Also see Equine Viral Encephalomyelitis.
West Nile virus (WNV), a flavivirus related to the St. Louis encephalitis/Japanese encephalitis complex, was first isolated from the blood of a febrile Ugandan woman in 1937. The virus was first described as the cause of a West Nile fever epidemic in people in Israel in 1951; in a later outbreak, severe meningoencephalitis was seen in elderly patients. The role of mosquitoes in viral transmission was clearly delineated in a series of field studies in Egypt in the 1950s. Wild birds were identified as the reservoir of the virus around the same time. Cases of West Nile fever in horses were reported several years later. WNV was first associated with disease in domestic avian species in 1997, when flocks of young geese in Israel were affected with a neuroparalytic disease. In August 1999, the disease appeared for the first time in the Western hemisphere when wild and zoo birds, horses, and humans died in the northeast USA, notably in the New York City area.
Etiology and Epidemiology
WNV is considered to be endemic in many countries of Africa, Asia, southern Europe, and North America. Since 2001, serologic evidence of the spread of WNV into Latin America, the Caribbean, and South America has been reported. Epidemics appear in the human population at infrequent intervals in some of these countries, and there is evidence for viral transmission between Africa and Europe by migrating birds. Most outbreaks have occurred during the summer months and can continue until cold nights reduce mosquito vector activity, notably Culex spp.
Geese are the only known natural hosts of WNV among domestic avian species. Most of the flocks affected in the Israel outbreaks were 5–9 wk old, but goslings as young as 3 wk and as old as 11 wk were also affected. Adult breeding flocks were clinically unaffected but virus neutralizing antibodies were found. Mortality of young Muscovy ducks but not young chickens or turkey poults was induced experimentally with a WNV isolate. While chickens are not killed by WNV, they do develop antibodies against the disease and have been used as sentinels to monitor WNV presence. Neither chickens nor turkeys develop high enough levels of viremia to infect mosquitoes or transmit the virus to other animals.
The principal route of viral transmission is by the bite of a mosquito (primarily Culex spp). In the USA during 1999 and 2000, most of the viral isolates were made from C pipiens and C restvans. WNV has been isolated, RNA detected, or antibodies found in 62 mosquito species in North America. In Africa and the Middle East, the usual vector is C univittatus, and in Europe, C pipiens and C modestus. WNV has also been isolated from at least 10 tick species.
Affected geese show various degrees of neurologic involvement ranging from recumbency to leg and wing paralysis. Affected birds are either reluctant or unable to move when disturbed. Signs of incoordination are pronounced and some birds flip over while attempting to stand. Naturally affected geese show torticollis and opisthotonos. Mortality rates of 20–60% have been reported, probably due to horizontal spread of the virus.
Pathologic changes include pallor of the myocardium and occasionally of the kidneys, splenomegaly, and hepatomegaly. The meningeal blood vessels are injected. Microscopic brain lesions consist of lymphocytic perivascular infiltration and neuronal degeneration. Small necrotic foci are present in the myocardium, but lymphocytic infiltration is minimal.
The tissues of choice for isolating virus from paralytic or dead birds are the brain, spleen, and kidneys. Homogenates are inoculated into the brain of newborn mice, embryonated eggs by the yolk sac route, or Vero and mosquito cell line cultures. Reverse transcriptase PCR with RNA extracted from either brain material or cell culture supernatant can also be performed. TakMan technology for rapid molecular diagnosis of field-collected mosquitoes and avian tissues is also available. Immunohistochemistry can be used on formalin-fixed paraffin-embedded tissues, in particular brain and kidney, to visualize viral antigens in infected birds. Several forms of ELISA have also been developed for flaviviruses.
Neurologic signs in young geese must be distinguished from those caused by Riemerella infections, especially R anatipestifer. Other bacteria include Streptococcus gallolyticus, and Erysipelothrix, Listeria, and Salmonella spp. Neurotropic viruses include Newcastle disease, which is rare in geese, and avian influenza. Ionophore intoxication can induce paralytic signs. Aspergillus also causes brain lesions and caseous nodules in the lungs.
Prevention and Control
Mosquito control is a mandatory component of any arboviral disease control program. Unfortunately, this is difficult to implement in a rural environment because of the distances that mosquitoes can fly or be carried by prevailing winds. Standing water and similar insect breeding sites in the vicinity of densely populated avian farms should be treated with larvicides. Poultry houses should be constructed to be insect free. Because many arboviral diseases are zoonoses, much can be achieved by cooperation with human disease surveillance agencies.
Control of WNV in geese is confined to vaccinating young flocks at risk, especially those raised during months when Culex spp are most numerous. Because of confounding factors such as possible horizontal transmission of virus, all birds in the flock should be vaccinated. Due to the age-related susceptibility to the virus, goslings should be immunized as young as possible, preferably at 3 wk old. Currently, WNV vaccines are not available commercially in North America, although several types have been developed and widely used in domestic geese in Israel. Laboratory trials have been performed with a formaldehyde-inactivated suckling mouse brain-derived product. Over 75% of geese vaccinated with a single dose of vaccine at 3 wk of age were protected, and 94% protection was achieved with 2 doses spaced 2 wk apart. The duration of immunity was estimated to last until 12 wk of age. Inactivated vaccines prepared from chick embryos or Vero cells are not protective because of their low antigenic mass. A single dose of a live attenuated vaccine derived from high mosquito cell passage induced immunity to intracerebral challenge in young geese. Mosquito feeding experiments and back passage reversions to virulence studies have yet to be completed.
Last full review/revision March 2012 by Scott D. Fitzgerald, DVM, PhD, DACVP, DACPV