West Nile virus (WNV; Flavivirus West Nile virus) is the most widespread flavivirus in the world and has been reported on all continents except Antarctica. It was one of the first arthropod-borne viruses (ie, arboviruses) identified to infect humans and was first isolated from the blood of a febrile Ugandan woman in 1937.
Outbreaks were initially reported in Israel in the 1950s, followed by France and Russia in the 1960s and Belarus and Ukraine in the 1970s. The roles of mosquitoes in virus transmission and of wild birds as virus reservoirs were described in the 1950s. WNV was first associated with disease in domestic avian species in 1997, when flocks of young geese in Israel were affected with a neurologic 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 northeastern US, notably in the New York City area.
Etiology and Epidemiology of West Nile Virus in Poultry
The virus family Flaviviridae, which includes West Nile virus, contains three genera:
flaviviruses, including WNV, Japanese encephalitis virus (JEV), dengue virus (DENV), and yellow fever virus (YFV)
hepaciviruses, including hepatitis B and C viruses
pestiviruses, which primarily affect hoofed mammals
The Flavivirus genus contains more than 70 viruses, which are further classified into tickborne and mosquito-borne virus groups. The mosquito-borne viruses may be roughly sorted into the Japanese encephalitis serocomplex (the encephalitic clade), which includes WNV and JEV, and the hemorrhagic fever clade (the nonencephalitic clade), which includes DENV and YFV.
Geographic distribution of the mosquito-borne flaviviruses largely depends on the preferred habitat of competent mosquito vectors, with mainly Culex spp mosquitoes transmitting encephalitic flaviviruses in the Northern Hemisphere. WNV is endemic in many countries of Africa, Asia, southern Europe, and North, Central and South America. Epidemics in human populations may occur at infrequent and unpredictable intervals, often based on environmental conditions that alter mosquito activity.
Most flaviviruses are transmitted by mosquito or tick vectors, although currently a few have no recognized vectors. WNV has been detected in 43 mosquito species in the US, the most important of which is C pipiens. It has also been isolated from hard (ixodid) and soft (argasid) tick species in regions of Europe, Africa, and Asia where WNV is endemic.
WNV is maintained in natural transmission cycles between mosquitoes and viremic avian hosts. Numerous wild bird species (eg, crows, robins, sparrows, grackles, among others) reach sufficient viremia titers to infect mosquitoes (based on laboratory studies in C pipiens mosquitoes), while viremia titers in chickens and domestic turkeys rarely reach this level. Because WNV is primarily transmitted by mosquito, disease detection and outbreaks are often seasonal (ie, from midsummer to mid-to-late fall in temperate regions).
Transmission of West Nile Virus in Poultry
The principal route of West Nile virus transmission is by the bite of a mosquito (primarily Culex spp). The predominant vector species vary geographically, and preferred host species vary among mosquito species. Bird-to-bird transmission has also been demonstrated experimentally when birds were housed in close quarters, likely via ingestion of shared virus-contaminated food and water sources since the virus is shed both orally and cloacally. Direct ingestion of infectious WNV (fluid, mosquitoes, or infected tissues) also resulted in infection in birds. Although ingestion is likely an uncommon and not epidemiologically meaningful transmission route, it remains a possibility in domestic birds (eg, poultry) in high-density housing with shared food and water.
Clinical Findings of West Nile Virus in Poultry
In general, birds that are susceptible to West Nile virus–associated disease can exhibit a variety of nonspecific (eg, emaciation, dehydration, feather loss, weakness, recumbency, drooped head, anorexia, lethargy, fluffed feathers) and neurologic signs (eg, ataxia, head tilt, nystagmus, tremors, hind limb paresis, seizures, blindness).
Younger birds of many species are more susceptible to disease, exhibiting higher viremia titers than do more mature (ie, adult) birds. For example, very young (eg, 1 day post-hatch) chickens have succumbed to experimental WNV infection after exhibiting fluffed feathers, weakness, and lethargy. However, older chicks and adult chickens and turkeys are not known to develop clinical signs of WNV-associated disease and are likely resistant. Many healthy WNV-seropositive chickens have been observed, and experimental infections have failed to induce disease.
Among other domesticated or semi-domesticated fowl, some breeds of geese and ducks are clinically affected by WNV infection. The most susceptible wild birds belong to the corvid family, and numerous raptor species (eg, owls, hawks, falcons) are also susceptible.
There are no pathognomonic gross lesions; however, irregular pale streaks or foci on the myocardium or a uniformly pale heart, as well as splenomegaly and hepatomegaly, may occur. Blood vessels within the meninges may be congested; however, this is a nonspecific and inconsistent finding.
Histopathology may include nonsuppurative (lymphoplasmacytic) myocarditis; encephalitis; endophthalmitis; nephritis; hepatitis; adrenalitis; and arteritis, and myocardial, adrenal gland, and pancreatic necrosis. In acute cases, the myocardium may have extensive degeneration and necrosis of myofibers, while more chronic cases may exhibit lymphoplasmacytic myocarditis. Similarly, brain lesions may progress after infection, with minimal changes in acute infections but with subsequent development of lymphoplasmacytic meningoencephalitis, gliosis, and neuronal degeneration.
Diagnosis of West Nile Virus in Poultry
Virus isolation or reverse transcriptase PCR assay
West Nile virus–associated disease in birds can clinically manifest as nonspecific (eg, emaciation, dehydration, feather loss, anorexia, lethargy, fluffed feathers) or neurologic disease (eg, ataxia, head tilt, nystagmus, tremors, hind limb paresis, seizures, and blindness). Diagnosis is by virus isolation or reverse transcriptase PCR (RT-PCR) assay of tissues or pooled tissues; high viral titers generally occur in tissues, blood and mucous membranes (oral and cloacal surfaces) of birds that succumb to acute infection. Postmortem diagnosis can also be confirmed by immunohistochemistry of affected tissues.
Tissues of choice for diagnosis of recent WNV infection by virus isolation are brain, heart, and kidney; pooling small pieces of each tissue for testing may increase the chances of detection. Tissues must be homogenized prior to testing by virus isolation on Vero cells. This diagnostic method requires biosafety level-3 containment. Tissues may have infectious virus for up to approximately 1–2 weeks after initial infection, after which the virus often is rapidly cleared from surviving birds.
Birds that succumb in the acute phase of infection generally have high WNV titers in most tissues as well as in oral and cloacal swabs. Tissue homogenates and swab samples also can be tested by RT-PCR assay, which is more widely available, more sensitive and may detect viral RNA for longer periods postinfection (especially in kidney and spleen) when compared to viral isolation. Immunohistochemistry also can be used to confirm infection via viral antigen detection in formalin-fixed paraffin-embedded tissues. This may involve a variety of tissues; however, heart, kidney, adrenal gland, spleen, and brain are helpful, and tissues with lesions are best.
Serology can demonstrate past infection, but anti-WNV antibodies likely persist lifelong in many avian species, and thus, timing of infection and causation of disease cannot be determined from a single serum sample. A four-fold or more increase in anti-WNV antibody titers in acute and convalescent sera collected 2–4 weeks apart can be used to diagnose recent infection.
Plaque reduction neutralization testing is the gold standard for WNV serology; however, the closely related St. Louis encephalitis virus (SLEV) must also be ruled out by paired serum titrations. Enzyme-linked immunosorbent assays have been developed for WNV but are not currently commercially available nor widely used for avian samples.
Neurologic signs in birds, including poultry, must be distinguished from those caused by other encephalitic viruses (such as highly pathogenic avian influenza viruses Avian Influenza Avian influenza is a viral infection found in domestic poultry and a wide range of other birds. Wild waterfowl and shorebirds are often subclinically affected carriers of the virus. In poultry... read more and eastern equine encephalitis virus Eastern Equine Encephalitis in Poultry Eastern equine encephalitis (EEE) virus can cause disease in poultry and game birds. Neurologic disease is the most common clinical outcome; however, this virus also may result in decreased... read more ) and from those that may cause neurologic signs (such as viscerotropic velogenic Newcastle disease Newcastle Disease in Poultry Newcastle disease is a severe, systemic, and fatal viral disease of poultry due to virulent strains of avian paramyxovirus type 1. Clinical signs in unvaccinated birds include sudden death,... read more ; avian paramyxovirus-1 Other Avian Paramyxovirus Infections Avian paramyxoviruses types 2–22 are predominantly harbored in wild bird populations. Infections of poultry with these viruses are mostly inapparent. Occasionally, types 2, 3, 6, and 7 have... read more , and avian bornavirus). Severe bacterial infections may manifest as neurologic to nonspecific clinical disease (eg, ataxia, weakness, fluffed feathers) and include Riemerella anatipestifer Riemerella anatipestifer Infection in Poultry Riemerella anatipestifer is a bacterial pathogen that affects ducklings, gosling, turkeys, and other fowl. Clinical signs include ocular and nasal discharge, mild coughing and sneezing... read more , Streptococcus gallolyticus Streptococcosis in Poultry Streptococci are opportunistic pathogens, often causing secondary infections. Clinical manifestations of avian streptococcosis in poultry include an acute septicemic form and a chronic form... read more , and Erysipelothrix, Listeria, and Salmonella spp.
Trauma, some toxins (eg, ionophores, organophosphates and carbamates, lead), and CNS and multicentric neoplasia (eg, lymphoma) also may cause nonspecific or neurologic signs and are additional differential diagnoses.
Treatment, Prevention and Control
Treatment is supportive and is limited to high value birds
Prevention is by decreasing or eliminating risk of contact with mosquitoes
Treatment of WNV is primarily supportive and includes parenteral fluids, assisted feeding, and confinement in a padded cage in case of seizures. Such measures are typically limited to high value birds such as those in zoos, endangered species and similar.
Mosquito control is an essential component of programs to prevent West Nile virus or any other mosquito-borne disease. Unfortunately, this is difficult to implement in large backyard and rural environments 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 backyard and other outdoor flock settings as well as avian farms should be treated with larvicides or emptied when possible, especially during seasons of known mosquito breeding. Poultry houses should be constructed to be mosquito-proof (eg, via use of fine-mesh screens or solid construction that prevents mosquito passage through walls, windows, or doors).
In some areas, local or regional mosquito control programs perform aerial insecticide spraying, which targets both adult and larval mosquitoes. Because WNV and many other arthropod-borne viruses are zoonotic, public health agencies may be involved in mosquito control and management in some areas.
Although there are no commercially available vaccinations licensed for use in birds, numerous formulations (eg, killed, canarypox-vectored, plasmid-mediated DNA) have been tested and used in a variety of avian species. Use is generally limited to highly valued captive individuals or flocks (eg, in threatened or endangered species recovery programs, zoological parks, educational collections). Immune protection resulting from these vaccinations is variable and should not be assumed. Further, passive transfer of maternal antibodies has been documented in some avian species and may interfere with vaccination of chicks; regular booster doses may be necessary.
In general, poultry and domestic turkeys are resistant to infection with WNV and are thus unlikely to develop clinical signs of disease, in contrast to some species of wild Galliformes and other avian taxa.
Due to lack of specific treatment options, prevention of WNV infection by avoiding mosquito contact with birds is key.
Vaccination may be used in some birds but response is variable, no commercially available vaccines are licensed for use in birds.
For More Information
West Nile Virus. Centers for Disease Control and Prevention. https://www.cdc.gov/westnile/index.html. Accessed February 2, 2023.
West Nile virus. USDA National Invasive Species Information Center. https://www.invasivespeciesinfo.gov/profile/west-nile-virus. Accessed February 2, 2023.