Post on 16-Apr-2017
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
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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
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HOST
All mammals HUMANS and HORSES are most sensitive Dogs are relatively resistant Cats are more resistant
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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
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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.
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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.
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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
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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
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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
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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
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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
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DIAGNOSIS
Clinical signs and history of recent trauma
Detecting tetanus toxin in serum
If wound is apparent –gram stained smears and by anaerobic culture
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Differential diagnosis
Strychnine poisoning Hypocalcemic tetany Eclampsia
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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
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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
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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
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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
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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)
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TRANSMISSION
IngestionOrganismSporesNeurotoxin
Wound contamination Inhalation Person-to-person not documented
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Human Disease
Three forms Food borne Wound Infant
All forms fatal and a medical emergency Incubation period: 12-36 hours
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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
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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
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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
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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
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Infant Clinical Signs
Constipation Lethargy Poor feeding Weak cry Bulbar palsies Failure to thrive
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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
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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
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Affected animal lie in strenal recumency with the head on the ground or turned to the flank
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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
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Adult Horses
“Forage poisoning” Ingest preformed toxin
Clinical Signs Dyspnea Flaccid tail Muscle tremors Severe paresis to rapid recumbency Unable to retract tongue, drooling
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Foals
“Shaker Foal” syndromeMost 2 weeks to 8 months oldOn a high nutrition plane
Spores in contaminated feed Usually type B
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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
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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
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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
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Dogs
Progressive symmetric ascending weakness Rear limbs to forelimbs
Cranial nerve deficits Respiratory paralysis Lose ability to urinate and defecate
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Dogs
Rare Type C; few cases type D Source
Ingestion of carrion Wetland areas with avian botulism epizootics
Incubation period Few hours to 6 days
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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)
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Differential diagnosis
Hypocalcemia Hypomagnesemia Carbohydrate overload Toxicosis, including from mycotoxin, lead, nitrate, organophosphate,
atropine or atropine-like alkaloid Tick paralysis Paralytic rabies
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Ruminants: Prevention
Good husbandry practices Rodent and vermin control Prompt disposal of carcasses Avoid spoiled feedstuff or poor quality silage Vaccination in endemic areas
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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
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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,
2013
World Organization for Animal Health (OIE), 2011
HOST
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
CAUSE
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
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