No other animal disease causes as much anxiety as rabies, though human cases have become extremely rare. The reason for the rarity is not because we have inoculated ourselves against rabies nor is the reason that we have decreased the incidence in the animal population. In fact the evidence indicates an increasing incidence of rabies in wildlife. Humans rarely come in contact with rabies because we have created a buffer of well-vaccinated pets between us and the wild mammal population. This article discusses what rabies is, the incidence, how it affects horses, treatment, and vaccination. .

The disease is caused by a single-stranded RNA virus in the family Rhabdoviridae, genus Lyssavirus. Within the genus there are currently some 25 viruses, but only serotype I rabies viruses are of any significance in domestic species. The serotype includes viruses isolated from bats in the Americas and viruses from historical disease syndromes such as Nigerian horse disease. Although these may present with distinct clinical signs, they cannot be distinguished by classic serologic techniques. The majority of wildlife vectors are bats, skunks, and raccoons in the United States, with spillover occurring into domestic animals from this reservoir. Rabies in rodents appears to be uncommon.

Rabies usually is transmitted by the saliva of an infected animal contaminating a bite wound. Other documented routes include, inhaled (aerosolized bat feces particles), oral, and transplacental. The sequence of events that occur after natural infection is still not clear but it has been suggested that the virus may replicate in muscle fibers as an amplification step before invading the nervous system. How the virus gains entry into the peripheral nerves is not known. Chemical receptors may serve as virus attachment sites. Then the virus is passed to the spinal cord and brain by retrograde axoplasmic transport. The location of the distribution of the virus to the CNS determines the clinical signs which are usually divided into either furious or paralytic forms. Spread throughout the rest of the CNS and sympathetic chain is quite rapid and is due, in part, to multiplication and active spread of the virus in neurons and possibly also passive transport in CSF. In addition to centripetal viral movement to the CNS, the virus also moves centrifugally to ultimately affect almost all other nerves in the body, as well as tissues in the eye and the salivary glands. Salivary secretion of the virus has been shown to predate the onset of clinical signs by as much as a month.

The incubation period for rabies in horses seldom has been documented but probably varies from two weeks to several months. As with the sequence of clinical signs and the survival time, it is dependent on the proximity of the bite wound to the brain and dose and pathogenicity of the viral strain. Horse to human transmission appears to be very rare.