West Nile virus (redirected from West Nile virus infection)

West Nile Virus 

Definition

West Nile virus is a mosquito-borne viral illness that can manifest with varying seriousness, ranging from no symptoms or mild flu-like symptoms to brain damage and death.

Description

West Nile virus (WNV) is a mosquito-borne flavivirus belonging to the Japanese encephalitis serocomplex, which includes St. Louis encephalitis, Murray Valley encephalitis, and Kunjin virus. Zoonotically maintained, 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 asymptomatical, the virus can cross the blood-brain barrier and cause severe illness, paralysis, and even death in humans and animals.

The 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, the first North American cases of WNV occurred in the New York City area. It is still unknown how the WNV reached the continental United States, but it is suspected that the transport of infected birds or the international travel of infected humans may have been to blame. After its arrival in the New Work area,, the virus spread rapidly across the United States, as well as northward into Canada and southward 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. During another outbreak a year, 9,858 cases of WNV infection were reported, of which over 2,900 were severe in nature and 262 of which resulted in fatality. As of January 2005, the CDC ArboNET has recorded avian or animal WNV infections in every state except Alaska, Hawaii, and Washington. Additionally, the CDC ArboNET recorded human WNV infections in every state except Alaska, Delaware, Hawaii, Massachusetts, New Hampshire, Rhode Island, Vermont, Washington, and West Virginia. Experts believe that WNV is now firmly established in the Western Hemisphere.

Life cycle and transmission

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 Culex 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. American crows, in particular, are extremely susceptible to WNV, and have become the virus' primary host population. Indeed, an unusual crow die-off can be used as an excellent indicator for the regional presence of the WNV. The virus has also been identified in more than 250 bird species in the United States, including blue jays, ravens, magpies, sparrows, and starlings. 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.

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 been evidenced 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.

Causes and symptoms

The exact mechanism of WNV-caused illnesses remains unclear. However, it is suspected that the virus enters the host's blood stream and multiples. It can then develop to the point where it crosses the blood brain-barrier, which separates the blood from the central nervous system. When this occurs, the virus can infect the brain, spinal cord, and other vital systems, creating a potentially deadly inflammatory response.

Symptoms

The incubation period for WNV after infection typical ranges between 3 to 14 days. Eighty percent of infected persons will exhibit no clinically apparent symptoms whatsoever. Roughly 20% of infected persons will exhibit a series of mild flu-like symptoms, also known as West Nile Fever. These mild symptoms can persist for 3 to 6 days, possibly weeks, and include:

• eye pain
• fever
• headache
• loss of appetite
• lymphadenopathy (abnormal enlargement of the lymph nodes)
• malaise (nonspecific bodily discomfort)
• myalgia (nonspecific muscular pain/tenderness)
• nausea
• rash (on the neck, torso, and limbs)
• vomiting

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 and elderly (>50 years of age) patients are at an increased risk for developing more severe syndromes; a 20-fold increase in incidence among older patients. Symptoms indicating the possible presence of severe West Nile-related syndromes include:

• severe headache
• high fever
• acute muscle weakness
• neck stiffness
• convulsions and tremors
• disorientation and stupor
• paralysis
• coma

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 even death. Severe WNV disease carries a mortality rate ranging between 3% and 15%, with elderly patients suffering the highest mortality rate. The majority of these deaths are as a result of complication 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-Barré syndrome, 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.

Diagnosis

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) that 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, health providers should remain constantly aware of the local presence of WNV activity, such as reports of recent animal and/or human cases. Similarities of symptomology between and serological cross-reactivity of WNV and other flaviviruses, may lead to confusion and an incorrect diagnosis. Health 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.

Non-neuroinvasive

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:

• no neuroinvasive symptomology
• presence of fever without other recognizable cause
• four-fold or greater increase in serum antibody titer
• virus isolated from and or deomonstrated in blood, tissue, cerebrospinal fluid (CSF), or other bodily fluid
• virus-specific immunoglobulin M (IgM antibodies demonstrated in CSF through antibody-capture methods

Neuroinvasive

In the rare cases (0.7%) of West Nile disease, the virus crosses the blood-brain barrier and manifests in severe and life-threatening symptomology. Clinical confirmation of neuroinvasive of neuroinvasive disease requires the presence of a fever and at least one of the following:

• acutely altered mental status, such as disorientation, stupor, or coma
• acute central or peripheral neurological difficulties, such as paralysis, nerve palsy, sensory deficits, and abnormal muscle function
• an increased white blood cell concentration in the CSF coupled with symptoms of meningitis, such as severe headache and neck pain

Treatment

Currently, there are no treatment modalities for WNV infection. Instead, supportive care is utilized 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 preventative measures against secondary infection.

Prognosis

The majority of WNV infections will manifest asymptomatically. West Nile fever offers an excellent prognosis associated with quick recovery and no adverse side-effects. The majority of symptoms will resolve within a few days or weeks of manifestation.

However, the prognosis is not a positive for patients suffering 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 amongst the elderly population. Patients with West Nile poliomyelitis 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 poliomyelitis affects muscles used for breathing, death from respiratory failure may result.

Prevention

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.

Prevention techniques of WNV typically coincide with avoidance measures against mosquito bites; the primary source of the virus. These include the use of insect repellant (with 5% to 20% DEET) on exposed body parts, wearing loose-fitting clothes over the limbs and torso while outdoors, using mosquito coils and/or citronella candles outdoors, and limiting outdoor activities during peak biting periods and/or in areas with high mosquito density. While camping outdoors, knockdown spray or bed netting with pyrethrum is suggested. Mosquito eradication programs have been instituted in most major cities. Public health authorities can utilize United States Environmental Protection Agency-approved "adulticidies" in areas suspected of the presence of WNV.

The Culex pipiens mosquito is the primary vector of WNV transmission and is also commonly live and feed 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 neighbourhood 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 eves. Swimming pools and hot tubs should be properly covered and chlorinated to prevent mosquitoes breeding in them.

Books

Mackenzie J., A.D.T. Barrett, and V. Deubel (eds.) Japanese encephalitis and West Nile viruses Berlin: Springer, 2002.

Periodicals

Fryer, J. "Interview with Joe Garret" Texas Journal of Rural Health 20 (#3, 2001): 5-7.

O'Leary D., A. Marfin, S. Montgomery, A. Kipp, J. Lehman, B. Biggerstaff, et al. "The Epidemic of West Nile Virus in the United States, 2002." Vector-borne and Zoonotic Diseases 4(March 2002): 61-.

Peterson L, and J. Roehrig. "West Nile Virus: A Reemerging Gobal Pathogen." Emerging Infectious Diseases 7(July-August 2001): 611-614.

Rappole J., S. Derrickson, and Z. Hubalek. "Migratory Birds and Spread of West Nile Virus in the Western Hemisphere." Emerging Infectious Diseases 6 (July-August 2000): 319-328.

Huhn G', J. Sejvar, S. Montgomery, and M. Dworkin. "West Nile Virus in the United States: An Update on an Emerging Infectious Disease." American Family Physician 68 (August 2003): 653-672.

Organizations

Centers for Disease Control and Prevention. 1600 Clifton Rd, Atlanta, GA 30333. (800)311-3435. http://www.cdc.gov.

Key terms

Flavivirus — An arbovirus that can cause potentially serious diseases, such as dengue, yellow fever, Japanese encaphilitis, and West Nile fever.

Guillain-Barré — A disorder in which the body's immune system attacks part of the peripheral nervous system. Weakness, tingling, and abnormal sensations in the arms and upper body can progress until the muscles become totally disabled and the patient is effectively paralyzed.

Meninges — A series of membranous layers of connective tissue that protect the central nervous system (brain and spinal cord). Damage or infection to the meninges, such as in meningitis, can cause serious neurological damage and even death.

Zoonotic diseases — Diseases caused by infectious agents that can be transmitted between (or are shared by) animals and humans. This can include transmission through the bite of an insect, such as a mosquito.

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virus /vi·rus/ (vi´rus) [L.] a minute infectious agent which, with certain exceptions, is not resolved by the light microscope, lacks independent metabolism and is able to replicate only within a living host cell; the individual particle (virion) consists of nucleic acid (nucleoid)—DNA or RNA (but not both)—and a protein shell (capsid), which contains and protects the nucleic acid and which may be multilayered.

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attenuated virus  one whose pathogenicity has been reduced by serial passage or other means.

Bayou virus  a virus of the genus Hantavirus that causes hantavirus pulmonary syndrome in the southwestern United States.

BK virus  (BKV) a human polyomavirus that causes widespread infection in childhood and remains latent in the host; it is believed to cause hemorrhagic cystitis and nephritis in immunocompromised patients.

Central European encephalitis virus  a species of tick-borne viruses of the genus Flavivirus that includes the agents of Central European encephalitis and the Russian spring-summer encephalitis virus.

cowpox virus  a virus of the genus Orthopoxvirus that is the etiologic agent of cowpox.

Coxsackie virus  coxsackievirus.

defective virus  one that cannot be completely replicated or cannot form a protein coat; in some cases replication can proceed if missing gene functions are supplied by other viruses; see helper v.

dengue virus  a flavivirus existing as four distinct types (designated 1, 2, 3, and 4) that causes dengue.

DNA virus  one whose genome consists of DNA.

eastern equine encephalomyelitis virus  see equine encephalomyelitis v.

EB virus  Epstein-Barr v.

Ebola virus 

1. an RNA virus almost identical to the Marburg virus but serologically distinct; it causes a similar disease.

2. a virus of the genus Filovirus that is the etiologic agent of Ebola virus disease.

EEE virus  eastern equine encephalomyelitis v.; see equine encephalomyelitis v.

encephalomyocarditis virus  an enterovirus that causes mild aseptic meningitis and encephalomyocarditis.

enteric viruses  an epidemiologic class of viruses that are normally acquired by ingestion and replicate in the intestinal tract, causing local rather than generalized infection.

enveloped virus  a virus having an outer lipoprotein bilayer acquired by budding through the host cell membrane.

Epstein-Barr virus  (EBV) human herpesvirus 4; a virus that causes infectious mononucleosis and is associated with Burkitt's lymphoma and nasopharyngeal carcinoma.

equine encephalomyelitis virus  a group of arbovirus species of the genus Alphavirus that cause encephalomyelitis in horses, mules, and humans, transmitted by mosquitoes; there are three strains: eastern, western, and Venezuelan.

fixed virus  one whose virulence and incubation period have been stabilized by serial passage and remained fixed during further transmission.

foamy viruses  Spumavirus.

helper virus  one that aids in the development of a defective virus by supplying or restoring the activity of the viral gene or enabling it to form a protein coat.

hepatitis virus  the etiologic agent of viral hepatitis. Six types are recognized: hepatitis A virus, the agent causing infectious hepatitis, acquired by parenteral inoculation or by ingestion; hepatitis B virus, the agent causing serum hepatitis, transmitted by inadequately sterilized syringes and needles, or through infectious blood plasma, or certain blood products; hepatitis C virus, which causes hepatitis C; hepatitis D virus, a defective RNA viral agent that can replicate only in the presence of hepatitis B virus and is transmitted with it and causes hepatitis D; hepatitis E virus, a calicivirus transmitting hepatitis E; and hepatitis G virus, flavivirus isolated from patients with hepatitis but whose etiologic role is uncertain.

hepatitis B–like viruses  Hepadnaviridae.

herpes virus  herpesvirus.

herpes simplex virus  (HSV) a virus of the genus Simplexvirus that is the etiologic agent of herpes simplex in humans. It is separable into two serotypes, designated 1 and 2 (called also human herpesvirus 1 and human herpesvirus 2 ); type 1 is transmitted by infected saliva and causes primarily nongenital lesions, and type 2 is sexually transmitted and causes primarily genital lesions.

human immunodeficiency virus  (HIV) a human T-cell leukemia/lymphoma virus, of the genus Lentivirus, with a selective affinity for helper T cells that is the agent of the acquired immunodeficiency syndrome.

human T-cell leukemia virus  human T-lymphotropic v.

human T-lymphotropic virus 1  (HTLV-1) a species of retroviruses of worldwide distribution, having an affinity for helper/inducer T lymphocytes; it causes chronic infection and is associated with adult T-cell leukemia and chronic progressive myelopathy.

human T-lymphotropic virus 2  (HTLV-2) a species of retroviruses having extensive serologic cross-reactivity with HTLV-1; no clear association with disease has been established.

igbo-ora virus  an arbovirus of the genus Alphavirus that has been associated with a dengue-like disease in Nigeria, the Central African Republic, and the Ivory Coast.

influenza virus  any of a group of orthomyxoviruses that cause influenza, including at least three genera: Influenzavirus A, Influenzavirus B, and Influenzavirus C. Serotype A viruses are subject to major antigenic changes (antigenic shifts) as well as minor gradual antigenic changes (antigenic drift) and cause the major pandemics.

influenza A virus , influenza B virus, influenza C virus species in the genera Influenzavirus A, Influenzavirus B, and Influenzavirus C; see influenza v.

Jamestown Canyon virus  a virus of the genus Bunyavirus, serologically related to California encephalitis virus, that occasionally causes encephalitis.

JC virus  (JCV) a polyomavirus that causes widespread infection in childhood and remains latent in the host; it is the cause of progressive multifocal leukoencepahalopathy.

La Crosse virus  a virus of the California serogroup of the genus Bunyavirus, the etiologic agent of La Crosse encephalitis.

lymphocyte-associated virus  any virus of the subfamily Gammaherpesviridae, members of which are specific for either B or T lymphocytes; infection is often arrested at a lytic or prelytic stage without production of infectious virions, and latent virus may frequently be demonstrated in lymphoid tissue.

lytic virus  one that is replicated in the host cell and causes death and lysis of the cell.

Marburg virus  an RNA virus occurring in Africa, transmitted by insect bite and causing Marburg disease.

masked virus  a virus that ordinarily occurs in a noninfective state and is demonstrable by indirect methods which activate it, as by blind passage in experimental animals.

measles virus  a paramyxovirus that is the cause of measles.

measles-like viruses  Morbillivirus.

monkeypox virus  an orthopoxvirus that produces mild exanthematous disease in monkeys and a smallpox-like disease in humans.

mumps virus  a virus of the genus Rubulavirus that causes mumps and sometimes tenderness and swelling of the testes, pancreas, ovaries, or other organs.

naked virus , nonenveloped virus a virus lacking an outer lipoprotein bilayer.

neurotropic virus  one that has a predilection for and causes infection in nervous tissues, e.g., the rabies virus.

Norwalk virus  a calicivirus that is a common agent of epidemics of acute gastroenteritis.

oncogenic viruses  an epidemiologic class of viruses that are acquired by close contact or injection and cause usually persistent infection; they may induce cell transformation and malignancy.

Oropouche virus  a virus of the genus Bunyavirus that causes illness in Brazil; infection is characterized by fever, chills, malaise, headache, myalgia, and arthralgia, sometimes nausea and vomiting, and occasionally central nervous system involvement.

orphan viruses  viruses isolated in tissue culture but not found specifically associated with any illness.

papilloma virus  papillomavirus.

parainfluenza virus  a group of viruses of the family Paramyxoviridae that cause upper respiratory tract disease in humans and other animals.

paravaccinia virus  pseudocowpox v.

Powassan virus  a tickborne virus of the genus Flavivirus that causes encephalitis in the eastern United States and Canada.

pox virus  poxvirus.

pseudocowpox virus  a virus of the genus Parapoxvirus that produces nodular lesions similar to those of cowpox and orf on the udders and teats of milk cows and the oral mucosa of suckling calves (paravaccinia), which can be transmitted to humans during milking.

Puumala virus  see Hantavirus.

rabies virus  an RNA virus of the rhabdovirus group that causes rabies.

rabies-like viruses  Lyssavirus.

respiratory viruses  an epidemiologic class of viruses that are acquired by inhalation of fomites and replicate in the respiratory tract, causing local rather than generalized infection; they are included in the families Adenoviridae, Coronaviridae, Orthomyxoviridae, Paramyxoviridae, and Picornaviridae.

respiratory syncytial viruses  (RSV) viruses belonging to the genus Pneumovirus, causing respiratory disease that is particularly severe in infants, and in tissue causing syncytium formation.

RNA virus  one whose genome consists of RNA.

Rous-associated virus  (RAV) a helper virus in whose presence a defective Rous sarcoma virus is able to form a protein coat.

Rous sarcoma virus  (RSV) see Rous sarcoma, under sarcoma .

rubella virus  the sole species of the genus Rubivirus, the etiologic agent of rubella.

St. Louis encephalitis virus  a virus of the genus Flavivirus, that is the etiologic agent of St. Louis encephalitis; transmitted by mosquitoes.

sandfly fever viruses  Phlebovirus.

satellite virus  a strain of virus unable to replicate except in the presence of helper virus; considered to be deficient in coding for capsid formation.

Seoul virus  see Hantavirus.

simian immunodeficiency virus  (SIV) a virus of the genus Lentivirus, closely related to human immunodeficiency virus, that causes inapparent infection in African green monkeys and a disease resembling acquired immunodeficiency syndrome in macaques.

Sin Nombre virus  a virus of the genus Hantavirus that causes hantavirus pulmonary syndrome in the western United States.

slow virus  any virus causing a disease characterized by a long preclinical course and gradual progression once the symptoms appear.

street virus  virus from a naturally infected animal, as opposed to a laboratory-adapted strain of the virus.

tanapox virus  a virus of the genus Yatapoxvirus that is the etiologic agent of tanapox.

Toscana virus  a virus of the Naples serogroup of the genus Phlebovirus, an etiologic agent of phlebotomus fever.

varicella-zoster virus  human herpesvirus 3

variola virus  the virtually extinct virus, belonging to the genus Orthopoxvirus, that is the etiologic agent of smallpox. No natural infection has occurred since 1977 and no reservoir of the virus now exists.

VEE virus , Venezuelan equine encephalomyelitis virus see equine encephalomyelitis v.

WEE virus , western equine encephalomyelitis virus see equine encephalomyelitis v.

West Nile virus  a virus of the genus Flavivirus that causes West Nile encephalitis; it is transmitted by Culex mosquitoes, with wild birds serving as the reservoir.

Yaba monkey tumor virus  a virus of the genus Yatapoxvirus that is the etiologic agent of yabapox.

yellow fever virus  a mosquito-borne species of the genus Flavivirus that causes yellow fever in Central and South America and Africa.

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West Nile virus (wst nl)

n.

A flavivirus that is transmitted by the bite of a mosquito and that can cause mild febrile illness as well as severe, sometimes fatal encephalitis and meningitis.

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West Nile virus

[west nīl]

a virus of the genus Flavivirus that causes West Nile encephalitis. It is transmitted by Culex mosquitoes, with wild birds serving as the reservoir, and occurs widely in Africa, Europe, the Middle East, and Asia; it has recently been reported in the United States.