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  1. 1. Rabies by:Dr. Mukesh Kini M A Department of veterinary Epidemiology and preventive medicine
  2. 2. Introduction • also known as hydrophobia, lyssa, mad dog, madness, hytta, hubhoo, rabera • all warm blooded animals susceptible • natural disease of dogs, cats, bats, and wild carnivores • acute viral infection characterized by encephalomyelitis • rabies has highest mortality rate of any known infectious agent, which is virtually 100%
  3. 3. Etiology • caused by rabies virus belonging to genus lyssa virus in the family rhabdoviridae in order mononegavirales. • large enveloped, bullet shaped, sRNA virus • MAB produced against nucleocapsids or glycoprotein moieties provided evidence that various rabies isolates have antigenic variants • the outer projection on the envelope are composed glycoprotein G, which is important in attachment of virus to host cell and production of serum neutralization antibodies
  4. 4. • virus is fragile, inactivated by organic solvents, detergent, UV, heat, light • virus survives on refrigerated tissue for long time • remains alive if stored in 50% glycerol @ RT
  5. 5. • Closely related lyssaviruses, which are known as rabies- related lyssaviruses or nonrabies lyssaviruses, can cause a neurological disease identical to rabies. Lagos bat virus, Duvenhage virus, European bat lyssavirus (EBLV) 1, EBLV 2, Australian bat lyssavirus (ABLV), Mokola virus and Irkut virus have caused clinical cases in
  6. 6. Epidemiology • most important infectious disease from public health point of view • present in most countries except Guyana, Jamaica, Uruguay, Japan, UK, Spain, Australia, New Guinea • responsible for high morbidity and mortality in India • estimate: 25k die from rabies and 500000 post bite vaccination • 90-95% dog bite transmission, rest by rodents and wild animals
  7. 7. Epidemiology • about 90 million dogs in India, most of them unvaccinated • canine rabies termed as urban rabies • all warm blooded animals susceptible to rabies • highly susceptible: dog and other canids,vampire bats felines • ruminants and equines moderately susceptible and dead end host
  8. 8. Epidemiology • sylvatic cycle (wild) sometimes epizoonotic spillover occurs • spread of disease by direct contact, mostly bite • salivary transmission possible • nosocomial transmission of rabies has occurred through organ transplant • oral exposure minimal risk due to acidic pH of stomach • arosolization has been done experimentally, though rarely occurs in nature, like in bat caves
  9. 9. Epidemiology • contact through intact skin transmission not possible • dogs come in contact of each other during breeding season, which provides opportunity for disease to spread
  10. 10. Pathogenesis • after entry virus replicates in myocytes and remains in site for weeks or months causing long and variable incubation period before entry into nervous system • replication in periphery is so weak it doesn't stimulate immune response • incubation period variable mostly 3-9 wk, up to 2 years has been reported in domestic animals • incubation period depends on the bite site severity of exposure, inversely related to viral dose
  11. 11. Pathogenesis • centripetal: virus reaches CNS through pns • nerve endings neuromuscular and neurotendinal spindal are spots for entry of virus into nervous system • transport to CNS via axon very rapid within nerve fibers • no transport through lymphatics and blood stream • in brain and SC virus replicates in neurons and in perikaryons of infected neurons,large accumulation of nuceocapsid form the pathognomic negri bodies
  12. 12. Pathogenesis • CS appears after replication in brain and spinal chord • then centrifugal movement of infection occurs in peripheral organs • the virus reaches salivary gland via peripheral organs and shedding of virus occurs • profound neuronal dysfunction occurs, results in failure in respiratory center, even with assisted preservation of airways and ventilation, may manifest autonomic instability to result in death
  13. 13. Pathogenesis • WHO has recommended that clinically normal dogs which has bitten, should be examined from 7-10 days to see if it suffers from rabies or not • but it is recommended for 30days to 6 months quarantine to rule out any chances of latent infection
  14. 14. Clinical signs • initial CS are non specific and may include general lethargy, inappetence,diarrhea, vomition • changes in behavior may be one of the first clinical signs • 2 forms: furious form (hyper excitable) and dumb(paralysis predominant • contrary to common belief dumb form is more common in our country
  15. 15. Clinical signs • high toned yelp or bark • bites abnormal/inanimate objects • increased nervousness, temperature elevated,partial paralysis of jaw, restlessness, increased tendency to bite object if kept in mouth • a combination of increased saliva and inability to swallow may present as profound contamination of mouth chin and forelegs with potential infection of saliva
  16. 16. Clinical signs • cranial nerve involvement may be focal and unilateral presenting animal with unequal pupil size, with dysfunction in facial or tongue paresis and change in phonation • at end stage animal becomes profoundly moribund • end stage paralysis • sometimes dog dies without showing clinical signs
  17. 17. Diagnosis • history and CS • isolation of virus: salivary gland, brain and other nervous tissue preserved in 50% glycerol. the sample is inoculated into mice/cell lines like bhk-21 • serological: dFA gold standard test(brain tissue, corneal impression). the tissue shouldn't be stored in formalin • immunohistochemistry for formalin fixed • sellar staining(histology): negri bodies found in hippocampus of dogs • amplification: rt-PCR
  18. 18. Treatment • wound management: wash wound with plenty of soap(carbonyl soaps preferred).after washing with soap, quaterinary ammonium compounds maybe applied as antiseptic along with antirabies serum • wound shouldnt be sutured • if unavoidable first infiltrate antirabies sera around wound
  19. 19. Prevention and control • post-exposure and pre-exposure immunoprophylaxis • two types of vaccine available in india: (1) nervous tissue antirabies vaccine (2) tissue culture arv • tissue culture vaccine(purified chick embryo cell culture) gives high titer of neutralizing antibodies and doesn't cause neuroparalytic complication as in nervous tissue arv(banned by WHO) • dose 1ml s/c or i/m
  20. 20. Prevention and control • pre-exposure prophylaxis in dogs and cats: primary dose 90th day booster 1 +21 days booster2 +21 days annual booster yearly
  21. 21. Prevention and control • post-exposure prophylaxis: 0,3,7,14,28,90(optional) • antirabies serum can also provide passive immunity at inital stages. dose: 40IU/kg bw i/m max 3000IU Equine antirabies serum in animals
  22. 22. humans post exposure • Updated Thai Red Cross Schedule (2-2-2-0-2). • This involves injection of 0.1ml of reconstituted vaccine per ID site and on two • such ID sites per visit (one on each deltoid area, an inch above the insertion • of deltoid muscle) on days 0, 3, 7 and 28. The day 0 is the day of first dose • administration of IDRV and may not be the day of rabies exposure/animal bite.
  23. 23. control programmes • canine rabies control programme(MoI GOI) • education to responsible ownership • mobilization of community participation • reduction of contact rate between susceptible dogs • stray dog control • mass immunization • rabies diagnosis and surveillance • recording of suspected cases of suspected rabies
  24. 24. Refrence • Ettinger, 2010. text book of veterinary internal medicine vol 1 • Sharma R D, 2010. textbook of preventive medicine and epidemiology • •