Page 1712 - Cote clinical veterinary advisor dogs and cats 4th

862 Rabies

○ Skunks: mainly in California and the north Etiology and Pathophysiology Advanced or Confirmatory Testing
central and south central states • Single-stranded RNA virus of the genus • Cerebrospinal fluid (CSF) analysis may
VetBooks.ir responsible for most human cases in the • Transmission • Direct IFA testing of nervous tissue is the
show nonspecific increases in protein and
○ Bats: 48 contiguous United States and
Lyssavirus, family Rhabdoviridae
leukocytes.
past 20 years
○ Virus in saliva is transmitted through a
wound or mucous membranes.
○ Foxes: Arctic fox in Alaska, red and gray
fox in southeast United States ○ Inhalation of aerosolized virus may occur confirmatory test of choice.
○ Chill—do not freeze—the body or brain
○ Mongoose: Puerto Rico with exposure to bats/bat caves. of any dead/euthanized rabies suspect.
• The dog is the primary species involved in ○ Ingestion of infected tissues is also possible ○ Immediately submit the brain to a
transmission of rabies in Central America as a route of infection but is rare. state-approved laboratory for rabies IFA
and the Southern Hemisphere. ○ By organ transplantation (humans) testing.
• Virus replicates in local tissues, where it enters ○ Use extreme caution in obtaining samples
Clinical Presentation neuromuscular junctions and neurotendinous and shipping specimens; zoonosis can
DISEASE FORMS/SUBTYPES spindles. occur if rabies virus is aerosolized (e.g.,
Clinical signs are variable but predominantly ○ Virus is vulnerable to immune-mediated when an electric saw is used for opening
arise from central nervous system (CNS) destruction (e.g., vaccine induced) in the skull and proper protection is not
dysfunction. local tissues but becomes protected after used) or is inadvertently inoculated.
• Prodromal form it reaches peripheral nerves or the CNS. • A new reverse transcription polymerase chain
○ Change in behavior, which may include • Spreads by intraaxonal flow through reaction (RT-PCR) method is useful with
anxiety, solitude, and apprehension peripheral nerves to the spinal cord and small samples such as saliva and spinal fluid
○ Fever may occur. brain, replicates in the CNS, and then moves and has been shown to be as rapid as the
○ Pruritus may occur at the site of exposure. outward through peripheral, sensory, motor, IFA test.
○ Lasts 2-3 days and cranial nerves. • Direct IFA testing of dermis: skin biopsy of
• Paralytic (dumb) form (majority of canine • Large amount of virus is present in salivary sensory vibrissae of the maxillary area should
cases, minority of feline cases) glands, where it is shed. Salivary virus excre- not be used (false-negative results).
○ Lethargy, difficulty swallowing, ptyalism, tion begins up to 2 weeks before the onset
voice or bark change, dropped jaw, and of neurologic signs. TREATMENT
lower motor neuron paralysis, often first • The incubation period varies and depends
in the wounded limb on innervation at the bite site, distance of Treatment Overview
○ Lasts 1-7 days, from onset of overt signs the bite site to the CNS, virus variant, and • Fatal; recovery is extraordinarily rare. There
to death amount of virus in the exposure; can range have been 15 reports of human survival after
• Furious form (majority of feline cases, from 2 weeks to > 6 months confirmed rabies infection to date, and the
minority of canine cases) • After clinical signs are apparent, death ensues best outcome appears to be after bat virus
○ Aggression, biting, altered voice, paralysis, within 10 days. transmission.
seizures, and ataxia • The first reported survival of a human who
○ Hyperesthesia and hyperresponsive- DIAGNOSIS did not receive rabies pre-exposure or post-
ness to auditory and visual stimuli are exposure prophylaxis was recently described,
possible. Diagnostic Overview with a treatment called the Milwaukee
○ Lasts 2-4 days, from onset of overt signs Diagnosis is suspected in any animal with an protocol: rifampin, amantadine, and the
to death unknown or incomplete rabies vaccination induction of a ketamine/midazolam coma.
history that develops acute neurologic signs. • Dogs or cats that have bitten a person or
HISTORY, CHIEF COMPLAINT Confirmation requires direct immunofluores- are believed to have had contact with a wild
• History of wound may or may not exist. cence assays of brain/nervous tissue. animal must be confined and quarantined.
Given the pathophysiology of rabies, neuro-
logic clinical signs beginning within 1 week Differential Diagnosis Recommended Monitoring
of the occurrence of a wound are extremely • Encephalitis: viral (canine distemper, feline • Management of rabies suspects varies with
unlikely to be related to rabies infection by leukemia virus, feline immunodeficiency immunization status and local laws. The
the wound. virus, feline infectious peritonitis); immune attending veterinarian should contact the
• Behavioral changes are very common and mediated (e.g., granulomatous meningo- local state/regional veterinarian.
can vary. encephalitis); rarely, protozoal, rickettsial, • Most public health laws require a 10-day
○ Aggression, viciousness, irritability, excit- bacterial, or fungal confined observation period for dogs/cats
ability, nervousness, apprehension, and • Pseudorabies that bite a human.
anxiety • Intoxication (e.g., lead) ○ Virus shedding in saliva begins 1-5 (pos-
○ Abnormal or erratic behaviors, such as • Cerebral cysticercosis caused by larval Taenia sibly up to 13) days before the onset of
licking, biting, wandering, disorientation, solium mimics rabies in dogs. neurologic signs in infected animals.
ataxia, seizures, or paralysis • Portosystemic shunt • A healthy dog or cat that bites or scratches
• Ptyalism and change in bark • Hypoglycemia an individual should be securely confined
• No clinical signs; exposure is suspected but • Neoplasia and monitored for behavioral changes and/
not confirmed. • Trauma or neurologic signs suggesting rabies for 10
• Trigeminal neuropathy days.
PHYSICAL EXAM FINDINGS • Causes of ptyalism (p. 833) ○ If clinical signs do not develop in the dog/
Timing of the onset of clinical signs varies: cat within 10 days of bite/scratch, there
signs begin 2 weeks to several months after Initial Database has been no human exposure to rabies
exposure. Signs include fever, dropped jaw, • The clinical suspicion of rabies is based on virus.
ptyalism, inability to swallow, and mandibular history and physical exam in unvaccinated ○ If clinical signs consistent with rabies
and laryngeal paralysis. Lower motor neuron or poorly vaccinated animals. develop in the dog/cat during the 10-day
limb signs, ataxia, and cranial nerve deficits • CBC, serum chemistry panel, and urinalysis quarantine period, or if there were neu-
may be present. are unhelpful. rologic signs consistent with rabies at the

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