West Nile virus is a mosquito-borne virus that causes viral illnesses of varying seriousness, ranging from no symptoms or mild flu-like symptoms to encephalitis or meningitis.
In the United States, the Centers for Disease Control and Prevention (CDC) monitors and records human WNV infections. In 2011, 714 cases and 43 deaths due to WNV were reported in the United States. In that year, only Maine, Alaska, and Hawaii were free of the virus, although South Carolina, New Hampshire, Washington, and Oregon reported no human cases. In those states the virus only detected only in animals. As of 2012, the virus was found from Canada to Venezuela and in Africa, Europe, the Middle East, North America and West Asia.
The primary hosts of West Nile virus (WNV) are birds, in which the virus numbers multiply before being transmitted by mosquitoes to the next victim. Over 140 species of birds can be infected with WNV. Besides birds, the virus can infect other vertebrates, including humans and horses.
WNV is a flavivirus that belongs to the Japanese encephalitis serocomplex, which includes St. Louis encephalitis, Murray Valley encephalitis, and Kunjin virus. Infections occur generally between late summer and early fall in temperate areas, and throughout the year in southern climates. Although typical manifestation of WNV is asymptomatic, the virus can cross the blood-brain barrier and cause severe illness and paralysis.
WNV was originally isolated in a feverish woman living in the West Nile District of Uganda during 1937. The virus was ecologically characterized in Egypt during the 1950s and later linked to severe human meningoencephalitis in elderly patients during a 1957 outbreak in Israel. Since 1937, subsequent outbreaks of WNV have been reported in Africa, Asia, Australia, Oceania, Western Europe, and the Middle East.
In the summer of 1999, WNV was first reported in the New York City area and then spread rapidly across the entire continent. It is suspected that the transport of infected birds or the international travel of infected humans from Israel and/or Tunisia may have imported the disease into North America. After its arrival in the New York area, the virus spread rapidly across the United States, as well as north into Canada and south into Mexico. In 2002, a severe outbreak of WNV in the United States killed 284 people and caused 2,944 cases of severe brain damage. This was the worst outbreak in the United States to date.
Like most flaviviruses, the WNV is maintained in a natural host-vector-host cycle, where the primary vector is the mosquito. The zoonotic cycle begins with a reservoir host, which is most commonly of avian origin. When a mosquito feeds on the infected bird, the virus is passed to the insect along with the blood meal. The virus then multiplies rapidly within the mosquito's body and salivary glands over the next few days. When the insect feeds on another animal or human, the virus can be transmitted through the bite and cause serious illness.
Most mosquitoes can become infected with the WNV. However, female mosquitoes of the Culex pipiens species are of particular concern, as they live in suburban and urban areas, can survive through the winter, prefer to feed on birds, and frequently bite humans. The C. pipiens, also known as the house mosquito, is also the most common vector for WNV transmission. Culex restuan, Culex quinquefasciatus, Aedes Albopictus, and Aedes Vexans are also common carriers of the WNV.
Common food sources for mosquitoes, birds represent the primary WNV reservoir species. A continent-wide study published in 2007 suggests that WNV has severely affected bird populations associated with human habitats in North America. Many in the scientific community believe that the rapid spread of WNV in North America may be due in part to the migratory nature of birds. Infected birds carry the virus with them as they travel in summer and winter, thus acting as reservoirs in their new nesting sites. Across the world, outbreaks occur most commonly along the main migration routes of migratory birds.
Most vertebrates, such as alligators, bats, chipmunks, skunks, squirrels, and rabbits, can also be infected with WNV. Horses, in particular, are commonly infected with WNV. Like humans, the majority of horses suffer either no or mild symptoms, but severe illness and death can and does occur. There are relatively few cases of dogs and cats becoming infected with WNV. Animals of all species exhibiting fever, weakness, poor coordination, spasms, seizures, and/or personality changes may be infected with WNV.
There is no evidence of WNV transmission from person-to-person through touch, kissing, or other contact. However, there is evidence of WNV transplacental (mother-to-child) transmission, as well as viral transmission through breastfeeding. As such, pregnant mothers should be aware of the presence of WNV in their area and take appropriate precautions. The transmission of WNV has also occurred in blood transfusions and organ transplants although the current blood supply is now tested for the presence of the WNV. People that are immunocompromised (from disease or chemotherapy, for example) and people aged 50 and older represent the highest risk group for serious WNV infection.
Most infected persons will exhibit a series of mild flu-like symptoms, also known as West Nile Fever. These mild symptoms can persist for 3–6 days, and occasionally for weeks. They include:
In rare cases, approximately 1 in 150 cases (0.7%), WNV can cross the blood-brain barrier and develop into a severe neuroinvasive disease. Immunocompromised individuals and those over age 50 years are at an increased risk for developing more severe syndromes; a 20-fold increase in incidence among older patients has been reported. Symptoms indicating the possible presence of severe West Nile-related syndromes include:
People exposed to WNV infection, especially the immunocompromised and elderly, should contact their health provider immediately if they develop a severe headache accompanied by high fever.
Typically, severe WNV syndromes manifest as one of three syndromes: West Nile encephalitis (inflammation of the brain); West Nile meningitis (inflammation of the meninges of the brain and spinal cord); or West Nile meningoencephalitis (inflammation of both the brain and the meninges). These three syndromes can cause severe brain damage and death. The majority of deaths result from complications attributable to West Nile meningoencephalitis. Additionally, severe WNV disease can cause acute vision loss due to inflammatory disorders of the eye, such as chorioretinitis, optic neuritis, retinal vasculitis, uveitis, and vitritis. Less frequently, the patient can exhibit acute flaccid paralysis, similar to poliomyelitis (polio) or Guillain-Barrésyndrome, caused by inflammation of the spinal cord and/or damage to the peripheral nerves. In some severe cases, this acute flaccid paralysis can disrupt muscles that control breathing and result in respiratory failure.
A proper diagnosis of WNV infection depends heavily upon clinical presentation, laboratory testing, and patient history. Patients with a known susceptibility to WNV (the elderly and immunocompromised) who exhibit symptoms during the late spring to early fall, or at any time in warmer climates, should be tested for WNV and other arboviral infections. Additionally, healthcare providers should remain aware of the local presence of WNV activity, such as reports of recent animal and/or human cases. Similarity of symptoms and serological cross-reactivity of WNV and other flaviviruses, may lead to confusion and an incorrect diagnosis. Healthcare providers must use thorough laboratory testing to differentiate WNV antibodies from those of other arboviruses.
Symptomatic WNV infection can be classified as either non–neuroinvasive or neuroinvasive, with each being identified according to certain criteria.
The majority of WNV infections are asymptomatic. In approximately 20% of WNV cases, clinically recognizable symptoms can manifest. However, to be clinically classified as non-neuroinvasive West Nile disease, the following must be true:
Antibiotics are ineffective against WNV as they are against all viruses. Instead, supportive care is used to treat the varying symptoms and syndromes associated with the various West Nile diseases. Although milder symptoms can be treated at home, severe symptoms can require hospitalization. Treatment of severe symptoms may require the use of intravenous infusions, airway and respiratory management and support, and use of preventive measures against secondary infection.
In severe cases of flaccid paralysis, physical therapy and occupational therapy may be used to help restore some muscle function.
The majority of WNV infections are asymptomatic. West Nile fever offers an excellent prognosis associated with quick recovery and no long-term side effects. The majority of symptoms resolve within a few days or weeks.
The prognosis is not as positive for patients experiencing the more severe syndromes attributable to WNV infection. Symptoms of West Nile encephalitis, West Nile meningitis, and West Nile meningoencephalitis can last for several weeks, as well as cause severe and permanent neurological damage. Inflammation can interfere with the brain and central nervous system and result in death, especially among the elderly population. Patients may suffer prolonged muscle weakness and loss of motor control. Long-term rehabilitation is typically required and a full recovery is not assured. If the muscles used for breathing are affected, death from respiratory failure may result.
The CDC requires that state and local public health offices report cases of WNV. These cases are tracked and updated weekly on the CDC website. When a major outbreak occurs, public service announcements are made reminding individuals of preventative measure. Internationally WHO also monitors outbreaks of WNV.
Local municipalities are responsible for mosquito abatement programs, which help control various mosquito-borne diseases including WNV. These programs usually involve widespread aerial spraying of insecticide. Often there is opposition to insecticide spraying by individuals concerned with exposure to chemicals. Mosquito abatement programs try to balance the need for disease control and the desire of residents to remain pesticide-free.
Although there is a vaccine used for horses and exotic birds in zoos, there is no WNV vaccine for humans at the current time. Several pharmaceutical companies, however, have WNV vaccines in development.
The C. pipiens mosquito is the primary vector of WNV transmission and also commonly lives and feeds in urban areas. Special precautions should be taken to reduce exposure to these potentially infected insects. Screen doors and enclosed porches can help keep mosquitoes from coming into the house. It should be noted that studies have shown that mosquito control devices such as “bug zappers” and CO2-baited traps do not significantly reduce the risk of being bitten.
Removing potential mosquito breeding areas from near the home and from the neighborhood can further reduce the risk of bites. Any container which can collect half an inch of standing water can become a potential breeding site in as little as five days. Old tires, empty plant pots, and empty trashcans should be removed, while water sources like ponds or birdbaths should be cleaned regularly. Standing water on any property should be drained, such as from clogged eaves. Swimming pools and hot tubs should be properly covered and chlorinated to prevent mosquitoes breeding in them.
See also Meningitis ; Polio ; Viruses .
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Monique Laberge, PhD
Revised by Tish Davidson, AM