Rabies is an acute, progressive encephalomyelitis caused by lyssaviruses. This zoonosis occurs worldwide in mammals, with dogs, bats, and wild carnivores as the principal reservoirs. Typical clinical signs include acute behavioral changes and progressive paralysis. The disease is fatal once clinical signs appear; however, appropriate and timely administration of local wound care, immune globulin, and vaccination can prevent disease in unvaccinated humans after exposure. Vaccines are available for domestic animals, wildlife, and humans to prevent rabies and to help control transmission in reservoir populations.
Rabies is a fatal viral zoonosis and serious public health concern. The disease principally affects carnivores and bats, although any mammal can be affected.
Etiology of Rabies in Animals
Rabies is caused by viruses in the genus Lyssavirus in the family Rhabdoviridae. Globally, rabies virus is the most important member of the genus. Information regarding the diagnosis, pathogenesis, clinical signs, and prevention of rabies virus infection is generally applicable to other lyssaviruses as well.
Classification of Viral Genome
Rabies virus has a nonsegmented single-stranded negative-sense RNA genome (~12 kb) encoding five viral proteins:
nucleocapsid protein (N)
matrix protein (M)
glycoprotein (G)
large protein (L), the enzymatically active RNA-dependent RNA polymerase
phosphoprotein (P), L protein’s cofactor
Besides rabies virus, the International Committee on Taxonomy of Viruses lists 16 other species in the genus Lyssavirus, demarcated according to their genomic sequences. Additional putative novel species have been reported but have yet to be fully characterized.1
Structure
Rabies virus is an enveloped virus; lipid bilayer primarily derived from host cell membrane comprises the outer envelope, which is lined by the matrix protein. Virions are distinctively bullet-shaped and measure approximately 75 nm wide and 180 nm long.
The surface of the virion is covered with transmembrane trimeric glycoprotein spikes, which recognize and bind cell receptors. Internally, the genomic RNA is encapsidated to form a helical ribonucleoprotein closely associated with a viral RNA polymerase complex.
Replication
Rabies virus replicates by budding from host cell membranes. Following adsorption via receptor-virion interaction, free virus particles infect new cells by fusing their envelopes with the host cell membrane, allowing entry of viral genetic material. Messenger RNA is transcribed from the RNA genome.
Translation into proteins occurs on free ribosomes, and viral nucleocapsid develops in the cytoplasm. Complete viral particles may be formed at the cell surface but more commonly bud from intracytoplasmic membranes.
Pathogenic Mechanisms
Rabies virus replicates initially in non-nervous tissue at the site of inoculation.
Lyssaviruses such as rabies virus are highly neurotropic. Rabies virus travels via the peripheral nerves to the spinal cord and ascends to the brain. After reaching the brain, the virus travels via peripheral nerves to the salivary glands and other organs.
If an animal is capable of transmission via its saliva, virus will be detectable in the brain. Virus is shed intermittently in the saliva.
Near the end of the clinical phase, after replication in the CNS, rabies virus may be found in nearly every innervated orga
The surface of the virion is covered with transmembrane trimeric glycoprotein spikes, which recognize and bind cell receptors. Internally, the genomic RNA is encapsidated to form a helical ribonucleoprotein closely associated with a viral RNA polymerase complex.
Replication
Rabies virus replicates by budding from host cell membranes. Following adsorption via receptor-virion interaction, free virus particles infect new cells by fusing their envelopes with the host cell membrane, allowing entry of viral genetic material. Messenger RNA is transcribed from the RNA genome.
Translation into proteins occurs on free ribosomes, and viral nucleocapsid develops in the cytoplasm. Complete viral particles may be formed at the cell surface but more commonly bud from intracytoplasmic membranes.
Pathogenic Mechanisms
Rabies virus replicates initially in non-nervous tissue at the site of inoculation.
Lyssaviruses such as rabies virus are highly neurotropic. Rabies virus travels via the peripheral nerves to the spinal cord and ascends to the brain. After reaching the brain, the virus travels via peripheral nerves to the salivary glands and other organs.
If an animal is capable of transmission via its saliva, virus will be detectable in the brain. Virus is shed intermittently in the saliva.
Near the end of the clinical phase, after replication in the CNS, rabies virus may be found in nearly every innervated organ.
Epidemiology of Rabies in Animals
Identification of different virus variants by laboratory procedures, such as monoclonal antibody analysis or genetic sequencing, has greatly enhanced understanding of rabies epidemiology.
Rabies virus is adapted to its reservoir host, and antigenically distinct rabies virus variants are maintained within specific animal reservoir species (eg, the virus variant associated with rabies maintained by dog-to-dog transmission is termed the canine rabies virus variant).
Generally, each rabies virus variant is responsible for virus transmission between members of a major reservoir species in the geographic area in which it is enzootic. However, cross-species transmission of rabies virus variants does occur (eg, rabies in a dog as a result of infection with a variant from a skunk would be referred to as skunk rabies virus variant infection in a dog).
At least 30 species are known reservoirs, primarily terrestrial carnivores, hematophagous bats, and insectivorous bats. Globally, the dog is the most important reservoir, particularly in Asia and Africa.
In North America, distinct virus variants are responsible for rabies perpetuation in red and Arctic foxes in Canada and Alaska, raccoons along the eastern seaboard from Maine to Florida, and gray foxes in the southwest, including Arizona and New Mexico.
Two variants are responsible for rabies in striped skunks, one in the south-central states and the other in the north-central states, often extending into the Canadian prairies. Another skunk rabies virus variant is found in California.
By comparison, the epidemiology of rabies in bats is complex. In general, each variant found in bats may be characterized with a predominant bat species. Spillover from bats to other mammals occurs infrequently.
Most indigenous human cases of rabies in the US are due to bat rabies virus variants (especially viruses associated with Lasionycteris noctivagans, the silver-haired bat; Perimyotis subflavus, the tricolored bat; and Tadaridabrasiliensis, the Brazilian free-tailed bat).
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