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. 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.
5. • 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
6.
7. • 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
8. 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
9.
10. 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
11. 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
12. 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
13. 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
14. 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
15. 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
16. 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
17.
18.
19. 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
20. 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
21. 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
22. 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: dFAgold 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
23.
24. 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
25.
26. 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
27. Prevention and control
• pre-exposure prophylaxis in dogs and cats:
primary dose 90th day
booster 1 +21 days
booster2 +21 days
annual booster yearly
28. 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
29. 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.
30.
31. 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
32. Refrence
• Ettinger, 2010. text book of veterinary internal medicine
vol 1
• Sharma R D, 2010. textbook of preventive medicine and
epidemiology
• http://www.cdc.gov/rabies/diagnosis/index.html
• http://www.ncdc.gov.in/Rabies_Guidelines.pdf
