Bacterial zoonoses affecting nervous system

transcript

BACTERIAL ZOONOSES

AFFECTING NERVOUS SYSTEM

SHARON A J15-MVM-044

Contents

Tetanus Botulism Lyme disease Leptospirosis Listeriosis Tuberculosis

BRUCELLOSIS It is one of the major bacterial zoonotic disease and in humans is also

known as undulent fever ,malta fever or mediterranean fever. it is caused by different species of brucella group of organisms

TETANUS

Synonyms Trisumus Lock jaw

ETIOLOGY Clostridium tetani Gram positive bacilli Motile, Non-encapsulated, Anaerobic, Slender endospore-forming

bacillus. Oval, colorless, terminal

spores – tennis racket or drumstick shape

11 known strain

All mammals HUMANS and HORSES are most sensitive Dogs are relatively resistant Cats are more resistant

EPIDEMIOLOGY

World wide Live in all anaerobic habitat-soil ,faeces &

intestinal tracts of various animals Especially in hot, damp climate with heavily

manured soils More in developing and under developing countries IMPORTANT ENDEMIC INFECTION IN INDIA

EPIDEMIOLOGY ( cont…)

The incubation period of tetanus may be up to several months, but is usually about eight days.

In general, the injury site is for from the central nervous system, the longer the incubation period.

The near the C.N.S incubation period IP is short, the more severe the symptoms.

Mode of transmission

Contaminated WOUNDS Tissue injury – surgery, animal

bites, parturation , (dystocia), deep puncture wounds

Naval infection –Tetanus neonatale

In neonatal tetanus, symptoms usually appear from 4 to 14 days after birth, averaging about 7 days.

PathogenesisWound

Exotoxins

Spore germinate –anaerobic condition

Disseminate via blood and lymphatics

Toxin reaches CNS along nerves

Producing clinical signs

Ascending tetanus

Descending tetanus

Tetanospasmin & Tetanolysin

CLINICAL SIGNS

Human beings Painless spasm of the

muscles of the jaw Difficulty in opening the

mouth “lock Jaw”, Contraction of the

muscles on the forehead and mouth

The board like rigidity of the abdominal wall are characteristic

CLINICAL SIGNS

RUMINANTS Bloat Constipation & retention of urine Lateral recumbency with extreme

extension of limbs, tail and all muscles

Rigidity of legs and opisthotonous SHEEP and GOAT Fall to the ground and opisthotonus

CLINICAL SIGNS

• HORSES• Erect ears• Tail- stiff and extended• Anterior nares –dialated• Third eyelid prolapsed• SAW HORSE stance• Sweating• Increased heart rate • Rapid breathing • Congestion of mucous membrane

CLINICAL SIGNS

DOGS AND CATS Long incubation period Localized tetanus Stiffness and rigidity in

limb ,stiffness may progress to opposing limb and may advances anteriorly.

Generalized tetanus is also there but rare

DIAGNOSIS

Clinical signs and history of recent trauma

Detecting tetanus toxin in serum

If wound is apparent –gram stained smears and by anaerobic culture

Differential diagnosis

Strychnine poisoning Hypocalcemic tetany Eclampsia

PREVENTION AND CONTROL

CLEANLINESS AND VACCINATION Active immunization –Tetanus Toxoid 2 week, 2 month, 12 month Mare last 8 weeks of pregnancy Sheep and Goat –late pregnancy (3rd and 4th month) Passive immunity -Anti toxin (non immunized animals) Proper wound healing Disinfectant-IODINE AND CHLORINE

BOTULISUM21

Animals

Cattle and sheep Horses Birds and poultry Mink and ferrets Uncommon in dogs and pigs

Fairly resistant No natural cases documented in cats

ETIOLOGY Clostridium botulinum

• Gram positive• Obligate anaerobic bacillus• Spores

UbiquitousResistant to heat, light, drying and radiationSpecific conditions for germination

Anaerobic conditionsWarmth (10-50oC)Mild alkalinity

Neurotoxins

Seven different types: A to G Different types affect different species All cause flaccid paralysis Only a few nano grams can cause illness Binds neuromuscular junctions

Toxin: Destroyed by boiling Spores: Higher temperatures to be

inactivated

NeurotoxinsNeurotoxin A B C D E F G

Human X X X XHorses X XCattle X X XSheep XDogs X XAvian X XMink & Ferret X X X

05/03/2023

HISTORY

1793, Justinius Kerner “Botulus” = Latin for

sausage 1895, Emile von Ermengem

Isolated organism during Belgium outbreak

U.S. outbreaks led to improved industry processing

Justinus Kerner (1786–1862)

TRANSMISSION

IngestionOrganismSporesNeurotoxin

Wound contamination Inhalation Person-to-person not documented

Human Disease

Three forms Food borne Wound Infant

All forms fatal and a medical emergency Incubation period: 12-36 hours

Infant Botulism

Most common form in U.S. Spore ingestion

Germinate then toxin released and colonize large intestine

Infants < 1 year old 94% < 6 months old

Spores from varied sources Honey, food, dust, corn syrup

Food borne Botulism

Preformed toxin ingested from contaminated food Most common from home-canned foods

Asparagus, green beans, beets, corn, baked potatoes, garlic, peppers, tomatoes; type A

Improperly fermented fish (Alaska); type E

Wound Botulism

Organism enters wound Develops under anaerobic conditions From ground-in dirt or gravel It does not penetrate intact skin Associated with addicts of black-tar heroin

Adult Clinical Signs

Nausea, vomiting, diarrhea Double vision Difficulty speaking or swallowing Descending weakness or paralysis

Shoulders to arms to thighs to calves Symmetrical flaccid paralysis Respiratory muscle paralysis

Infant Clinical Signs

Constipation Lethargy Poor feeding Weak cry Bulbar palsies Failure to thrive

Cattle and Sheep

Ingestion of toxin Incubation

24 hours to 7 days Sources

Spoiled stored silage or grain Silage using poultry litter or products Phosphorus deficiency in cattle Carcasses: Baled or chopped into hay

Ruminants: Clinical Signs

Progressive ascending ataxia(Symmetric muscular paralysis)

Recumbent & Head turned into flanks Cranial nerve dysfunction(dysphagia, drooling, tongue

paresis, and facial muscle paresis) Eye effects include decreased pupillary light reflex,

ptosis and mydriasis Rumen stasis; bloat Atonic bladder - loss of urination

Affected animal lie in strenal recumency with the head on the ground or turned to the flank

Horses

Horses, especially foals, are highly sensitive to botulism toxin Type B & C toxins Incubation period

24 hours to 7 days Sources

Contaminated feed Wound infections

Adult Horses

“Forage poisoning” Ingest preformed toxin

Clinical Signs Dyspnea Flaccid tail Muscle tremors Severe paresis to rapid recumbency Unable to retract tongue, drooling

“Shaker Foal” syndromeMost 2 weeks to 8 months oldOn a high nutrition plane

Spores in contaminated feed Usually type B

Birds and Poultry

“Limber neck” Types C and E Good sentinel species Sources:

Decomposed vegetation or invertebrates

Ingest toxin or invertebrates with toxin

Contaminated feed or water of chickens

Birds and Poultry:Clinical Signs

Occurs 12-48 hours after ingestion Droopy head Drowsy Wing and leg paralysis

Unable to hold their head up Unable to use their wings or legs

Eyelid paralysis

Mink and Ferrets

Type C Occasionally A and E

Sources Chopped raw meat or fish Improper storage of meat by-products

Vaccine available for type C

Progressive symmetric ascending weakness Rear limbs to forelimbs

Cranial nerve deficits Respiratory paralysis Lose ability to urinate and defecate

Rare Type C; few cases type D Source

Ingestion of carrion Wetland areas with avian botulism epizootics

Incubation period Few hours to 6 days

Cattle and Sheep: Diagnosis

History Bloodwork and CSF tap: Normal ELISA test available for type C & D Definitive diagnosis

Demonstration of toxin in serum, gut contents or organs(mouse bioassay) Electromyography (EMG)

Differential diagnosis

Hypocalcemia Hypomagnesemia Carbohydrate overload Toxicosis, including from mycotoxin, lead, nitrate, organophosphate,

atropine or atropine-like alkaloid Tick paralysis Paralytic rabies

Ruminants: Prevention

Good husbandry practices Rodent and vermin control Prompt disposal of carcasses Avoid spoiled feedstuff or poor quality silage Vaccination in endemic areas

Product name BoNT type Animal species

Dosage

Ultravac botulinum(Pfizer Animal Health)

C ,D Cattle, sheep 2.5 ml cattle1 ml sheep

1st dose; 2nd dose after 4-6 weeks Annual booster

Long range(Pfizer Animal Health)

C ,D Cattle 2.5 ml 1st dose from 6 weeks Annual booster

Singvac 1-year botulinum (Virbac Animal Health)

C ,D cattle 2 ml 1 dose Booster after 36 months

Botulism Vaccine (Onderstepoort Biological Products)

C,D Cattle Horses Mules Sheep Goats

1.0ml sheep and goats 2.0ml cattle, horses, and mules

1st dose; 2nd dose after 4-7 weeks Annual booster

TUBERCULOSIS

Acnitis Consumption Great white plaque Great white scourge Pearl disease Pott’s disease Pthisis Rajayakshman

Swollen gland Caption of the men of

death Going into a decline

ETIOLOGY

Tubercle bacilli, causing tuberculosis belongs to Mycobacterium tuberculosis complex.

Mycobacterium tuberculosis Mycobacterium bovis Mycobacterium africanum Mycobacterium microti

Mycobacterium bovis: tuberculosis in cattle

Mycobacterium avium complex (MAC) Mycobacterium avium & Mycobacterium intracellulare causes generalised TB in cattle zoonotic disease called

mycobacteriosis

EPIDEMIOLOGY

1882- Robert Koch isolated M.tuberculosis 1898- differentiated M.bovis and M.tuberculosis Many countries have eradicated bovine

TB Prevalent in many African, Asian and

middle East countries.

Robert Koch

TB- second most leading cause of death by single infectious agent

128 out of 155 countries reported the presence of M. bovis infection and/or clinical disease in their cattle population between 2005 and 2008 (Michel et al, 2010)

2013, world: 9 million (1.1 m with HIV)- affected 1.5 million (360000 with HIV)- death 2013, India: 22,00,000 – new cases of TB reported 38,000- death WHO,

World Organization for Animal Health (OIE), 2011

M.tuberculosis reservoirs in man M.bovis mainly cattle, domestic and

wild animals and man. M.avium causing generalized TB

TRANSMISSION

Tubercle bacilli transmit from person to person, person to animal man can infect animals with both strains self limiting in animals Ingestion- unpasteurized and contaminated meat

Animal-to-animal Inhalation of droplets Ingestion of milk Bite of infected hard tick Infected pastures

Animal-to-man Direct exposure Ingestion of infected material

Man-to-animal

Urination by farm workers with renal tuberculosis Direct exposure

DISEASE IN MAN

PRIMARY TUBERCULOSIS

SECONDRY TUBERCULOSIS

EXTRAPULMONARY TUBERCULOSIS

PRIMARY TUBERCULOSIS

Formation of tubercle May break and heal by calcification

SECONDRY TUBERCULOSIS

Dormant bacilli reactivates Violent coughing Greenish or blood in sputum Fever Anorexia Weight loss Fatigue Night sweats

EXTRAPULMONARY TUBERCULOSIS

1. TB meningitis headache, drowsiness, intermitted vomiting, mental deterioration, permanent retardation, blindness, deafness.

2. MILIARY TUBERCULOSIS

3. SCROFULA

PEARLY DISEASEMiliary nodules on serous membrane

lymphadenitis of the cervical lymph nodes

4. TUBERCULOUS ARTHRITIS

5. SCROFULODERMA

POTT’S DISEASECollapse of vertebral column and spinal code damage

Consumption of contaminated milk

CULANEOUS TUBERCULOSIS

TB METASTATIC ABSCESS

TUBERCULUS VERRUCOSA

TUBERCULOIDLUPUS VULGARIS

DISEASE IN ANIMAL

CATTLE: Lymphadenitis Progressive hardening and swelling of udder Watery, flakes in milk Emaciation Diarrhea with capricious appetite Fluctuating temperature

CATS AND DOGS:

Marked emaciation Nasal discharge Cough Pleurisy Dypsnea Abdominal and chest swelling

DIAGNOSIS1. Microscopic detection of organism

2. Delayed type hypersensitivity assay a. single intradermal tuberculin test b. stormont test

Acid fast bacilli detected in the impression smear from omentum

c. short thermal test d. subcutaneous tuberculin test e. opthalmic test

3. Animal inoculation

4. Isolation and identification of pathogen

Suspected material

Guinea pig

Tubercular lesions

Lowenstein jensen medium

1. Microscopic detection of organisms

2. Montoux test

Fluorescent auramine staining showing Mycobacterium sp in sputum sample

3. Radiography4. Gas chromatography5. Radiometric determination of bacterial

growth6. PCR7. ELISA8. Isolation of pathogens

PREVENTION AND CONTROL

Test and slaughter – best Test and segregation Slaughter surveillance Cleaning and disinfection 5% phenol, iodine solutions, moist heat(121˚C, 15min), glutaraldehyde and formaldehyde Herd density Vaccination

Condemnation of milk from infected animal

Treatment of infected meat Abattoir control Milk pasteurization Health education

LYME DISEASE

The spirochete bacteria Borrelia burdorferi A zoonotic disease A disease affecting the many organ systems Lyme borreliosis, is an infectious disease caused by bacteria of

the Borrelia type In North Americai Borrelia burgdorferi sensu stricto, Europe and Asia, the bacteria Borrelia afzelii and Borrelia garinii are

also causes of the disease.

SYMPTOMS

Erythematous lesions Fever Headache, Joint pains, Severe headaches with neck stiffness, Heart palpitations, If untreated, symptoms may include loss of the ability to move one or

both sides of the face,

Left facial palsy (Bell's palsy) in early Lyme disease

SYMPTOMS

TRANSMISSION

Lyme disease is transmitted to humans by the bite of infected ticks of the Ixodes genus. The tick must be attached for 36 to 48 hours before the bacteria can spread

Deer tick

Lyme disease is classified as a zoonosis, as it is transmitted to humans from a natural reservoir among rodents by ticks that feed on both sets of hosts.

Hard-bodied ticks of the genus Ixodes are the main vectors of Lyme disease (also the vector for Babesia).

Most infections are caused by ticks in the nymphal stage, as they are very small and may feed for long periods of time undetected

Larval ticks are very rarely infected. Although deer are the preferred hosts of deer ticks, and the size of the

tick population parallels that of the deer population, ticks cannot acquire Lyme disease spirochetes from deer.

ZOONOTIC IMPORTANCE

Lyme disease is the most common disease spread by ticks in the Northern Hemisphere

It is estimated to affect 300,000 people a year in the United States and 65,000 people a year in Europe(Shapiro, ED (1 May 2014). "Clinical practice. Lyme disease.". The New England Journal of Medicine 370 (18): 1724–31.doi:10.1056/NEJMcp1314325. PMID 24785207.)

NERVOUS SYSTEM IMPLICATION

B. burgdorferi may induce astrocytes to undergo astrogliosis which may contribute to neurodysfunction.

The spirochetes may also induce host cells to secrete Quinolinic acid, which stimulates the NMDA receptor on nerve cells, which may account for the fatigue and malaise observed with Lyme encephalopathy

In addition, diffuse white matter pathology during Lyme encephalopathy may disrupt grey matter connections, and could account for deficits in attention, memory, visuospatial ability, complex cognition, and emotional status.

COUNTRIES WITH REPORTED LYMES DISEASES

LEPTOSPIROSIS

Leptospirosis field Fever, Rat catcher's yellows, Pretibial fever t is also known as Weil's disease L interrogans most pathogenic Leptospira is a flexible, spiral-shaped, Gram-negative spirochete with

internal flagella. Leptospira interrogans has many serovars based on cell surface antigens.

Infection caused by corkscrew-shaped bacteria called Leptospira. Signs and symptoms can range from none to mild such as headaches,

muscle pains, and fevers; to severe with bleeding from the lungs or meningitis.

Up to 13 different genetic types of Leptospira may cause disease in humans.

It is transmitted by both wild and domestic animals. The most common animals that spread the disease are rodents. It is often transmitted by animal urine or by water or soil containing

animal urine coming into contact with breaks in the skin, eyes, mouth, or nose.

In the developing world the disease most commonly occurs in farmers and poor people who live in cities. In the developed world it most commonly occurs in those involved in outdoor activities

Pathogenesis

Leptospira Damage to small

blood vesselsVasculitis

Direct cytotoxic injuryImmunological injury

Massive migration of fluid from Intravascular to interstitial compartment

Renal dysfunction, vascularInjury to internal organs

SIGNS AND SYMPTOMS

Leptospirosis is a biphasic disease that begins suddenly with fever accompanied by chills, intense headache, severe myalgia (muscle ache), abdominal pain, conjunctival suffusion (red eye), and occasionally a skin rash.

The symptoms appear after an incubation period of 7–12 days. The first phase (acute or septicemic phase) ends after 3–7 days of illness.

The disappearance of symptoms coincides with the appearance of antibodies against Leptospira and the disappearance of the bacteria from the bloodstream. The patient is asymptomatic for 3–4 days until the second phase begins with another episode of fever.

The hallmark of the second phase is meningitis (inflammation of the membranes covering the brain).

CLINICAL MANIFESTATION

VASCULITISCONJUNCTIVITIS

COMMON RISK FACTORS

PREVENTION

Effective rat control Avoidance of urine contaminated water sources Pre-exposure prophylaxis may be beneficial for individuals traveling to

high-risk areas for a short stay.

Epidemiology

Leptospirosis is a worldwide zoonosis affecting many wild and domestic animals. Humans acquire the infection by contact with the urine of infected animals. Human-to-human transmission is extremely rare.

It is estimated that seven to ten million people are infected by leptospirosis annually.

One million cases of severe leptospirosis occur annually, with 58,900 deaths.

Annual rates of infection vary from 0.02 per 100,000 in temperate climates to 10 to 100 per 100,000 in tropical climates.

This leads to a lower number of registered cases than likely exists.

LISTERIOSIS

Listeria primarily causes infections of the central nervous system (meningitis, meningoencephalitis,brain abscess, cerebritis) and bacteremia in those who are immunocompromised.

Synonyms Silage Disease Circling disease Listerellosis mononucleosis

Special features of organism

Can withstand refrigeration temperatures

Can withstand batch method of pasteurisation

Can withstand high salt concentration

Can grow over a wide pH range 4.5-9

Extensive survivability

Listeria monocytogenes is ubiquitous in the environment and most pathogenic organism.

The main route of acquisition of Listeria is through the ingestion of contaminated food products. Listeria has been isolated from raw meat, dairy products, vegetables, fruit and seafood. Soft cheeses, unpasteurized milk are potential dangers.

Rarely listeriosis may present as cutaneous listeriosis. This infection occurs after direct exposure to L. monocytogenes by intact skin and is largely confined to veterinarians who are handling diseased animals, most often after a Listerial abortion.

Route of transmission

Direct indirect contact through conjunctiva & Intact mucous membrane

Ingestion of Milk and meat

]Through water and soil

Perinatal infection –Through trans placental and trans mammary route

Organism excreted through semen

Through inhalation –very rare

Treatment

Bacteremia should be treated for 2 weeks,

Meningitis for 3 weeks,

Brain abscess for at least 6 weeks.

Ampicillin generally is considered antibiotic of choice; gentamicin is

added frequently for its synergistic effects.

Prevention

The main means of prevention is through the promotion of safe handling, cooking and consumption of food. This includes washing raw vegetables and cooking raw food thoroughly

Another aspect of prevention is advising high-risk groups such as pregnant women and immunocompromised patients to avoid unpasteurized milk and foods such as soft cheese

REFERENCES:

ZOONOSES AND COMMUNICABLE DISEASES COMMON TO MAN AND ANIMALS-Third edition ZOONOTIC DISEASES OF PUBLIC HEALTH IMPORTANCE-

NATIONAL INSTITUTE OF COMMUNICABLE DISEASES (DIRECTORATE GENERAL OF HEALTH SERVICES)

www.WHO.in www.cdc.in www.oie.org

THANK YOU

Bacterial zoonoses affecting nervous system

Health & Medicine