Canine Rabies

Introduction
• Rabies is caused by an acute, progressive viral encephalomyelitis
that affects all mammals but mainly affects carnivores and bats

• Rabies is the oldest known zoonotic disease and canine disease and
fatal in infected humans and animals that show clinical signs.
• Rabies is the oldest fatal zoonotic diseases

• Rabies is found throughout the world(all continent), with the

exception of Antarctica

• Worldwide, the dog is the most important reservoir, particularly in

less developed countries
Etiology
• Disease is caused by the Rabies virus
• Rhabdovirus family
• Lyssavirus genus
• >16 different lyssaviruses have been described.
• But Globally, rabies virus is the most important member of the genus.
• Lyssaviruses are highly neurotropic.

• Rabies is a Large, bullet-shaped RNA lyssavirus {family Rhabdoviridae)

• Rabies is perpetuated by wildlife reservoirs in aII parts of the world,

which includes foxes, mongooses, skunks and raccoons, bats.
Etiology
• Rabies maintained by dog-to-dog transmission is termed
Canine rabies
• The name of the mammalian species acting as the source of
Rabies infection is used as an adjective to describe their
involvement in the infection process.

• For instance, rabies in a dog as a result of infection with a

variant from a different reservoir mammal, is named with
the name of the animal in the case description
• eg skunk (or raccoon or fox), would be referred to as skunk (or
raccoon or fox, etc) rabies in a dog.
Etiology
•All rabies reservoirs are also vectors of the virus
•Not all vectors are reservoirs

•For example, cats can effectively transmit rabies

virus
• Virus is present in the saliva of rabid cats, and people
have developed rabies after being bitten by rabid cats.

• But no unique feline rabies virus variant has been

documented.
Transmission
• Transmission of rabies principally occurs via introduction of
virus-laden saliva into tissues, usually by the bite of a rabid
animal

• Virus from saliva, salivary glands, or neurological tissues

such as brain can also cause infection by entering the body
through fresh wounds or intact mucous membranes

• The rabies virus is not transmitted through intact skin

• Hematogenous spread does not occur.

Transmission
• Under most circumstances, there is no danger of aerosol transmission of
rabies virus.

• However, aerosol transmission has occurred under very specialized

conditions in which the air contained a high concentration of suspended
particles or droplets carrying viral particles.
• Aerosol infection may occur via direct attachment of the virus to olfactory nerve
endings.
• Under laboratory condition/ bat cave condition

• Rabies virus has been transmitted by transplantation of tissues and

organs from infected people.

• Consumption of infected meat

 Transmission
• Typically, rabies virus remains at the inoculation site for
a considerable time.

• Helps to explain the effective action of local infiltration of

rabies immune globulin during human postexposure
prophylaxis, even days after exposure.
Pathogenesis
• After a bite, virus is inoculated at site of bites.
• Rabies virus travels via the peripheral nerves to the spinal
cord and ascends to the brain.
• The virus multiples in the central nervous system with the
animals beginning to show signs
• After reaching the brain, the virus travels via peripheral
nerves to the salivary glands and other organs.
• Centrifugal spread along nerves from the brain results in
localization in salivary glands and excretion in saliva.
• Virus is shed intermittently in the saliva.
Pathogenesis

Peripheral
Spinal cord brain
nerves

Salivary gland
 Clinical signs
•Most rabies cases in dogs develop within 10
days to 6 months after exposure, but this
period may be shorter or considerably longer,
as short as 1week

•In humans typically 2–3 months

•Can be as far as >8 years.
Clinical signs
• The incubation period is can be both prolonged and
variable.
• The incubation period is affected by:
• the amount of implanted virus
• the richness of local innervation
• the distance of the wound to the CNS.

• Saliva is infectious at, or before, the time clinical signs

occur.

• Domestic dogs and cats may shed virus up to 10 days

before onset of clinical signs.
Clinical signs
•Typical signs of CNS disturbance are acute
behavioral changes and unexplained progressive
paralysis.(The most reliable signs, in all species)

•Behavioral changes may include:

•sudden anorexia
•signs of apprehension or nervousness
•irritability
•hyperexcitability (including priapism)
Clinical signs
•The animal may seek solitude
•Ataxia
•altered phonation
•Uncharacteristic aggressiveness may develop—a
normally docile animal may suddenly become
vicious.
•Lost of fear of people, and normally nocturnal
species(wildlife) may be seen wandering about
during the daytime.
The clinical course
Divided into three general phases.
1. prodromal – First stage
2. Acute neural excitative(furious rabies)- second
stage
3. paralytic/end stage(dumb rabies) – third stage

• However, this division is of limited practical value because

of the variability of signs and the irregular lengths of the
phases.
Clinical course
Initial Prodromal phase
•Altered temperament and behavior.
•A friendly dog suddenly turns shy and nervous
•Reserved animals suddenly become friendly
•The disease progresses rapidly after the onset of
paralysis, and death is virtually certain a few days
thereafter.
•Some animals die rapidly without marked clinical
signs.
Clinical course
The furious form
• Aggression (the acute neural excitative phase) is pronounced.
• This is the classic “mad-dog syndrome,” although it may be seen in
all species.
• There is rarely evidence of paralysis during this stage.
• The animal becomes irritable and, with the slightest provocation,
may viciously and aggressively use its teeth, claws, horns, or
hooves.
• The posture and expression is one of alertness and anxiety, with
pupils dilated.
• Noise may invite attack.
• Such animals lose caution and fear of people and other animals.
 Clinical course
The furious form 2
• frequently extensively roaming, attacking other animals, including people,
and any moving object.
• They commonly swallow foreign objects, eg, feces, straw, sticks, and
stones.
• Rabid dogs may chew the wire and frame of their cages, breaking their
teeth, and will follow a hand moved in front of the cage, attempting to
bite.
• Young pups can seek human companionship and are overly playful, but
bite even when petted.
• Rabid skunks may seek out and attack litters of puppies or kittens. Rabid
domestic cats and bobcats can attack suddenly, biting and scratching
viciously.
• As the disease progresses, muscular incoordination and seizures are
common. Death may results from progressive paralysis.
Clinical coarse
The paralytic form
• manifest by ataxia
• paralysis of the throat and masseter muscles, often with
profuse salivation and the inability to swallow.
• Dropping of the lower jaw is common in dogs.
• Owners frequently examine the mouth of dogs and
livestock searching for a foreign body or administer
medication with their bare hands, thereby exposing
themselves to rabies.
• These animals may not be vicious and rarely attempt to
bite.
• The paralysis progresses rapidly to all parts of the body, and
coma and death follow in a few hours.
 Diagnosis
Laboratory diagnosis
• Rabies must be considered in any dog/cat showing unusual mood /behavioral
change or exhibiting any unaccountable neurologic signs

• Therefore, when rabies is suspected and definitive diagnosis is required,

laboratory confirmation is indicated.

• Immunofluorescence microscopy on fresh brain tissue is the test of choice

• Suspect animals should be euthanized, and the head removed for laboratory
shipment.

• There are no clinical or gross pathognomonic lesions for the diagnosis of

rabies in animals; therefore, confirmation of infection can only be achieved by
laboratory techniques
Diagnosis
• The rabies virus is usually identified by Direct immunofluorescence
in a brain sample taken at necropsy.
• the hippocampus, cerebellum and the medulla oblongata are the
recommended brain tissue of choice

• Direct Fluorescent Antibody (dFA) test – gold standard/test of

choice
• The test is based upon the microscopic detection of inclusions in the
brain of rabid animals.
• Brain impressions are made upon microscope slides, which are fixed
and incubated with fluorescein isothiocyanate (FITC)-labeled
antibodies to rabies virus (RABV).
• These stained impressions are viewed using epi-fluorescence
microscopy.
Positive Direct florescent antibody test
Diagnosis
•Seller’s stain test – for the detection of
Negri bodies- provide diagnosis under 1
hour- low sensitivity
•Negri bodies- eosinophilic, sharply outlined,
pathognomonic inclusion bodies (2–10 μm in
diameter) of viral proteins found in the
cytoplasm of rabies infected neurons

•PCR
Pathogenesis of Rabies
Treatment

• There is no treatment once the clinical signs appear.

Prevention
• Rabies can be prevented in dogs and cats by vaccination.
• 100% vaccine preventable.
• Suspected animals are generally kenneled for a period of 10
days/2 weeks and observed.

• If the animal is alive and healthy after that time, the animal is
considered not to have been shedding rabies virus in its saliva at
the time of the encounter

• If animals exhibits any of the signs of rabies after the period of

quarantine then animal is euthanized and tested.
Prevention
• Veterinary workers should handle potentially rabid
animals with extreme caution.

• Protective clothing such as thick rubber gloves, eye

goggles and a plastic or rubber apron should be worn
when doing autopsies or in other circumstances when
exposure to infectious tissues could occur.

• A human vaccine is available for any populations at

risk.
Prevention
•Education of pet owners and general public
on responsible pet keeping.

•Stray dog population control.

•Serology is occasionally used to test

seroconversion in domesticated animals
before international travel