West Nile fever

In clinical cases in horses, owners first notice incoordination and weakness, usually in the hind limbs and often asymmetric, sometimes with fever, depression, reduced appetite and muscle twitching or tremors. Signs can progress to stumbling, facial paralysis, impaired vision, head pressing, teeth grinding, circling, difficulty swallowing, convulsions, and ascending paralysis ending in recumbency; fatal cases usually die within about five days. Susceptible birds such as geese and corvids show wing and leg paralysis and incoordination. Histology shows non-suppurative encephalomyelitis centred on the spinal cord and brainstem.

West Nile fever is caused by West Nile virus, a flavivirus of the Japanese encephalitis complex (family Flaviviridae), related to St. Louis encephalitis and yellow fever viruses. A mosquito that has fed on a viraemic bird injects the virus when biting. Birds develop enough viraemia to infect further mosquitoes, whereas horses and people usually do not, so they are dead-end hosts. In horses that become ill, the virus reaches the central nervous system and causes a mild to moderate non-suppurative encephalomyelitis. Lesions sit mainly in the spinal cord and lower brainstem, involve both grey and white matter, and are most severe in the thoracic and lumbar cord, which accounts for the hind-limb weakness.

Birds are the reservoir, and Culex mosquitoes are the main vectors; ticks have also been implicated. Horses and humans are incidental hosts, and the virus also replicates in reptiles, amphibians and other mammals. First isolated in Uganda in 1937, it was found in Israel in 1951 and Egypt in the 1950s, and is present in parts of the Middle East and Europe; it reached North America in 1999 and later Mexico and South America. Transmission tracks mosquito activity, peaking at dusk and dawn, and cases in endemic northern-hemisphere areas are suspected mainly from June to October. It is a zoonosis, and a disease listed in the WOAH Terrestrial Animal Health Code.

Other equine neurological diseases: rabies, botulism, equine protozoal myeloencephalitis, cervical vertebral stenotic myelopathy, equine herpesvirus 1 myeloencephalopathy, equine degenerative myeloencephalopathy, and eastern, western and Venezuelan equine encephalitis. Signs overlap, so separation depends on the laboratory: IgM-capture ELISA and neutralisation tests on serum in the living horse, and PCR, virus isolation or immunohistochemistry on brain and spinal cord after death.

Central nervous system: spinal cord (especially thoracic and lumbar segments), brainstem, brain; peripheral musculature (weakness, fasciculation)

Vaccination of horses in endemic areas before mosquito season (killed, canarypox-vectored and DNA vaccines exist); mosquito control and breeding-site reduction, stable screening, repellents, limiting dusk and dawn exposure; dead bird surveillance.

No specific treatment; supportive care only. Case fatality in clinically ill horses 25-45% across outbreaks (38% in the US in 2000); about 40% of survivors still had neurological deficits at six months. Geese mortality 20-60%.

Wild birds