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West Nile Virus (WNV)

By: Dr. Branson Ritchie

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West Nile virus (WNV) was initially isolated in 1937 from the blood of a woman with a fever in Uganda. It was one of the first viruses shown to be transmitted by mosquitoes. This virus is in the family Flaviviridae, which contains other notable arthropod-transmitted viruses like yellow-fever virus, dengue hemorraghic fever virus and St. Louis encephalitis virus. The later is endemic in the eastern United States causing sporadic, seasonal outbreaks of disease in humans and horses. Historically, free-ranging birds from multiple families have been considered highly susceptible to WNV infection but relatively resistant to disease. While transiently infected, free-ranging birds can serve as a source of virus for mosquitoes, and occasionally other biting insects, who can then transmit the virus to other birds, humans, horses or other mammals. Direct transmission (transmission not involving an insect) would only be a concern with blood to blood transfer during the brief period when high concentrations of virus are found in the blood.

West Nile virus is considered one of the most widely distributed of all flaviviruses, but until recently had not been isolated from a host in North America. In the fall of 1999, a strain of WNV was recovered from humans, birds and mosquitoes during a disease outbreak that started in New York City. The outbreak was first recognized in August when free-ranging crows from the area began dying with clinical changes suggestive of nervous system damage (ie. abnormal head positioning, circling, wing droop, stumbling, tremors and convulsions). During the subsequent months, WNV was confirmed as the cause of death in more than 20 species of captive and free-ranging birds from New York State, New Jersey and Connecticut. Deaths were also reported in some humans and horses from the same areas.

Since its initial description, WNV has been associtated with occasional outbreaks of disease in humans and horses in Africa and Asia. Sporadic outbreaks have also been described in Europe but WNV associated problems are less common in Europe than in Africa and Asia. This virus has rarely been associated with disease in birds, making the US outbreak particularly unusual.

The recent immigration of WNV to the United States is concerning. If WNV, presumably introduced to New York in the summer of 1999, is able to overwinter in a manner similar to endemic flaviviruses, then recurring seasonal outbreaks of WN fever should be expected. The immigration of WNV to North America, reminds us that any pathogen is only a plane ride away.

Symptoms in Birds

In general, naturally acquired flaviviruses (like WNV) and togaviruses (like EEE virus) infections generally cause no recognizable problems in birds that coevolved with endemic strains of virus, but often fatal infections in birds that evolved elsewhere. Numerous species of birds have been shown to be susceptible to WNV infection including two species of Psittaciformes, the ringed-neck parakeet and the vasa parrot. Species of companion birds that evolved in Euroasia would be considered relatively resistant to WNV associated disease, while those species that evolved elsewhere might be more likely to develop clinical changes or die.

Birds with clinical changes suggestive of nervous system damage (ie. abnormal head positioning, circling, wing droop, stumbling, tremors and convulsions) should be evaluated by an avian veterinarian immediately. Most cases of nervous system disease in birds will caused by bacteria, fungi, toxins, cancers or viruses other than WNV. West Nile virus, or other arthropod-transmitted viruses, would be most likely to cause problems in birds during seasons when mosquito activity increases. Increases in mosquito density, and thus WNV activity, would be favored by flooding, intensive irrigation procedures and higher than normal temperatures.

Symptoms in Humans and Horses

The majority of humans and horses infected with WNV remain clinically unaffected or develop only a mild transient disease followed by complete recovery. When they occur, clinical changes in horses typically include sluggishness, stumbling, limb paralysis and convulsions. Affected humans typically develop a flu-like illness characterized by high fever, headache, sore throat, fatigue, muscle pain, nausea, diarrhea and signs of respiratory disease. The incubation period is usually 3 to 6 days with an acute onset of symptoms. The virus is only in the blood for an average of 4 to 8 days in immunocompetent people, but may persist in the blood for a month in those that are immunocompromised.

Less than 15 percent of infected humans develop more severe forms of disease characterized by aseptic meningitis or encephalitis, hepatitis, pancreatitis or myocarditis. In the few humans that are more severely affected, the virus causes progressive damage of the nervous system that can lead to death. West Nile virus disease rates in humans and horses are highest with aggressive strains of the virus. For example, 5 percent of the humans with symptoms of disease died when a particularly aggressive strain began circulating in Romania. By comparison, the reported case-fatality rate in humans for St. Louis encephalitis virus is usually 10 percent.


Cases of suspected WNV should be referred to the State Veterinarian. West Nile virus infections can be documented through demonstration of a rising antibody titer in paired serum samples (tested in the same assay at the same time) or by culture of the virus. Virus neutralization assays can be used in birds and is necessary to determine if antibodies detected by ELISA are specific for WNV and not cross-reactive antibodies generated against a related flavivirus. Because of the human health risk, virus isolation should be performed only in laboratories with biosafety level 3 facilities. Isolation of the virus from blood is most successful during the first few days of infection. Polymerase chain reaction (PCR) based assays have been developed and are useful for detecting target segments of WN viral nucleic acid in clinical samples.


As is the case for most viral infections, there are no specific treatments for WNV. The clinical changes in birds associated with WNV infections can also be caused by bacteria, fungi, toxins, cancers or viruses other than WNV. Following appropriate diagnostic testing, an avian veterinarian may use antibiotics, immunostimulants, supportive nutrition and anticonvulsants (in birds with seizures).


Currently, WNV infections in birds can only be prevented by stopping an infected or contaminated mosquito from feeding on susceptible birds, humans or horses. Mosquitoes develop in standing water and removing any vesicles for water to accumulate around the home, barn or aviary may help decrease mosquito populations. Bats, some birds and many species of wasp consume large quantities of flying insects, including mosquitoes, and neighborhood programs to increase these mosquitoe predators should be encouraged. Spraying of pesticides can be used in local areas to decrease mosquito populations but the advantage of reduced concentrations of mosquitoes must be weighed against any environmental or health risk associated with pesticide exposure. When mosquito populations increase, avoid being out-of-doors in the early morning or evening when mosquitoes are most active. Companion birds maintained indoors should be at minimal risk of developing WNV associated problems.

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