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*'''West Nile Fever (WNF)''', which occurs in 20 percent of cases, is a [[fever|febrile]] [[syndrome]] which causes [[flu-like symptoms]].<ref>{{cite journal |author=Olejnik E |title=Infectious adenitis transmitted by ''Culex molestus |journal=Bull Res Counc Isr |volume=2 |issue= |pages=210–1 |year=1952}}</ref>Most characterizations of WNF generally describe it as a mild, [[acute (medicine)|acute]] syndrome lasting 3–6 days after symptom onset. Systematic follow-up studies of patients with WNF had not previously been done, so this information is largely [[Anecdotal evidence|anecdotal]]. In addition to a high fever, headache, chills, [[diaphoresis|excessive sweating]], weakness, fatigue, [[lymphadenopathy|swollen lymph nodes]], drowsiness, pain in the joints and [[flu-like symptoms]]. [[Gastrointestinal tract|Gastrointestinal]] symptoms which may occur include [[nausea]], [[emesis|vomiting]], [[Anorexia (symptom)|loss of appetite]], and [[diarrhea]]. Fewer than 1/3 of patients develop a [[rash]].
*'''West Nile Fever (WNF)''', which occurs in 20 percent of cases, is a [[fever|febrile]] [[syndrome]] which causes [[flu-like symptoms]].<ref>{{cite journal |author=Olejnik E |title=Infectious adenitis transmitted by ''Culex molestus |journal=Bull Res Counc Isr |volume=2 |issue= |pages=210–1 |year=1952}}</ref>Most characterizations of WNF generally describe it as a mild, [[acute (medicine)|acute]] syndrome lasting 3–6 days after symptom onset. Systematic follow-up studies of patients with WNF had not previously been done, so this information is largely [[Anecdotal evidence|anecdotal]]. In addition to a high fever, headache, chills, [[diaphoresis|excessive sweating]], weakness, fatigue, [[lymphadenopathy|swollen lymph nodes]], drowsiness, pain in the joints and [[flu-like symptoms]]. [[Gastrointestinal tract|Gastrointestinal]] symptoms which may occur include [[nausea]], [[emesis|vomiting]], [[Anorexia (symptom)|loss of appetite]], and [[diarrhea]]. Fewer than 1/3 of patients develop a [[rash]].


*'''West Nile [[Neurotropic virus|Neuroinvasive Disease]] (WNND)''', which occurs in less than 1 percent of cases, is when the virus infects the [[central nervous system]] resulting in [[meningitis]], [[encephalitis]], meningoencephalitis or a [[poliomyelitis]]-like syndrome.<ref name="ReferenceA">Davis LE, DeBiasi R, Goade DE, ''et al.'' West Nile virus neuroinvasive disease. Ann Neurol. 2006 Sep;60(3):286-300. PMID 16983682</ref> Many patients with WNND have normal [[neuroimaging]] studies, although abnormalities may be present in various cerebral areas including the [[basal ganglia]], [[thalamus]], [[cerebellum]], and [[brainstem]].<ref name="ReferenceA"/>
*'''West Nile [[Neurotropic virus|Neuroinvasive Disease]] (WNND)''', which occurs in less than 1 percent of cases, is when the virus infects the [[central nervous system]] resulting in [[meningitis]], [[encephalitis]], meningoencephalitis or a [[poliomyelitis]]-like syndrome.<ref name="ReferenceA">{{cite journal | author = Davis LE, DeBiasi R, Goade DE ''et al.'' | year = 2006 | month = Sep | title = West Nile virus neuroinvasive disease | url = | journal = Ann Neurol | volume = 60 | issue = 3| pages = 286–300 | pmid = 16983682 }}</ref> Many patients with WNND have normal [[neuroimaging]] studies, although abnormalities may be present in various cerebral areas including the [[basal ganglia]], [[thalamus]], [[cerebellum]], and [[brainstem]].<ref name="ReferenceA"/>


*'''West Nile virus encephalitis (WNE)''' is the most common neuroinvasive manifestation of WNND. WNE presents with similar symptoms to other viral encephalitis with fever, headaches, and altered mental status. A prominent finding in WNE is [[muscular weakness]] (30–50% of patients with encephalitis), often with [[lower motor neuron]] symptoms, [[flaccid paralysis]], and [[hyporeflexia]] with no [[Sensory system|sensory]] abnormalities.<ref>Anticona EM, Zainah H , Ouellette DR ''et al.'': Two Case Reports of Neuroinvasive West Nile Virus Infection in the Critical Care Unit. Case Reports in Infectious Diseases; Volume 2012 (2012), Article ID 839458, 4 pages doi:10.1155/2012/839458</ref>"WNV is now the most common cause of epidemic viral encephalitis in the United States, and it will likely remain an important cause of neurological disease for the foreseeable future.("Carson PJ, ''et al.'' 2006)<ref>{{cite journal | pmid = 16912946 | doi=10.1086/506939 | volume=43 | issue=6 | journal = Clinical Infectious Diseases | year=2006 | title = Long‐Term Clinical and Neuropsychological Outcomes of West Nile Virus Infection | month=September | pages=723–30 | author=Carson PJ, Konewko P, Wold KS, ''et al.''}}</ref>
*'''West Nile virus encephalitis (WNE)''' is the most common neuroinvasive manifestation of WNND. WNE presents with similar symptoms to other viral encephalitis with fever, headaches, and altered mental status. A prominent finding in WNE is [[muscular weakness]] (30–50% of patients with encephalitis), often with [[lower motor neuron]] symptoms, [[flaccid paralysis]], and [[hyporeflexia]] with no [[Sensory system|sensory]] abnormalities.<ref>Anticona EM, Zainah H , Ouellette DR ''et al.'': Two Case Reports of Neuroinvasive West Nile Virus Infection in the Critical Care Unit. Case Reports in Infectious Diseases; Volume 2012 (2012), Article ID 839458, 4 pages doi:10.1155/2012/839458</ref>"WNV is now the most common cause of epidemic viral encephalitis in the United States, and it will likely remain an important cause of neurological disease for the foreseeable future.("Carson PJ, ''et al.'' 2006)<ref>{{cite journal | pmid = 16912946 | doi=10.1086/506939 | volume=43 | issue=6 | journal = Clinical Infectious Diseases | year=2006 | title = Long‐Term Clinical and Neuropsychological Outcomes of West Nile Virus Infection | month=September | pages=723–30 | author=Carson PJ, Konewko P, Wold KS, ''et al.''}}</ref>
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==Prognosis==
==Prognosis==
While the general prognosis is favorable, current studies indicate that West Nile Fever can often be more severe than previously recognized, with studies of various recent outbreaks indicating that it may take as long as 60–90 days to recover.<ref>Watson J., Patel P. Jones R., ''et al.'' Clinical Characteristics and Functional Outcomes of West Nile Fever[66.39.42.45/topics/west_nile/pdf/wnv_clinical_characteristics.pdf]</ref><ref>Carson1 P, Konewko P., Wold k., ''et al.'' Long-Term Clinical and Neuropsychological Outcomes of West Nile Virus Infection. Oxford Journals Medicine Clinical Infectious Diseases Volume 43, Issue 6 Pp. 723-730.</ref> Patients with milder WNF are just as likely as those with more severe manifestations of neuroinvasive disease to experience multiple long term (>1+ years) [[somatic]] complaints such as tremor, and dysfunction in [[motor skill]]s and [[executive functions]]. Patients with milder illness are just as likely as patients with more severe illness to experience adverse outcomes.<ref>Klee AL, Maidin B, Edwin B, ''et al.'' Long-term prognosis for clinical West Nile virus infection. Emerg Infect Dis. 2004 Aug;10(8):1405-11. PMID 15496241</ref> Recovery is marked by a long [[convalescence]] with [[Fatigue (medical)|fatigue]]. One study found that neuroinvasive WNV infection was associated with an increased risk for subsequent kidney disease.<ref>{{cite journal
While the general prognosis is favorable, current studies indicate that West Nile Fever can often be more severe than previously recognized, with studies of various recent outbreaks indicating that it may take as long as 60–90 days to recover.<ref>Watson J., Patel P. Jones R., ''et al.'' Clinical Characteristics and Functional Outcomes of West Nile Fever[66.39.42.45/topics/west_nile/pdf/wnv_clinical_characteristics.pdf]</ref><ref>Carson1 P, Konewko P., Wold k., ''et al.'' Long-Term Clinical and Neuropsychological Outcomes of West Nile Virus Infection. Oxford Journals Medicine Clinical Infectious Diseases Volume 43, Issue 6 Pp. 723-730.</ref> Patients with milder WNF are just as likely as those with more severe manifestations of neuroinvasive disease to experience multiple long term (>1+ years) [[somatic]] complaints such as tremor, and dysfunction in [[motor skill]]s and [[executive functions]]. Patients with milder illness are just as likely as patients with more severe illness to experience adverse outcomes.<ref>{{cite journal | author = Klee AL, Maidin B, Edwin B ''et al.'' | year = 2004 | month = Aug | title = Long-term prognosis for clinical West Nile virus infection | url = | journal = Emerg Infect Dis | volume = 10 | issue = 8| pages = 1405–11 | pmid = 15496241 }}</ref> Recovery is marked by a long [[convalescence]] with [[Fatigue (medical)|fatigue]]. One study found that neuroinvasive WNV infection was associated with an increased risk for subsequent kidney disease.<ref>{{cite journal
|url=http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0040374
|url=http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0040374
|title= Prevalence of Chronic Kidney Disease and Progression of Disease Over Time among Patients Enrolled in the Houston West Nile Virus Cohort
|title= Prevalence of Chronic Kidney Disease and Progression of Disease Over Time among Patients Enrolled in the Houston West Nile Virus Cohort

Revision as of 14:09, 23 September 2012

West Nile Virus
Virus classification
Group:
Group IV ((+)ssRNA)
Family:
Flaviviridae
Genus:
Flavivirus
Species:
West Nile virus

West Nile virus (WNV) is a mosquito-borne zoonotic arbovirus belonging to the genus Flavivirus in the family Flaviviridae. This flavivirus is found in temperate and tropical regions of the world. It was first identified in the West Nile subregion in the East African nation of Uganda in 1937. Prior to the mid 1990s, WNV disease occurred only sporadically and was considered a minor risk for humans, until an outbreak in Algeria in 1994, with cases of WNV-caused encephalitis, and the first large outbreak in Romania in 1996, with a high number of cases with neuroinvasive disease. WNV has now spread globally, with the first case in the Western Hemisphere being identified in New York City in 1999;[1] over the next 5 years, the virus spread across the continental United States, north into Canada, and southward into the Caribbean Islands and Latin America. WNV also spread to Europe, beyond the Mediterranean Basin [a new strain of the virus was recently (2012) identified in Italy]. WNV is now considered to be an endemic pathogen in Africa, Asia, Australia, the Middle East, Europe and in the United States, which in 2012 has experienced one of its worst epidemics.

The main mode of WNV transmission is via various species of mosquitoes which are the prime vector, with birds being the most commonly infected animal and serving as the prime reservoir host - especially passerines which are of the largest order (Passeriformes) of birds. WNV has been found in various species of ticks, but current research suggests they are not important vectors of the virus. WNV also infects various mammal species, including humans, and has been identified in reptilian species, including alligators and crocodiles, and also in amphibians. Not all animal species which are susceptible to WNV infection – humans included, and not all bird species develop sufficient viral levels to transmit the disease to uninfected mosquitoes, and are thus not considered major factors in WNV transmission.[2][3]

Approximately 80% of West Nile virus infections in humans are subclinical, which cause no symptoms.[4] In the cases where symptoms do occur – termed West Nile fever in cases without neurological disease – the time from infection to the appearance of symptoms (incubation period) is typically between 2 and 15 days. Symptoms may include fever, headaches, fatigue, muscle pain or aches, malaise, nausea, anorexia, vomiting, myalgias and rash. Less than 1% of the cases are severe and result in neurological disease when the central nervous system is affected. People of advanced age, the very young, or those with immunosuppression, either from medical induced such as those taking immunosupressive drugs or due to a pre-existing medical condition such as HIV infection, are most susceptible. The specific neurological diseases which may occur are West Nile encephalitis, which causes inflammation of the brain, West Nile meningitis, which causes inflammation of the meninges which are the protective membranes that cover the brain and spinal cord, West Nile meningoencephalitis, which causes inflammation of the brain and also the meninges surrounding it, and West Nile poliomyelitis - spinal cord inflammation which results in a syndrome similar to polio, which may cause acute flaccid paralysis.

Currently, no vaccine against WNV infection is available. The best method to reduce the rates of WNV infection is mosquito control on the part of municipalities, businesses and individual citizens to reduce breeding populations of mosquitoes in public, commercial and private areas via various means including eliminating standing pools of water where mosquitoes breed, such as in old tires, buckets, disused swimming pools, etc. On an individual basis, the use of personal protective measures to avoid being bitten by an infected mosquito, via the use of mosquito repellent, window screens, avoiding areas where mosquitoes are more prone to congregate, such as near marshes, areas with heavy vegetation etc., and being more vigilant from dusk to dawn when mosquitoes are most active offers the best defense. In the event of being bitten by an infected mosquito, familiarity of the symptoms of WNV on the part of laypersons, physicians and allied health professionals affords the best chance of receiving timely medical treatment which may aid in reducing associated possible complications and also appropriate palliative care.

West Nile fever
SpecialtyInfectious diseases, neurology Edit this on Wikidata

Signs and symptoms

U.S. West Nile virus (WNV) Neuroinvasive Disease incidence. Current 9-4-2012

The incubation period for WNV – the amount of time from infection to symptom onset – is typically from between 2–15 days. Headache can be a prominent symptom of WNV fever, meningitis, encephalitis, menigoencephalitis and it may or may not be present in poliomyelytis-like syndrome thus headache is not a useful indicator of neuroinvasive disease.(CDC)

  • West Nile virus encephalitis (WNE) is the most common neuroinvasive manifestation of WNND. WNE presents with similar symptoms to other viral encephalitis with fever, headaches, and altered mental status. A prominent finding in WNE is muscular weakness (30–50% of patients with encephalitis), often with lower motor neuron symptoms, flaccid paralysis, and hyporeflexia with no sensory abnormalities.[7]"WNV is now the most common cause of epidemic viral encephalitis in the United States, and it will likely remain an important cause of neurological disease for the foreseeable future.("Carson PJ, et al. 2006)[8]
  • West Nile meningitis (WNM) usually involves fever, headache, and stiff neck. Pleocytosis is present. Changes in consciousness are not usually seen and are mild when present.
  • West Nile meningoencephalitis is inflammation of both the brain (encephalitis) and meninges (meningitis).
  • West Nile poliomyelitis (WNP), an acute flaccid paralysis syndrome associated with WNV infection, is less common than WNM or WNE. This syndrome is generally characterized by the acute onset of asymmetric limb weakness or paralysis in the absence of sensory loss. Pain sometimes precedes the paralysis. The paralysis can occur in the absence of fever, headache, or other common symptoms associated with WNV infection. Involvement of respiratory muscles, leading to acute respiratory failure, can sometimes occur.
  • Cutaneous manifestations specifically rashes are not uncommon in WNV-infected patients, however there is a paucity of detailed descriptions in case reports and there are few clinical images widely available. Punctate erythematous, macular, and papular eruptions, most pronounced on the extremities have been observed in WNV cases and in some cases histopathologic findings have shown a sparse superficial perivascular lymphocytic infiltrate, a manifestation commonly seen in viral exanthems. A literature review provides support that this punctate rash is a common cutaneous presentation of WNV infection. (Anderson RC et al.)[15]

Virology

WNV is one of the Japanese encephalitis antigenic serocomplex of viruses. Image reconstructions and cryoelectron microscopy reveal a 45–50 nm virion covered with a relatively smoothprotein surface. This structure is similar to the dengue fever virus; both belong to the genus Flaviviruswithin the family Flaviviridae. The genetic material of WNV is a positive-sense, single strand of RNA, which is between 11,000 and 12,000 nucleotides long; these genes encode seven nonstructural proteins and three structural proteins. The RNA strand is held within a nucleocapsid formed from 12-kDa protein blocks; the capsid is contained within a host-derived membrane altered by two viral glycoproteins.

Phylogeny

Phylogenetic tree of West Nile viruses based on sequencing of the envelope gene during complete genome sequencing of the virus.[16]

Studies of phylogenetic lineages determined WNV emerged as a distinct virus around 1000 years ago.[17] This initial virus developed into two distinct lineages, lineage 1 and its multiple profiles is the source of the epidemic transmission in Africa and throughout the world. Lineage 2 was considered an Africa zoonosis. However, in 2008, lineage 2, previously only seen in horses in sub-Saharan Africa and Madagascar, began to appear in horses in Europe, where the first known outbreak affected 18 animals in Hungary in 2008.[18] Lineage 1 West Nile virus was detected in South Africa in 2010 in a mare and her aborted fetus; previously, only lineage 2 West Nile virus had been detected in horses and humans in South Africa.[19] A 2007 fatal case in akiller whale in Texas broadened the known host range of West Nile virus to include cetaceans.[20]

The US virus was very closely related to a lineage 1 strain found in Israel in 1998. Since the first North American cases in 1999, the virus has been reported throughout the United States, Canada, Mexico, the Caribbean and Central America. There have been human cases and equine cases, and many birds are infected. The Barbary macaque, Macaca sylvanus, was the first nonhuman primate to contract WNV.[21] Both the US and Israeli strains are marked by high mortality rates in infected avian populations; the presence of dead birds—especially Corvidae—can be an early indicator of the arrival of the virus.

Transmission

The West Nile virus maintains itself in nature by cycling between mosquitoes and certain species of birds. A mosquito (the vector) bites an uninfected bird (the host) , the virus amplifies within the bird, an uninfected mosquito bites the bird and is in turn infected. Other species such as humans and horses are incidental infections, as they are not the mosquitoes' preferred blood meal source. The virus does not amplify within these species and they are known as dead-end hosts.

The West Nile virus (WNV) is transmitted through female mosquitoes, which are the prime vectors of the virus. Only females feed on blood, and different species have evolved to take a blood meal on preferred types ofvertebrate hosts. The infected mosquito species vary according to geographical area; in the US,Culex pipiens (Eastern US), Culex tarsalis (Midwest and West), and Culex quinquefasciatus(Southeast) are the main sources.[22]

The proboscis of a female mosquito – here a Southern House Mosquito (Culex quinquefasciatus) - pierces the epidermis and dermis to allow it to feed on humanblood from a capillary: this one is almost fully engorged. The mosquito injects saliva which contains ananesthetic, and an anticoagulant into the puncture wound; and in infected mosquitoes, the West Nile virus.

The various species that transmit the WNV prefer birds of the Passeriformes order, the largest order of birds. Within that order there is further selectivity with various mosquito species exhibiting preference for different species. In the United States WNV mosquito vectors have shown definitive preference for members of theCorvidae and Thrush family of birds. Amongst the preferred species within these families are the American crow, a Corvid and the American Robin (Turdus migratorius), a thrush.

The birds develop sufficient viral levels after being infected, to transmit the infection to other biting mosquitoes which in turn go on to infect other birds. In crows and robins, the infection is fatal in 4-5 days. This epizootic viral amplification cycle has been shown to peak 15-16 days before humans become ill. This may be due to the high mortality, and thus depletion of the preferred hosts, i.e., the specific bird species. The mosquitoes become less selective and begin feeding more readily on other animal types such as humans and horses which are considered incidental hosts.[23]

In mammals, the virus does not multiply as readily (i.e. does not develop high viremia during infection), and mosquitoes biting infected mammals are not believed to ingest sufficient virus to become infected,[24] making mammals so-called dead-end infections.

Direct human-to-human transmission initially was believed to be caused only by occupational exposure,[25] or conjunctive exposure to infected blood.[26] The US outbreak identified additional transmission methods through blood transfusion,[27] organ transplant,[28] intrauterine exposure,[29] and breast feeding.[30] Since 2003, blood banks in the US routinely screen for the virus among their donors.[31] As a precautionary measure, the UK's National Blood Service initially ran a test for this disease in donors who donate within 28 days of a visit to the United States, Canada or the northeastern provinces of Italy and theScottish National Blood Transfusion Service[32] asks prospective donors to wait 28 days after returning from North America or the northeastern provinces of Italy before donating.

Recently, the potential for mosquito saliva to impact the course of WNV disease was demonstrated.[33][34][35] Mosquitoes inoculate their saliva into the skin while obtaining blood. Mosquito saliva is a pharmacological cocktail of secreted molecules, principally proteins, that can affect vascular constriction, blood coagulation, platelet aggregation, inflammation, and immunity. It clearly alters the immune response in a manner that may be advantageous to a virus.[36][37][38][39] Studies have shown it can specifically modulate the immune response during early virus infection,[40] and mosquito feeding can exacerbate WNV infection, leading to higherviremia and more severe forms of disease.[33][34][35]

Vertical transmission

Vertical transmission; the transmission of a viral or bacterial disease from the female of the species to her offspring, has been observed in various West Nile virus studies, amongst different species of mosquitoes in both the laboratory and in nature.[41] Mosquito progeny infected vertically in autumn, may potentially serve as a mechanism for WN virus to overwinter and initiate enzootic horizontal transmission the following spring.[42]

Risk factors

Risk factors independently associated with developing a clinical infection with WNV include a suppressed immune system and a patient history of organ transplantation.[43] For neuroinvasive disease the additional risk factors include older age (>50+), male sex, hypertension, and diabetes mellitus.[44][45]

A genetic factor also appears to increase susceptibility to West Nile disease. A mutation of the gene CCR5 gives some protection against HIV but leads to more serious complications of WNV infection. Carriers of two mutated copies of CCR5made up 4.0 to 4.5% of a sample of West Nile disease sufferers, while the incidence of the gene in the general population is only 1.0%.[46][47]

Diagnosis

An Immunoglobulin M (IgM) antibody molecule. Definitive diagnosis of WNV is obtained through detection of virus-specific IgM and neutralizing antibodies.

Preliminary diagnosis is often based on the patient's clinical symptoms, places and dates of travel (if patient is from a non-endemic country or area), activities, and epidemiologic history of the location where infection occurred. A recent history of mosquito bites and an acute febrile illness associated with neurologic signs and symptoms should cause clinical suspicion of WNV.

Diagnosis of West Nile Virus infections is generally accomplished by serologic testing of blood serum or cerebrospinal fluid (CSF), which is obtained via a lumbar puncture. Typical findings of WNV infection include lymphocytic pleocytosis, elevated protein level, reference glucose and lactic acid levels, and no erythrocytes.

Definitive diagnosis of WNV is obtained through detection of virus-specific antibody Immunoglobulin M, (IgM) and neutralizing antibodies. Cases of West Nile virus meningitis and encephalitis which have been serologically confirmed produce similar degrees of CSF pleocytosis and are often associated with substantial CSF neutrophilia.[48] Specimens collected within 8 days following onset of illness may not test positive for West Nile IgM, and testing should be repeated. A positive test for West Nile IgG in the absence of a positive West Nile IgM is indicative of a previous flavavirus infection and is not by itself evidence of an acute West Nile virus infection.[49]

If cases of suspected West Nile virus infection, sera should be collected on both the acute and convalescent phase of the illness. Convalescent specimens should be collected 2-3 weeks after acute specimens.

It is common in serologic testing for cross-reactions to occur among flaviviruses such as Dengue virus (DENV) and tick-borne encephalitis virus, this necessitates caution when evaluating serologic results of flaviviral infections.[50]

Four FDA-cleared WNV IgM ELISA kits are commercially available from different manufacturers in the U.S., each of these kits is indicated for use on serum to aid in the presumptive laboratory diagnosis of WNV infection in patients with clinical symptoms of meningitis or encephalitis. Positive WNV test kits obtained via use of these kits should be confirmed by additional testing at a state health department laboratory or CDC.

In fatal cases, nucleic acid amplification, histopathology with immunohistochemistry and virus culture of autopsy tissues can also be useful. Only a few state laboratories or other specialized laboratories, including those at CDC, are capable of doing this specialized testing

Differential diagnosis

A number of various diseases may present with symptoms similar to those caused by a clinical West Nile virus infection. Those causing neuroinvasive disease symptoms include the enterovirus infection and bacterial meningitis. Accounting for differential diagnoses is a crucial step in the definitive diagnosis of WNV infection. Consideration of a differential diagnosis is required when a patient presents with unexplained febrile illness, extreme headache, encephalitis or meningitis. Diagnostic and serologic laboratory testing utilizing PCR testing and viral culture of CSF to identify the specific pathogen causing the symptoms, is the only currently available means of differentiating between causes of encephalitis and meningitis.

Prevention

Low-cost, ceiling hung mosquito netting for a bed.
Mosquito coil

Personal protective measures can be taken to greatly reduce the risk of being bitten by an infected mosquito:

  • Using insect repellent on exposed skin to repel mosquitoes. EPA-registered repellents include products containing DEET (N,N-diethylmetatoluamide) and picaridin (KBR 3023). DEET concentrations of 30% to 50% are effective for several hours. Picaridin, available at 7% and 15% concentrations, needs more frequent application. DEET formulations as high as 50% are recommended for both adults and children over 2 months of age. Protect infants less than 2 months of age by using a carrier draped with mosquito netting with an elastic edge for a tight fit.
  • When using sunscreen, apply sunscreen first and then repellent. Repellent should be washed off at the end of the day before going to bed.
  • Wear long-sleeved shirts which should be tucked in, long pants, and hats to cover exposed skin.
  • The application of permethrin-containing (e.g., Permanone) or other insect repellents to clothing, shoes, tents, mosquito nets, and other gear for greater protection. Permethrin is not labeled for use directly on skin. Most repellent is generally removed from clothing and gear by a single washing, but permethrin-treated clothing is effective for up to 5 washings.
  • Be aware that most mosquitoes that transmit disease are most active during twilight periods (dawn and dusk or in the evening). A notable exception is the Asian Tiger mosquito which is a daytime feeder and is more apt to be found in, or on the periphery of, shaded areas with heavy vegetation. They are now widespread in the United States and in states such as Florida they have been found in all 67 counties.[51]
  • Staying in air-conditioned or well-screened housing, and/ or sleeping under an insecticide treatedbed net. Bed nets should be tucked under mattresses and can be sprayed with a repellent if not already treated with an insecticide.


Monitoring and control

A carbon dioxide-baited CDC light trap at NPSmonitoring site. The highest individual light trap total for 2010 was from a trap located in a salt marsh in the Fire Island National Seashore: approximately 25,142 mosquitoes were collected during a 16-hour period on August 31.[52]
Eggs of permanent water mosquitoes can hatch, and the larvae survive, in only a few ounces of water. Less than half the amount that may collect in a discarded coffee cup. Floodwater species lay their eggs on wet soil or other moist surfaces. Hatch time is variable for both types; under favorable circumstances, i.e.warm weather; the eggs of some species may hatch in as little as 1-3 days after being laid.[53]
Used tires often hold stagnant water and are a breeding ground for many species of mosquitoes. Some species such as the Asian Tiger mosquito prefer manmade containers; such as tires, to lay their eggs in. The rapid spread of this aggressive daytime feeding species beyond their native range has been attributed to the used tire trade.[54][55]

West Nile virus can be sampled from the environment by the pooling of trapped mosquitoes via carbon dioxide-baited light traps and gravid traps, testing avian blood samples drawn from wild birds, dogs and sentinel monkeys, as well as testing brains of dead birds found by various animal control agencies and the public.

Testing of the mosquito samples requires the use of RT-PCR to directly amplify and show the presence of virus in the submitted samples. When using the blood sera of wild birds and sentinel chickens, samples must be tested for the presence of WNV antibodies by use of immunohistochemistry (IHC)[56] or Enzyme-Linked Immunosorbent Assay (ELISA).[57]

Dead birds, after necropsy, have their various tissues tested for virus by either RT-PCR or IHC, where virus shows up as brown-stained tissue because of a substrate-enzyme reaction.

West Nile control is achieved through mosquito control, by elimination of mosquito breeding sites such as abandoned pools, applying larvacide to active breeding areas and targeting the adult population via aerial spraying of pesticides.

Environmentalists have condemned attempts to control the transmitting mosquitoes by spraying pesticide, saying the detrimental health effects of spraying outweigh the relatively few lives which may be saved, and more environmentally friendly ways of controlling mosquitoes are available. They also question the effectiveness of insecticide spraying, as they believe mosquitoes that are resting or flying above the level of spraying will not be killed; the most common vector in the northeastern US, Culex pipiens, is a canopy feeder.

Treatment

No specific treatment is available for WNV infection. In severe cases treatment consists of supportive care that often involves hospitalization, intravenous fluids, respiratory support, and prevention of secondary infections.

Prognosis

While the general prognosis is favorable, current studies indicate that West Nile Fever can often be more severe than previously recognized, with studies of various recent outbreaks indicating that it may take as long as 60–90 days to recover.[58][59] Patients with milder WNF are just as likely as those with more severe manifestations of neuroinvasive disease to experience multiple long term (>1+ years) somatic complaints such as tremor, and dysfunction in motor skills and executive functions. Patients with milder illness are just as likely as patients with more severe illness to experience adverse outcomes.[60] Recovery is marked by a long convalescence with fatigue. One study found that neuroinvasive WNV infection was associated with an increased risk for subsequent kidney disease.[61][62]

Epidemiology

Global distribution of West Nile virus.(2006)
West Nile virus cases in the continental United States in 2012.(Aug. 28, 2012)

WNV was first isolated from a feverish 37-year-old woman at Omogo in the West Nile District ofUganda in 1937 during research on yellow fever virus.[63] A series of serosurveys in 1939 in central Africa found anti-WNV positive results ranging from 1.4% (Congo) to 46.4% (White Nile region, Sudan). It was subsequently identified in Egypt (1942) andIndia (1953), a 1950 serosurvey in Egypt found 90% of those over 40 years in age had WNV antibodies. The ecology was characterized in 1953 with studies in Egypt[64] and Israel.[65] The virus became recognized as a cause of severe human meningoencephalitis in elderly patients during an outbreak in Israel in 1957. The disease was first noted in horses in Egypt and France in the early 1960s and found to be widespread in southern Europe, southwest Asia and Australia.

The first appearance of WNV in the Western Hemisphere was in 1999[1] with encephalitis reported in humans, dogs, cats, and horses, and the subsequent spread in the United States may be an important milestone in the evolving history of this virus. The American outbreak began in College Point, Queens in New York Cityand was later spread to the neighboring states of New Jersey and Connecticut. The virus is believed to have entered in an infected bird or mosquito, although there is no clear evidence.[66] West Nile virus is now endemic in Africa, Europe, the Middle East, west and central Asia, Oceania(subtype Kunjin), and most recently, North America and is spreading into Central and South America.

Recent outbreaks of West Nile virus encephalitis in humans have occurred in Algeria (1994), Romania (1996 to 1997), theCzech Republic (1997), Congo (1998), Russia (1999), the United States (1999 to 2009), Canada (1999–2007), Israel (2000) and Greece (2010).

Epizootics of disease in horses occurred in Morocco (1996), Italy (1998), the United States (1999 to 2001), andFrance (2000), Mexico (2003) and Sardinia (2011).

Treatment research

A vaccine for horses (ATCvet code: QI05AA10 (WHO)) based on killed viruses exists; some zoos have given this vaccine to their birds, although its effectiveness is unknown. Dogs and cats show few if any signs of infection. There have been no known cases of direct canine-human or feline-human transmission; although these pets can become infected, it is unlikely they are, in turn, capable of infecting native mosquitoes and thus continuing the disease cycle.[67] AMD3100, which had been proposed as an antiretroviral drug for HIV, has shown promise against West Nile encephalitis. Morpholino antisense oligos conjugated to cell penetrating peptides have been shown to partially protect mice from WNV disease.[68] There have also been attempts to treat infections using ribavirin, intravenous immunoglobulin, or alpha interferon.[69] GenoMed, a U.S. biotech company, has found that blocking angiotensin II can treat the "cytokine storm" of West Nile virus encephalitis as well as other viruses.[70]

In 2007, the World Community Grid launched the Discovering Dengue Drugs – Together project. This uses a distributed network of volunteers' computers via the Berkeley Open Infrastructure for Network Computing to perform computer simulations of interacting molecules. Thousands of small molecules are screened for potential antiviral properties with respect to West Nile and related viruses.

See also

Notes

  1. ^ a b Nash D, Mostashari F; et al. (2001). "THE OUTBREAK OF WEST NILE VIRUS INFECTION IN THE NEW YORK CITY AREA IN 1999". NEJM. 344 (24): 1807–12. PMID 11407341. {{cite journal}}: Explicit use of et al. in: |author= (help)
  2. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 12899140, please use {{cite journal}} with |pmid=12899140 instead.
  3. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 15663852, please use {{cite journal}} with |pmid= 15663852 instead.
  4. ^ "West Nile Virus: What You Need to Know CDC Fact Sheet". www.CDC.gov. Retrieved 2012-04-09.
  5. ^ Olejnik E (1952). "Infectious adenitis transmitted by Culex molestus". Bull Res Counc Isr. 2: 210–1.
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  7. ^ Anticona EM, Zainah H , Ouellette DR et al.: Two Case Reports of Neuroinvasive West Nile Virus Infection in the Critical Care Unit. Case Reports in Infectious Diseases; Volume 2012 (2012), Article ID 839458, 4 pages doi:10.1155/2012/839458
  8. ^ Carson PJ, Konewko P, Wold KS; et al. (2006). "Long‐Term Clinical and Neuropsychological Outcomes of West Nile Virus Infection". Clinical Infectious Diseases. 43 (6): 723–30. doi:10.1086/506939. PMID 16912946. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  9. ^ D. S. Asnis, R. Conetta, A. A. Teixeira, et al., “The West Nile virus outbreak of 1999 in New York: the Flushing Hospital experience,” Clinical Infectious Diseases, vol. 30, no. 3, pp. 413–418, 2000
  10. ^ Montgomery SP, Chow CC, Smith SW, etal. Rhabdomyolysis in patients with West Nile encephalitis and meningitis. Vector Borne Zoonotic Dis. 2005 Fall;5(3):252-7. PMID 16187894
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  14. ^ Shaikh1 S, Trese. West Nile virus chorioretinitis MT Br J Ophthalmol. 2004 December; 88(12): 1599–1600. PMCID: PMC1772450 doi: 10.1136/bjo.2004.049460
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  52. ^ [[National Park Service: Mosquito Management
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