Page 1090 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Nervous system 1065

VetBooks.ir Prognosis RABIES
Approximately 30% of horses with neurological dis-
ease die or are euthanased 3–4 days after the onset Definition/overview
of clinical signs. The prognosis is reasonable for ani- Rabies is a fatal neurological disease of mammals.
mals that remain standing. The prognosis is poor for Disease in horses is rare, but is of concern because of
horses that are unable to stand because of hindlimb the severity of the disease and risk to humans. Rabies
paralysis or that have signs of cerebral lesions (e.g. has been identified in horses in many parts of the world.
seizures or coma). The 70% that recover usually
have a complete resolution of clinical signs in weeks Aetiology/pathophysiology
to months; however, persistent neurological deficits Rabies virus is a highly neurotropic Lyssavirus
have been reported. (Rhabdoviridae) with strain differences in pathoge-
nicity and host range. Rabies has two classic cycles:
OTHER ARBOVIRAL DISEASES canine (urban) rabies and wildlife (sylvatic) rabies. The
majority of wildlife vectors are small to medium-sized
Equine encephalosis is an acute arthropod-borne omnivores such as skunks and raccoons. Dogs may be
viral disease caused by the equine encephalosis virus, at higher risk in certain countries with higher levels of
which is classified in the genus Orbivirus of the fam- endemic rabies in the feral canine population. Domestic
ily Reoviridae. It is endemic in most parts of South animals are generally regarded as dead-end hosts and
Africa, with Culicoides spp. the presumed vector of the are usually infected following contact with the wildlife
disease. Most infections are subclinical, with clinical vectors. Rabies is most commonly transmitted by sali-
cases developing ataxia, stiffness and facial swell- vary contamination of a bite wound, although infection
ing that is similar to African horse sickness (AHS). by inhalation, oral or transplacental routes has been
Infected horses are viraemic for 4–7 days and can be demonstrated in some species. The incubation period
infective for vectors during this time. There is no varies from 2 weeks to several months depending on
evidence that horses become carriers of the disease. the site of inoculation and the dose and pathogenicity
Equine infectious anaemia (EIA) is another of the strain. Following inoculation, the rabies virus
arboviral infection of horses that may result in neu- replicates locally and, after several days, attaches to
ropathological changes. EIA virus (EIAV) is a mem- peripheral nerve receptors. The virus is then passed to
ber of the Retroviridae family. The most common the CNS via retrograde axoplasmic transport. Rabies
neurological abnormality is symmetrical ataxia of virus has a predilection for replication in the cell bodies
the trunk and limbs. Other reported abnormalities (grey matter) of the CNS, with subsequent dysfunction
include circling, gait alterations and behavioural of these neurons leading to behavioural changes and
changes. Hydrocephalus has also been found at abnormalities of the cranial and peripheral nerves. The
necropsy. These signs may rarely occur alone, but cause of death may be respiratory paralysis as a result of
usually are present with clinical signs related to hae- infection of the medulla. Shedding of the virus in nasal
molymphatic dysfunction (see also p. 1018). and salivary secretions has been shown to pre-date the
Other than those discussed above, there is a onset of clinical signs by up to 29 days.
variety of neurotropic arboviruses that have been
reported to infect horses, leading to seroconversion Clinical presentation
and occasional disease. These include louping ill, The presentation can be highly variable and rabies
Japanese B, St. Louis, Murray valley, Semliki for- should be considered in any horse with neurological
est, Russian spring–summer, Powassan and Ross abnormalities in an endemic area, particularly in acute
River encephalitis viruses, which are all members and progressive cases. The presenting signs and clini-
of the family Flaviviridae. Members of the fam- cal course are extremely variable. Reported signs have
ily Bunyaviridae such as Main Drain viruses and included any of the following: anorexia, depression,
California group viruses may also cause neurologi- blindness, mania, hyperaesthesia, muscle twitching,
cal disease in horses. lameness, paresis, ataxia, colic, urinary incontinence