Bacterial zoonoses affecting nervous system
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This document discusses several bacterial zoonoses that can affect the nervous system. It focuses on tetanus, botulism, and tuberculosis. For tetanus, it describes the causative agent (Clostridium tetani), pathogenesis, clinical signs in humans and various animals, diagnosis, prevention including vaccination, and control. For botulism, it discusses the seven neurotoxins produced by Clostridium botulinum, clinical signs in humans and different species, and prevention in livestock. Finally, it provides background on Mycobacterium tuberculosis complex as the cause of tuberculosis, its epidemiology, and the diseases it can cause in cattle and humans.
![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](https://image.slidesharecdn.com/bacterialzoonosesaffectingnervoussystem-160428181225/85/Bacterial-zoonoses-affecting-nervous-system-101-320.jpg)
Bacterial zoonoses affecting nervous system
- 1. BACTERIAL ZOONOSES AFFECTING NERVOUS SYSTEM SHARON A J 15-MVM-044
- 2. Contents Tetanus Botulism Lyme disease Leptospirosis Listeriosis Tuberculosis
- 3. 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
- 4. TETANUS Synonyms Trisumus Lock jaw 4
- 5. 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 5
- 6. HOST All mammals HUMANS and HORSES are most sensitive Dogs are relatively resistant Cats are more resistant 6
- 7. 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 7
- 8. 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. 8
- 9. 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. 9
- 10. Pathogenesis Wound Exotoxins Spore germinate –anaerobic condition Disseminate via blood and lymphatics Toxin reaches CNS along nerves Producing clinical signs Ascending tetanus Descending tetanus Tetanospasmin & Tetanolysin 10
- 11. 11
- 12. 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 12
- 13. 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 13
- 14. 14
- 15. 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 15
- 16. 16
- 17. 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 17
- 18. DIAGNOSIS Clinical signs and history of recent trauma Detecting tetanus toxin in serum If wound is apparent – gram stained smears and by anaerobic culture 18
- 19. Differential diagnosis Strychnine poisoning Hypocalcemic tetany Eclampsia 19
- 20. 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 20
- 21. BOTULISUM 21
- 22. Animals Cattle and sheep Horses Birds and poultry Mink and ferrets Uncommon in dogs and pigs Fairly resistant No natural cases documented in cats 22
- 23. ETIOLOGY Clostridium botulinum • Gram positive • Obligate anaerobic bacillus • Spores Ubiquitous Resistant to heat, light, drying and radiation Specific conditions for germination Anaerobic conditions Warmth (10-50oC) Mild alkalinity 23
- 24. 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 24
- 25. Neurotoxins Neurotoxin A B C D E F G Human X X X X Horses X X Cattle X X X Sheep X Dogs X X Avian X X Mink & Ferret X X X 4/28/2016
- 26. 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) 26
- 27. TRANSMISSION Ingestion Organism Spores Neurotoxin Wound contamination Inhalation Person-to-person not documented 27
- 28. Human Disease Three forms Food borne Wound Infant All forms fatal and a medical emergency Incubation period: 12-36 hours 28
- 29. 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 29
- 30. 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 30
- 31. 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 31
- 32. 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 32
- 33. Infant Clinical Signs Constipation Lethargy Poor feeding Weak cry Bulbar palsies Failure to thrive 33
- 34. 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 34
- 35. 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 35
- 36. Affected animal lie in strenal recumency with the head on the ground or turned to the flank 36
- 37. 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 37
- 38. Adult Horses “Forage poisoning” Ingest preformed toxin Clinical Signs Dyspnea Flaccid tail Muscle tremors Severe paresis to rapid recumbency Unable to retract tongue, drooling 38
- 39. Foals “Shaker Foal” syndrome Most 2 weeks to 8 months old On a high nutrition plane Spores in contaminated feed Usually type B 39
- 40. 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 40
- 41. 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 41
- 42. 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 42
- 43. Dogs Progressive symmetric ascending weakness Rear limbs to forelimbs Cranial nerve deficits Respiratory paralysis Lose ability to urinate and defecate 43
- 44. 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 44
- 45. 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) 45
- 46. Differential diagnosis Hypocalcemia Hypomagnesemia Carbohydrate overload Toxicosis, including from mycotoxin, lead, nitrate, organophosphate, atropine or atropine-like alkaloid Tick paralysis Paralytic rabies 46
- 47. Ruminants: Prevention Good husbandry practices Rodent and vermin control Prompt disposal of carcasses Avoid spoiled feedstuff or poor quality silage Vaccination in endemic areas 47
- 48. Product name BoNT type Animal species Dosage Ultravac botulinum (Pfizer Animal Health) C ,D Cattle, sheep 2.5 ml cattle 1 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 48
- 49. TUBERCULOSIS
- 50. 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
- 51. ETIOLOGY Tubercle bacilli, causing tuberculosis belongs to Mycobacterium tuberculosis complex. Mycobacterium tuberculosis Mycobacterium bovis Mycobacterium africanum Mycobacterium microti
- 52. Mycobacterium bovis: tuberculosis in cattle Mycobacterium avium complex (MAC) Mycobacterium avium & Mycobacterium intracellulare causes generalised TB in cattle zoonotic disease called mycobacteriosis
- 53. 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
- 54. 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)
- 55. 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
- 56. World Organization for Animal Health (OIE), 2011
- 58. HOST M.tuberculosis reservoirs in man M.bovis mainly cattle, domestic and wild animals and man. M.avium causing generalized TB
- 59. 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
- 60. 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
- 61. Man-to-animal Urination by farm workers with renal tuberculosis Direct exposure
- 63. PRIMARY TUBERCULOSIS Formation of tubercle May break and heal by calcification
- 64. SECONDRY TUBERCULOSIS Dormant bacilli reactivates Violent coughing Greenish or blood in sputum Fever Anorexia Weight loss Fatigue Night sweats
- 65. EXTRAPULMONARY TUBERCULOSIS 1. TB meningitis headache, drowsiness, intermitted vomiting, mental deterioration, permanent retardation, blindness, deafness.
- 66. 2. MILIARY TUBERCULOSIS 3. SCROFULA PEARLY DISEASE Miliary nodules on serous membrane lymphadenitis of the cervical lymph nodes
- 67. 4. TUBERCULOUS ARTHRITIS 5. SCROFULODERMA POTT’S DISEASE Collapse of vertebral column and spinal code damage Consumption of contaminated milk
- 68. CULANEOUS TUBERCULOSIS TB METASTATIC ABSCESS TUBERCULUS VERRUCOSA
- 70. DISEASE IN ANIMAL CATTLE: Lymphadenitis Progressive hardening and swelling of udder Watery, flakes in milk Emaciation Diarrhea with capricious appetite Fluctuating temperature
- 71. CATS AND DOGS: Marked emaciation Nasal discharge Cough Pleurisy Dypsnea Abdominal and chest swelling
- 72. DIAGNOSIS 1. 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
- 73. 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
- 74. 1. Microscopic detection of organisms 2. Montoux test Fluorescent auramine staining showing Mycobacterium sp in sputum sample
- 75. 3. Radiography 4. Gas chromatography 5. Radiometric determination of bacterial growth 6. PCR 7. ELISA 8. Isolation of pathogens
- 76. 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
- 77. Condemnation of milk from infected animal Treatment of infected meat Abattoir control Milk pasteurization Health education
- 78. 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.
- 79. 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,
- 80. Left facial palsy (Bell's palsy) in early Lyme disease
- 81. SYMPTOMS
- 82. 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
- 83. 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.
- 84. 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.)
- 85. 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.
- 86. COUNTRIES WITH REPORTED LYMES DISEASES
- 87. 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.
- 88. 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
- 90. Pathogenesis Leptospira Damage to small blood vessels Vasculitis Direct cytotoxic injury Immunological injury Massive migration of fluid from Intravascular to interstitial compartment Renal dysfunction, vascular Injury to internal organs
- 91. 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).
- 95. 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.
- 96. 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.
- 98. 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
- 99. 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
- 100. 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.
- 101. 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
- 102. 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.
- 103. 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
- 104. 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