment betwee
n animals. Replace examination gloves and sleeves between animals. Use milk replacer to feed preweaned calves. Heat-treat or pasteurize colostrum. Use BLV-seronegative recipients for embryo transfer. Wash and rinse instruments in warm water, then submerge in an
appropriate disinfectant.
Eradication
Tested all calves >six months of age removal or segregation of infected cattle from
non-infected cattle Three consecutive negative herd tests at 60-
to 90-day intervals are then required for the herd to be certified as BLV-free.
recertified annually by a repeated negative test of the entire herd
Foot and Mouth Disease(FMD)
Etiology
Family Picornaviridae Genus Aphthovirus Serotypes
O, A, C, Asia1, SAT1, SAT2 and SAT3 Asia1 in Asia and Middle East SAT1-3 in Africa O, A, C in European country and world wide Free from FMD: Scandinavia, Great Britain, North
and Central America, Australia and New Zealand
Resistant and Sensitivity
Sensitive Sunlight UV Temp >50 C pH changes
FMD survival times in animal samples
Organ and condition Time
Lymphnode at 4 C 120 days
Bone marrow at 4 C 210 days
Skeletal muscle at 4 C 2 days
Frozen carcass (no rigor) 6 months
Host
All domestic and wild cloven-footed animals Susceptibility: cattle>pig>sheep>goat Pigs are amplifying host which can cause airborne
transmission.
Transmission
2 main routes of infection: Aerosal Ingestion
Modes of Transmission: Direct contact Indirect contact (mechanical transfer)
Air borne spread up to 10 kms
Factors favoring the spread of FMD 1. Massive production and excretion of FMDV by
infected animals (incubatory carrier) 2. Prolonged survival of FMDV outside animal body 3. Airborne spread of virus over long distances 4. Persistent carrier stage in domestic and wild
animals recovered from apparent and inapparent infection.
5. The ready spread of infection either by direct contact or through animal products, formites or aerosals.
6. The multiplicity of virus antigenic forms which do not confer cross-protection against each other.
Clinical signs (1)
Incubation period 2-14 days Fever (usually fall in about 48 hrs) Anorexia Depression Drop in milk production Development of vesicles on mouth and feet Ruptured vesicles leading to salivation and
lameness
Clinical signs (2)
Vesicular lesions occuring on udder and teats may become permanently infected.
Loss of condition and cessation of growth which may prolonged.
Lameness is prominent sign in pig. Mortality is limited to young animals. Inapparent infection: goat>sheep>pig>cattle
Period of excretion of FMDV related to onset of clinical signs
Source Time (days)
Saliva -10 to +9
Airborne -1 to +4
Milk -4 to +4
Semen -4 to +7
Feces/urine -1 to +6
Lesions 0 to +11
Pillars of rumens
Biological Basis for Vaccination (1) Lack of cross-protection RNA virus, like FMDV, mutate at a rate higher than
DNA virus. The wide range of antigenic variants within the
serotypes. Vaccinated ruminants may become subclinical
carrier of FMDV following contact with virus. Parenteral immunization with inactivated FMDV
vaccine is poor stimulator of mucosal humoral immunization.
The rapidity of FMDV replication allows little opportunity for immunological memory to play a role in immunity to infection.
Repeated prophylactic vaccination is necessary for the maintenance of protective serum antibody titers in susceptible livestock.
Recovery from and protection against reinfection with FMD are related to the development of serum-neutralizing antibody in the cattle.
Biological Basis for Vaccination (2)
The Role of Vaccination in FMD Control Strategy (1) Antigenically appropriate vaccine Regularly ascertained the relationship
between field isolates and the vaccine strains In calf, the primary vaccination should be 4
months. Revaccination may be given 4-12 mths
intervals depending upon local epidemiological advice and the quality of vaccine.
Prophylactic Annually, bi-annually, tri-annually Common practice: >1 strain of a particular serotype in FMD
vaccine Mass prophylactic vaccination
Emergency in FMD free country Slaughter of all infected and susceptible in-contacted
animals Define zone around the outbreak Control virus spread by movement control and disinfection Emergency vaccination: ring vaccination
The Role of Vaccination in FMD Control Strategy (2)
Emergency in FMD infected country Treat animal, mild disinfection, protective dressing
to inflammed area, administration of flunixin meglumine.
Declare infected zone, ring zone within a radius of 16-24 km.
Control human and animal movement Disinfection: 1-2% of NaOH or Formaline,
4% of Sodium carbonate Mass Vaccination
The Role of Vaccination in FMD Control Strategy (3)
Cautions and Remarks
The maintenance of a serum antibody-negative national herd is essential for international trade.
Find the source of outbreak Confirm subtype of virus
Complement fixation test ELISA RT-PCR and sequencing for molecular epidemiology
Careful imitative virus The carrier stage in vaccinated and unvaccinated
cattle may persist for as long as 6 mths and be capable of causing new out break in all species.
Bovine Spongiform Encephalopathy
BSE, Mad cow disease
Etiology
Prion protein
(PrP)
History
Great Britain in 1985: Dead cattle with clinical signs of nervous system
abnormality: atxia, salivation, etc. “Mad cow disease” 167,000 cases and death animals Infectious agent: prion protein (PrP) Contaminated in meat and bone meal
Jekyll and Hydes PrionsThe wild type prion (PrPc) is found in the secretory pathway of
cells expressing the protein(1) and moves to the plasmamembrane where it is anchored by its GPI tail (2). There it maybind to an extracellular ligand (possibly copper) (3) before beingcycled from the membrane into endocytic vesicles (4). At some point its cargo is released and the protein either passes to the
lysozome for degradation or back to surface for another round ofligand binding. In this respect it resembles many other
membrane-resident proteins. The pathogenic form(PrPSc) alsofinds its way to endocytic vesicles where it co-opts some of thewild type form to become pathogenic (5). PrPSc is resistant todegradation, a hallmark of the infectious form, so accumulates.Neurotoxicity is probably linked to the conversion event itself,perhaps through its interference with normal PrPc turnover,
because there is considerable evidence to show that the accruedPrPSc is not inherently toxic.
RESISTANCE TO PHYSICAL AN D CHEMICAL ACTION
Temperature:Preserved by refrigeration and freezing. Recommended physical inactivation is porous load autoclaving at 134–138°C for 18 minutes (this temperature range may not completely inactivate).
pH:Stable over a wide range of pH.
Disinfectants:Sodium hypochlorite containing 2% available chlorine, or 2 N sodium hydroxide, applied for >1 hour at 20°C, for surfaces, or overnight for equipment.
Survival:Recommended decontamination measures will reduce titres but may be incompletely effective if dealing with high titre material, when agent is protected within dried organic matter, or in tissue preserved in aldehyde fixatives. Survives in tissues post-mortem after a wide range of rendering processes. Related hamster scrapie infectivity can survive interment in soil for 3 years and dry heat of 1 hour at temperatures as high as 360°C.
Transmission BSE occurs as a result of dietary exposure to feedstuffs containing infec
ted meat and bone meal (MBM).
No cases of BSE have been recorded as a result of iatrogenic transmission, but this is a potential means.
There is some evidence of a maternally associated risk for calves born to affected cows. The biological mechanisms involved are unknown, but this effect is insignificant in the epidemiology.
There is no evidence of horizontal transmission of BSE between cattle.
Occurrence of new variant Creutzfeldt-Jakob disease (CJD) suggests zoonotic potential via oral exposure.
SOURCES OF AGENT
Central nervous system (including eye) of naturally occurring clinically affected cases. Infectivity detected in the distal ileum of experimentally infected cattle is presumed associated with lymphoreticular tissues.
Clinical signs (1)
Mean incubation period is 4-5 years. Subacute or chronic, progressive disorder
The main clinical signs are neurological: Apprehension, fear, increased startle, or depression Hyper-aesthesia or hyper-reflexia Adventitial movements: muscle fasciculations, tremor and
myoclonus Ataxia of gait, including hypermetria Autonomic dysfunction: reduced rumination, bradycardia an
d altered heart rhythm.
Pruritis, seen in scrapie, occurs also but is not usually a prominent sign.
Loss of body weight and condition.
Clinical signs (2)
Lesions
There are no gross post-mortem changes.
A characteristic spongiform encephalopathy is present in most cases.
Diagnosis (1)
Identification and Isolation of the agent There is no available diagnostic test for the BSE a
gent. Bioassay of brain tissue of terminally affected cattl
e or other species by parenteral inoculation of mice is the only method currently available for detection of infectivity. This is impractical because of minimum incubation periods approaching 300 days.
Serological test The absence of detectable immune responses in BSE or other
transmissible spongiform encephalopathies precludes serological tests.
Other test Histopathological examination of the brain from clinically affected
cases for characteristic bilaterally symmetrical spongiform changes of grey matter and subsequent immunohistochemical demonstration of accumulations of disease specific PrP.
Examination for fibrils, homologous with scrapie-associated fibrils (SAF) by electron microscopy or electrophoretic separation and immunoblotting for detection of the disease specific isoform of PrP in extracts of unfixed, fresh or frozen brain.
Diagnosis (2)
Prevention and control
Free countries Targeted pathological surveillance to occurrences of clinica
l neurological disease. Safeguards on importation of live ruminant species and thei
r products. Policy and procedures for importation of embryos.
Countries with cases in cattle Slaughter and compensation for ascertainment of cases. Controls on recycling of mammalian protein. Effective identification and tracing of cattle.
http://www.oie.int/eng/maladies/fiches/a_B115.htm
Thailand Actions to Prevent BSE กระทรวงเกษตรและสหกรณ์�
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Chantaraprateep et al., 1998. Thai J Vet Med. Vol. 28, No. 1:17-55
Rinderpest
Cattle Plague
Etiology
Family Paramyxoviridae Genus Morbilivirus Only one serotype Susceptible species
Cattle and buffaloes Sheep and goats Asiatic pigs Wildlife
History
Host: cattle, sheep, goats, camels, wild ruminants and pigs
First established in 1754 A major disease of livestock through most of
the 19th century in Great Britain An OIE Class A disease reflecting its serious
economic impact
Transmission
By direct or close indirect contacts Shedding of virus begins 1-2 days before
pyrexia in tears, nasal secretions, saliva, urine and faeces
Blood and all tissues are infectious before the appearance of clinical signs
Infection is via the epithelium of the upper or lower respiratory tract
No carrier state
Clinical signs (1)
Incubation period: 3 to 15 days (usually 4 to 5 days)
Peracute form This form is seen in highly susceptible and young
animals. The only signs of illness are a fever of 104-107o F
(40-41.7o C), congested mucous membranes, and death within 2 to 3 days after the onset of fever.
Classical form: four stages Incubation period Febrile period (40-42°C) with depression, anorexia, reduction of
rumination, increase of respiratory and cardiac rate Mucous membrane congestion (oral, nasal, ocular and genital
tract mucosae) intense mucopurulent lachrymation and abundant salivation anorexia - necrosis and erosion of the oral mucosae this phase lasts 2-3 days
Gastrointestinal signs appear when the fever drops: profuse haemorrhagic diarrhoea containing mucus and necrotic debris. Severe tenesmus. Dehydration, abdominal pain, abdominal respiration, weakness, recumbency and death within 8-12 days. In rare cases, clinical signs regress by day 10 and recovery occurs by day 20-25
Clinical signs (2)
Conjunctivitis and mucopurulent exudate in the early stage of RP infection.
Purulent discharge and conjuctivitis
Excessive salivation in the early stage
of RP infection.
Oral erosions
Erosions of buccal mucosa and gingiva
Subacute form Clinical signs limited to one or more of the classic
signs. Low mortality rate
Atypical form Irregular pyrexia and mild or no diarrheoa. The lymphotropic nature of rinderpest virus
favours recrudescence of latent infections and/or increased susceptibility to other infectious agents.
Clinical signs (3)
Gross lesions
Either areas of necrosis and erosions, or congestion and haemorrhage in the mouth, intestines and upper respiratory tracts
Enlarged and oedematous lymph nodes White necrotic foci in Peyer's patches 'Zebra striping' in the large intestine Carcass emaciation and dehydration
Sloughing of the epithelium over a necrotic Peyer's patch
Ulcerations in the mucosa of the upper colon
Hyperemia of the cecum and colon with accentuation of lesions (hemorrhage) at the ceco-colic junction
Hyperemia and hemorrhages in the longitudinal folds of the colon - Zebra striping
Hemorrhage in the mucosa of the gall bladder
EpidemiologyThe Global Rinderpest Eradication Program (FAO)
Eradication
Only one serotype Recovered or properly vaccinated animals
are immune for life No vertical transmission, arthropod vector, or
carrier state RPV is an ideal virus to be targeted for
eradication. Thailand is a rinderpest free country.
Lumpy Skin Disease
Pseudo-urticaria, Neethling virus disease, exanthema nodularis bovis, knopvelsiekte
Etiology and Host
Family Poxviridae Genus Capripoxvirus Host: Cattle, Buffaloes, Giraff First described in Northern Rhodesia in 1929 An OIE list A disease
Transmission
Insect vector Mosquitoes (e.g. Culex mirificens and Aedes
natrionus) Flies (e.g. Stomoxys calcitrans and Biomyia
fasciata)
Clinical signs
Inapparent to severe disease Fever (40-41.5°C) either transitory or lasting up to 2 weeks Swellings or nodules in the skin and generalization. Depression, anorexia, excessive salivation, oculonasal discharge,
agalactia and emaciation The nodules may become necrotic and sometimes deep scabs form
(which are called 'sittast') Lameness resulting from inflammation and necrosis of tendons, and
from severe oedema of brisket and legs Superficial lymph nodes enlarged to four-to-ten times their normal
size Complications: severe mastitis and loss of the quarter
permanent lameness abortion, intrauterine infection, and temporary
sterility in bulls and cows may occur.
A calf affected with LSD; note the large skin nodules
Nodules (N) and sittasts (S) in a Balidy cow in Egypt affected with LSD
An LSD (pox) lesion in the trachael mucosa
LSD lesions in the lung are areas of atelectasis and interlobular edema
Eradication
Slaughter of all infected and in-contact cattle Vaccination
Papillomavirus or Warts
Pseudocowpox
Pseudocowpox
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