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Diseases / List of Viral Diseases / Disease description:

West Nile Virus Disease

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INDEX - INFORMATION AVAILABLE

GENERAL INFORMATION

SUSCEPTIBILITY, DISEASE CHARACTERISTICS & DIAGNOSIS

TREATMENT & CONTROL

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THE FOLLOWING INFORMATION IS HELD ON THE INFECTIOUS AGENT INFORMATION PAGE
Flaviviridae: West Nile Virus:
 

  • Virus Structure and Identification
  • Associated Host Species of Virus (Animal Types Affected) and Hazard / Risk
  • Virus Life Cycle, Transmission and Effects of Chemicals
  • Transmission and Biogeographical / Climatic Range for Virus

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General and References

Disease Summary

West Nile Virus (WNV) Disease is caused by a virus which is transmitted mainly by mosquitoes (Culicidae - Mosquitoes (Family)), but may also be transmitted by ticks (Argasidae - Soft ticks (Family) and Ixodidae - Soft ticks (Family)) and some other arthropods. It may cause illness in a wide range of species including birds (Aves - Birds (Class)), humans (Homo sapiens - Human), horses (Equidae - Horses (Family)) and possibly other mammals (Mammalia - Mammals (Class)). Clinical signs vary widely from mild non-specific signs, particularly fever to severe central nervous signs. Severe clinical disease is uncommon but may be fatal. 

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Alternative Names (Synonyms)

  • West Nile Fever
  • West Nile encephalitis
  • West Nile viral encephalitis
  • Near Eastern equine encephalitis (in horses, in Egypt). (J84.5.w2)
  • Lourdige (in horses, in France).(J84.5.w2)

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Disease Type

 Viral

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Infectious/Non-Infectious Agent (directly associated with the Disease)

Species/Taxa

Mosquitoes (Main Vectors)

Ticks (Vectors)

Chemical

  • --

Physical

  • --

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References

Disease Author

Debra Bourne (V.w5)

Referee

Suzanne I. Boardman (V.w6); Becki Lawson (V.w26);  Dr Robert G. McLean (V.w42)

References

Detailed references are provided attached to specific sections.

ORGANISATIONS
(USA Contacts for Managing WNV Disease)

ELECTRONIC LIBRARY
(Further Reading)
Click image for full contents list of ELECTRONIC LIBRARY

Click here for further reading on "Managing for West Nile Virus"
Library

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Epidemiology and Host Susceptibility Factors

Incubation Period, Time Course and Persistence of Disease

General Editorial Description The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.

1) INCUBATION PERIOD:

  • The incubation period is usually fairly short and may vary between species.
  • In humans the incubation period is recorded within the range of 1 to 15 days, more usually 3 to 6 days.

(J39.84.w1, J71.54.w1, J71.75.w1, J84.5.w2, J84.7.w20, J84.8.w4, J88.36.w1, J100.93.w1, J101.86.w2, J116.5.w1, J120.20.w1, J120.20.w1, J122.77.w1, J123.31.w1, J127.46.w1, J129.42.w1, J133.951.w9, J133.951.w12, B241.49.w49, P32.1.w13, B240.14.w14, B243.31.w1, W170.Nov01.WNV2, N7.51.w3)

2) DISEASE DURATION (TO RECOVERY) IN INDIVIDUAL ANIMALS:

  • In birds the course of clinical illness is usually less than one week, but may range from 1 day to 2 -3 weeks before recovery or death.
  • In horses, signs usually resolve in survivors in 2 - 7 days and recovery is usually complete. Progression from first signs to severe disease requiring euthanasia has been reported to take as little as 24 hours in one case following experimental infection but in outbreaks a duration of several days of clinical illness has been reported.
    • A recent study of 125 horses surviving the initial illness indicated a longer average duration of clinical abnormalities (mean 35 days, median 21 days, range 1-180 days) in those which were considered to have recovered, and abnormalities of gait and/or behaviour remaining in 40% of horses six months after the initial diagnosis of WNV infection.
    • Another study found a mean duration of 22 days (range up to 90 days) in those which fully recovered, but 20% of equines had continuing clinical signs.
  • In humans, the course of the disease is usually three to six days, but may range from one day to several weeks. Sometimes there may be a milder relapse a few days after the first attack. Convalescence may be slow, lasting sometimes 1 to 2 weeks, and accompanied by general fatigue. There have been reports of prolonged convalescence in some individuals, and in some cases long term sequelae have followed severe disease in the USA. The overall presentation and duration of illness appears to vary with different outbreaks of WNV disease.
  • Concern has been expressed regarding possible long term complications in mammal and bird species.

(J4.218.w2, J4.225.w2, J6.32.w1, J71.75.w1, J84.5.w2, J84.7.w27, J84.8.w4, J85.108.w1, J91.3.w2, J100.93.w1, J101.59.w1, J101.64.w1, J102.17.w1, J103.3.w1, J106.55.w1, J120.20.w1, J122.77.w1, J129.42.w1, J215.24.w1, B240.14.w14, B241.49.w49, B243.31.w1, B244.w1, P30.1.w3, P51.49.w1, W27.13Nov01.wnv1, W214.Nov01.WNV6, V.w46)

3) TIME COURSE / PERSISTENCE OF DISEASE IN A SUSCEPTIBLE POPULATION:

  • West Nile virus infection is usually an endemic disease, with few clinical cases apparent. As a result, clinical cases tend to be seen sporadically, particularly in horses and humans. However, when a species is extremely susceptible, such as the Corvus brachyrhynchos - American Crow, mortality in a relatively naive population may be seen throughout the season during which mosquitoes (Culicidae - Mosquitoes (Family)) are active. 
  • Epidemics, and the main period of endemic transmission, occur during the summer months in temperate and subtropical areas.
  • Transmission in subtropical and tropical areas may peak in the rainy season. 

(J64.19.w1, J84.5.w2, J84.7.w16, J84.7.w17, J84.7.w27, J84.7.w32, J84.9.w8, J85.108.w1, J87.32.w1, J91.61.w1, J98.352.w1, J100.93.w1, J101.59.w1, J102.17.w1, J103.3.w1, J111.72.w1, J129.42.w1, J133.951.w26, J257.168.w2, B240.14.w14, B241.49.w49, B244.w1, P31.6.w1, P39.3.w1, P39.4.w1, P39.4.w6, P39.4.w7, N7.48.w2, N7.48.w3, W8.Nov01.WNV9, W27.20Feb02.wnv1)

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Mortality / Morbidity / Susceptibility / Life stage affected

General Editorial Description The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.

1) NUMBER OF DEATHS

  • Mortality rates have varied between different outbreaks and are difficult to determine as the total number of individuals infected is frequently not known.
  • In horses (Equus caballus - Domestic horse) and humans (Homo sapiens - Human), the fatality rate usually has been recorded as a percentage of confirmed or clinically detected cases - NOT as a percentage of the susceptible population (in humans the fatal cases are usually in elderly or immunocompromised individuals) and the indicated mortality rate for confirmed or clinically detected cases varies between approximately:
  • Experimentally, intracerebral inoculation in mammals caused a very high mortality rate in a variety of species whilst intraperitoneal and subcutaneous inoculation resulted in fatalities, but at a lower overall mortality rate.
  • Corvus brachyrhynchos - American Crow infected by subcutaneous inoculation of a recent USA WN virus strain had a 100% mortality rate. The crow family (Corvidae - Crows, Birds-of-Paradise etc. (Family)) appear to be particularly susceptible to the strain of WN virus circulating in the USA, and it should be remembered that high mortalities could occur in other species groups that have not yet been exposed to this strain of the virus.
  • In a collection in New York in 1999, 55% of clinically infected individuals died; however further serological studies showed that the dead birds totalled only 11.7% of the 94 birds which had been infected.
  • However, the large number of clinically normal animals that have been found with circulating WN virus antibodies would indicate that the mortality rate is usually very low in the majority of species (birds (Aves - Birds (Class)) and mammals (Mammalia - Mammals (Class))) affected.

(J2.40.w3, J3.105.w5, J3.151.w1, J4.222.w1, J5.47.w2, J42.100.w2, J64.19.w1, J71.75.w1, J84.7.w9, J84.7.w10, J84.7.w12, J84.7.w14, J84.7.w16, J84.7.w17, J84.7.w24, J84.7.w27, J84.7.w29, J84.7.w32, J84.8.w3, J84.9.w17, J84.9.w20, J84.10.w1, J85.108.w1, J87.32.w1, J88.36.w1, J90.1999.w2, J90.16.w4, J90.16.w5, J91.4.w1, J98.352.w1, J100.93.w1, J101.59.w1, J110.11.w1, J111.72.w1, J116.5.w1, J120.20.w1, J122.77.w1, J129.42.w1, J133.951.w9, J133.951.w26, J257.168.w2, B241.49.w49, P30.1.w3, W8.Nov01.WNV8, W27.19Sept02.wnv1, N7.51.w6, N7.52.w6, P39.4.w4, P39.4.w16, P48.1.w3, P87.10.w3, V.w42)

2) NUMBER OF ANIMALS AFFECTED

  • When the large number of humans and animals with circulating antibodies and the low number of clinical cases reported are considered together, it appears likely that the number of infected individuals showing clinical signs, even during outbreaks, is generally only a low percentage of those infected. 
  • The exception may be the recent outbreaks in the USA where high mortality and morbidity has been seen in free-ranging birds, particularly the crow family (Corvidae - Crows, Birds-of-Paradise etc. (Family)).
  • In horses it appears from natural and experimental data that about one in ten infected individuals develops clinical signs.

(J64.19.w1, J84.7.w17, J84.7.w27, J84.8.w11, J84.9.w20, J90.1999.w2, J90.16.w4, J91.3.w1, J98.352.w1, J98.358.w1, J100.93.w1, J112.13.w1, J129.42.w1, J133.951.w26, J238.118.w1, B240.14.w14, P30.1.w3, P39.4.w16, P48.1.w16, P51.49.w2, W30.Nov01.WNV7, N7.52.w4, N7.52.w6)

3) EFFECTS OF AGE, SEX AND REPRODUCTIVE STATUS

  • In outbreaks of WNV encephalitis in horses (Equus caballus - Domestic horse), animals of all ages appear to be affected, although it has been suggested (J85.108.w1) that adults may be affected more than young animals and data from the USA (1999-2001) suggest that older animals may be more likely to die than younger animals (P39.3.w3). Draft horses may be more likely to become clinically affected.
  • In humans (Homo sapiens - Human), encephalitis appears to occur more frequently in elderly individuals and mortality is also commonly reported to be higher for elderly patients; although fatal encephalitis cases in children have been recorded, illness is rarely recorded in very young children.
  • In Grus canadensis - Sandhill crane, young chicks may be more susceptible than adults.
  • In birds of prey, there are some indications that illness may be more severe in juveniles than in adults.
  • In laboratory rodents (Rodentia - Rodents (Order)), resistance to WNV infection generally increases with age, the greatest susceptibility being seen in neonates.
  • There are no apparent differences in susceptibility related to gender or reproductive status in any species; although slightly more male than female horses were affected in the USA in 1999-2001, the opposite was found in some later studies.

(J2.40.w3, J4.222.w1, J4.225.w2, J4.225.w5, J4.228.w1, J19.68.w7, J71.54.w1, J84.7.w12, J84.7.w14, J84.7.w16, J84.7.w17, J84.7.w27, J84.7.w32, J84.14.w5, J85.108.w1, J90.16.w5, J98.352.w1, J101.86.w2, J111.72.w1,  J129.42.w1, J133.951.w26, J257.168.w2, J279.7.w2, B241.49.w49, B243.31.w1, B244.w1, P31.6.w1, P39.3.w3, P39.4.w1, P39.4.w2, P39.4.w7, P48.1.w5, P87.10.w2, N7.51.w6, N7.52.w6)

4) EFFECTS OF BODY CONDITION AND OTHER DISEASES

The following factors appear to increase susceptibility to the development of clinical signs associated with West Nile virus:

  • Lymphoproliferative disorders have been associated with protracted WN viraemia and severe illness in humans.
  • Immunosuppression has been associated with an increased fatality rate in humans.
  • A weakened immune system from another disease was considered to be a possible relevant factor in a dog which died from WNV infection.
  • In geese in Hungary, immunosuppression due to circovirus infection was considered to be a possible factor increasing susceptibility.
  • The dose of the virus appears to affect the speed of onset of clinical signs, whereby virus invasion of the central nervous system (CNS) seems to occur earlier with a larger viral dose. 
  • Stress due to cold, or due to isolation, was associated with increased mortality due to WN virus inoculation in mice.
  • Dexamethasone administration increased the mortality rate in experimentally infected mice.
  • Immunosuppression through administration of cyclophosphamide, corticosterones or bacterial endotoxin increased the mortality rate in experimentally infected rodents (Rodentia - Rodents (Order)).
  • It was considered possible that extrinsic stressors may have increased susceptibility in some Florida alligators (Alligator mississippiensis - American alligator (Alligatoridae - Alligators & Caimans (Family)))

(J19.68.w7, J71.109.w1, J84.5.w2, J84.9.w8, J84.9.w17, J84.9.w19, J91.3.w1, J130.46.w1, J257.168.w2, P39.4.w3, W27.19Sept02.wnv1)

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Clinical & Pathological Characteristics, and Diagnosis

Clinical Signs (by physiological system)

Overall Clinical Presentation The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.
  • The presentation of this disease may vary from inapparent infection through a mild non-specific illness, to severe nervous signs and death; there are no pathognomonic findings.
  • The course of the disease is usually short, but convalescence can be prolonged, particularly in the elderly.
  • The predominant presentation in humans is usually pyrexia (fever) and headache, often with fatigue and myalgia/arthralgia; skin rash, enlarged lymph nodes, conjunctival congestion and gastrointestinal signs are also commonly seen. Other less common signs in humans include sore/congested throat and coughing.
  • In severe disease in humans, neurological signs and sometimes profound muscular weakness may be seen while signs such as rash and lymphadenopathy may be absent.
  • In horses, neurological signs usually predominate in clinically apparent cases; fever may or may not be present. Common signs include ataxia/incoordination, muscle fasciculations, limb paresis or paralysis (particularly of the hind limbs) and leading to recumbency in severe cases, altered behaviour and hyperaesthesia.
  • In other mammals when clinical illness occurs this may include mild non-specific signs such as lethargy and reduced appetite and/or overt neurological signs such as head tilt, torticollis, ataxia and incoordination, tremors, hindlimb paralysis, tetraplegia, loss of righting ability and recumbency. Pyrexia may be present. Continuing neurological signs may occur in survivors.
  • Many affected birds in the USA have been found dead (sudden death) although non-specific, neurological, and respiratory signs have sometimes been noted prior to death.
  • In affected reptiles, neurological signs have been seen.

(References are available in the detailed literature reports below)

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Clinical Pathology (Testing Samples incl. Serology)

Overall Clinical Pathology findings The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.
  • There are no pathognomonic findings.
  • In clinically affected humans, haematology may show a mild leucopaenia with relative lymphocytosis and a left shift. In equines, there may be a mild absolute lymphopaenia. Biochemistry is frequently within normal ranges although mild electrolyte imbalances have been noted, sometimes accompanied by raised bilirubin levels in horses and urea levels in humans. A positive diagnosis of WNV disease is usually based on either a four-fold rise in antibody titres for paired serum samples (acute and convalescent sera), or detection of WN viral antigen, accompanying indicative clinical signs.
  • In patients with central nervous system involvement, the CSF is clear, often with raised protein but normal sugar levels, and pleocytosis (mononuclear cell or polymorphonuclear cell). Virus may be isolated and antibodies may be detected in the CSF.
  • Antibodies may be detected in CSF before they are detectable in serum.
  • Virus has been detected in oral swabs and cloacal swabs from a variety of WNV infected birds although it is not detected in all infected birds. 
  • In humans presenting with acute flaccid paralysis, asymmetric muscle denervation with reduced compound muscle potentials but normal sensory nerve potentials has been detected in electrodiagnostic studies.
  • Brain scans with CT and MRI are not diagnostic.
  • Leptomeningeal enhancement of the lumbar spine has been reported with MRI of a patient with WNV infection associated leg weakness (acute flaccid paralysis).
  • Feather pulp from growing flight feathers of WNV infected corvids (Corvidae - Crows, Birds-of-Paradise etc. (Family)) contains relatively high quantities of virus and this can be used for detection during the moult, which is during the height of the WN virus transmission season.

(References are available in the detailed literature reports below)

Sampling

For humans, the following advice for the most appropriate specimens to test for viral encephalitides has been provided through the Emerging Infections Encephalitis Project, funded by the Centers for Disease Control and Prevention (CDC) (D72): [Text copied directly]

This project includes testing CSF specimens on patients with encephalitis of unknown etiology for 13 different viruses.

Appropriate specimens for testing include:

  1. CSF - can be tested by IgM capture ELISA and RT-PCR

    If there is insufficient quantity of CSF for both ELISA and RT-PCR, testing priority should be determined by the ordering physician.

    1. Capture ELISA is more sensitive than RT-PCR for WNV testing and should be considered when there is stronger suspicion of WNV than other etiologic agents.
    2. RT-PCR is less sensitive for WNV, but provides testing for 13 different viruses. This test should be considered if suspicion of the etiologic agent is stronger for viruses other than WNV.
  2. Serum - Acute and convalescent sera can be tested by IgM Capture and IgG ELISA testing, with indeterminate and positive specimens confirmed by PRNT.
  3. Brain Tissue - Can be tested by RT-PCR and viral culture.

(D72)

See also:

Click for Video: Bird Necropsy Protocol for West Nile Virus Surveillance Video Available: Blood Collection Techniques for Birds:
  Internet (Web) Version (Smaller files - quicker to load)
  CD-ROM Version (Larger files - higher quality images)

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Pathological Findings (by anatomical system)

Overview The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.

GROSS PATHOLOGY

  • In birds, brain haemorrhage, splenomegaly, meningoencephalitis and myocarditis are the most frequent findings although there may be no gross lesions on post mortem examination (necropsy). 
  • In horses, traumatic lesions may be evident, associated with falling while ataxic or struggling while recumbent. Often there are no gross lesions of the central nervous system. One or more gross lesions such as submeningeal oedema, meningeal congestion, cerebral surface congestion and congestion within the spinal cord have been recorded in a few horses.
  • In humans, there may be no gross pathological changes. Where present, lesions in patients with meningoencephalitis may include perivascular haemorrhage, dilation of the ventriculi of the brain, foci of encephalomalacia, dislocation of the brain trunk, hydropericarditis, cardiac muscle flabbiness. Acute haemorrhagic pancreatitis has been described also.

HISTOLOGY

  • Histological findings have generally been concentrated in the central nervous system (CNS) where lesions of mild to severe nonsuppurative encephalitis or encephalomyelitis may be found. 
  • Myocarditis is relatively common, particularly in birds.
  • Hepatitis or pancreatitis, as well as mild lung lesions, and adrenal lesions, have been noted occasionally. 

VIRUS ISOLATION

  • Virus may be isolated from a variety of tissues sampled at necropsy.
  • In birds (Aves - Birds (Class)) virus is most commonly isolated from the kidney and nearly as often from the brain and heart.
  • In horses (Equus caballus - Domestic horse) virus has been isolated from the brain and spinal cord (natural infection).
  • In humans (Homo sapiens - Human) virus has been isolated from brain tissue.

(References are available in the detailed literature reports below)

See also:

Click for Video: Bird Necropsy Protocol for West Nile Virus Surveillance Video Available: Bird Necropsy Protocol for West Nile Virus Surveillance:
Internet (Web) Version (Smaller files - quicker to load)
CD-ROM Version (Larger files - higher quality images)

CLICK THE LINKS FOR Literature Reports on Specific Pathological Findings Descriptions available
CLICK THE LINKS FOR Editorial Overviews Available

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Diagnostic Criteria

General Indicative Signs

Aves - Birds (Class):

  • While infection may be asymptomatic, clinical signs which may be seen include general signs such as depression, anorexia, weakness, recumbency and weight loss, and/or neurological signs such as abnormal posture of the head or neck, ataxia, incoordination, inability to stand, tremors, circling, disorientation, impaired vision, posterior paresis (unilateral or bilateral) and disorientation. Clinical signs are variable and may include nervous and nonspecific signs. Birds may also be found dead without any clinical signs having been observed. (J26.37.w1, P30.1.w3) At necropsy, signs of trauma may or may not be present and gross lesions are not always present; suggestive findings are those of meningoencephalitis and necrotising myocarditis. (J26.37.w1)
  • In a 37-year-old male Florida sandhill crane at the International Crane Foundation, Baraboo, Wisconsin, USA in 2006, WNV was suspected on the basis of rapid onset, clinical signs, seasonality and increase in cases in Wisconsin. (P87.10.w3)

Equidae - Horses (Family):

  • WNV infection may cause a range of signs in equines from inapparent infection (no clinical signs) to severe neurological signs which may be fatal or require euthanasia. Ataxia (stumbling, staggering, incoordination, wobbly gait), weakness, paresis or paralysis and recumbency, muscle fasciculation and altered mental status are common; apparent blindness, proprioceptive defects, lip droop and teeth grinding may be noted in some horses; seizures occur only occasionally. Fever may or may not be present. Signs are non-specific and are not sufficient, in themselves, for diagnosis. (J4.218.w2, J84.7.w17, J84.7.w27, J89.16.w1, J484.35.w1, P51.49.w3)
    • Diagnosis in the living horse is based on assessment of clinical signs, epidemiology (geographical location, season, known occurrence in other horses or in birds, presence of potential vectors) and serological testing. (J89.22.w1, J484.35.w1)
    • In areas of North America where this disease has become common in horses, clinically affected animals may "look like" WN virus infection cases, particularly because of the muscle fasciculations and the hypersensitivity they often show. (J487.14.w1)
    • WNV infection should be suspected "for any horse with rapid onset of neurological disease in an area with confirmed West Nile virus activity during periods of high mosquito activity." (J4.218.w2)
    • Note: clustering of cases in an area where WN virus is known to be active would increase the level of suspicion. (V.w117)
    • Pathologically, abnormalities are found in the lower brainstem and spinal cord, rather than the cerebral and cerebellar cortices (unlike in Eastern Equine Encephalitis and Western Equine Encephalitis). (J484.35.w1, P51.49.w3)
    • For a list of other diseases which may cause similar clinical signs in horses see: Equine Surveillance for West Nile Virus - Other Diseases that look like WNV Infection

Homo sapiens - Human (Species Link Page):

  • WN virus infection may be inapparent or result in a range of signs and symptoms from classical West Nile fever (fever and headache, with or without rash and/or enlarged lymph nodes, and sometimes other symptoms) to severe neurological manifestations of meningitis or encephalitis, sometimes with profound muscle weakness or acute flaccid paralysis. Other manifestations, such as hepatitis or respiratory signs, have been noted occasionally. 
    • The signs and symptoms of WNV infection are not specific to this disease and are not diagnostic. West Nile fever cannot be distinguished clinically from other viral fevers and WNV meningitis or encephalitis cannot be distinguished clinically from similar syndromes caused by other viruses. 

    (B244.w1, B241.49.w49, B243.31.w1, J84.7.w14, J93.38.w5, W170.28Jan03.wnv1)

  • The CDC 2001 Case Definition for arboviral infections states: "Arboviral infections may be asymptomatic or may result in illnesses of variable severity sometimes associated with central nervous system (CNS) involvement. When the CNS is affected, clinical syndromes ranging from febrile headache to aseptic meningitis to encephalitis may occur, and these are usually indistinguishable from similar syndromes caused by other viruses. Arboviral meningitis is characterized by fever, headache, stiff neck, and pleocytosis. Arboviral encephalitis is characterized by fever, headache, and altered mental status ranging from confusion to coma with or without additional signs of brain dysfunction (e.g., paresis or paralysis, cranial nerve palsies, sensory deficits, abnormal reflexes, generalized convulsions, and abnormal movements)." (W170.28Jan03.wnv1)
  • The CDC case definition for West Nile fever describes this as: "A non-specific, self-limited, febrile illness caused by infection with WNV, a mosquito-borne flavivirus. Clinical disease generally occurs 2-6 days (range, 2-15 days) following the bite of an infected mosquito. Typical cases are characterized by the acute onset of fever, headache, arthralgias, myalgias, and fatigue. Maculopapular rash and lymphadenopathy generally are observed in less than 20% of cases. Illness typically lasts 2-7 days." [2002 definition] (D147)
  • In the USA, due to year-round transmission in some geographical regions and the reported occurrence of severe disease in persons of all ages it has been recommended that a diagnosis of WNV infection should be considered in all cases of unexplained human encephalitis and meningitis but particularly in adults 50 years old or older developing unexplained meningitis or encephalitis in late summer or early autumn (fall). (W170.Aug02.WNV1)
  • It is important to consider the possibility of WNV infection in patients presenting with acute flaccid paralysis, even if other signs of central nervous system involvement are absent. (J84.9.w13)
Definitive Diagnosis Detailed information on clinical-pathological findings, necropsy findings and laboratory tests for antigen or antibody are provided in the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.

Aves - Birds (Class):

In dead birds:

  • In dead bird surveillance, testing involves isolation of infectious virus, or specific RNA detection by RT-PCR. Immunohistochemistry may also be used to detect the virus in tissues. Kidney, heart and brain are the preferred tissues for testing. (D67, D147, J5.47.w2, J133.951.w12, P48.4.w13)
    • In a 37-year-old male Florida sandhill crane at the International Crane Foundation, Baraboo, Wisconsin, USA in 2006, WNV was confirmed by positive RT-PCR of brain tissue. (P87.10.w3)
  • In the USA for surveillance infection is considered to be laboratory-confirmed if WN virus is isolated, WN viral RNA is detected and further validated or WN viral antigen is detected and further validated, or in live birds if seroconversion to WN virus is demonstrated by PRNT in serially-collected serum specimens (with cross-neutralisation to rule out other flavivirus infections) or IgM antibody to WN virus is detected and validated by demonstration of neutralising antibody. A laboratory-probable individual is one in which IgM antibody is detected or seroconversion to WN virus is detected in serially collected serum specimens, strongly reactive by EIA or IFA, or antigen is detected but not validated by another procedure, or a single RT-PCR test is positive for WN viral RNA. (D147)

In live birds:

  • Definitive diagnosis of infection requires detection of seroconversion. Tests which may be used include HI, ELISA and PRNT. It must be remembered that in birds other than hatch-year birds, and which have not been previously bled and determined to be seronegative, presence of antibodies may not indicate recent infection.
    • In a 37-year-old male Florida sandhill crane at the International Crane Foundation, Baraboo, Wisconsin, USA in 2006, WNV was confirmed by  a flavivirus positive at titre 1:80, compared to WNV seronegative in previous years). (P87.10.w3)

(D67, D72, D147, J84.8.w9, J133.951.w10, P32.1.w1, P39.2.w2)

Equidae - Horses (Family):

  • Definitive diagnosis of WNV infection in horses requires detection of virus, specific viral antigen or genomic sequences from blood, CSF, tissue or other body fluid, or demonstration of seroconversion. In areas where vaccination against WNV infection may be used it is important to ensure that a full vaccination history is obtained if results of serological tests are to be interpreted correctly. Depending on the serological test used and whether other flaviviruses may be present in the geographical area, cross-reaction with other flaviviruses must be considered. (J215.April 2002.w1, D67, D147, W30.Nov01.WNV4)
  • For the purposes of West Nile virus surveillance in the USA, definitions have been agreed on "confirmed" and "probable" cases for  equine infections. (D67, D72, D147).
  • Details of the criteria for laboratory diagnosis and for "confirmed" and "probable" cases in the USA are provided in:  Equine Surveillance for West Nile Virus - How to make a definite diagnosis
  • For further information on different serological tests and virus identification see:

In Homo sapiens - Human (Species Link Page):

Diagnosis of West Nile Virus disease is generally based on compatible clinical signs associated with the confirmed presence of West Nile virus (detection of virus or of specific viral antigen or genomic sequences in serum, CSF or tissues) or serological indications of recent infection. (B243.31.w1, B244.w1, J64.19.w1, J129.42.w1, D67, D72, W170.28Jan04.WNV1) 

It is important to remember that:

  • Cross-reactions with other flaviviruses may occur with standard serological tests, which complicates interpretation of the tests. (B243.31.w1)
  • In immunosuppressed individuals, development of antibodies may be delayed or may not occur. (D147)
  • Virus is most likely to be detected (rarely isolated, more commonly detected by RT-PCR on the first days of illness in serum or more often in acute-phase samples of CSF. (B244.w1, J129.42.w1, D147)
    • In immunosuppressed individuals, virus or viral RNA may be detected in the serum or CSF for longer periods than normal. (D147)

In general for definition of arboviral encephalitis the accepted diagnostic categories are:

  • Confirmed case: compatible clinical syndrome together with either virus-specific IgM in CSF or four-fold rise in serum antibody titre detected by ELISA, IFA, CF, HI or virus neutralization or isolation of virus from tissue, blood or CSF;
  • Probable case: compatible clinical syndrome together with elevated antibody titre in a single serum sample (examples of elevated titres are >320 by HI, >256 by IFA, >128 by CF, >160 by 90% PRNT) or presence of virus-specific IgM in serum;
  • Suspected case: compatible clinical syndrome occurring during a period of likely arbovirus transmission.

(J93.38.w5, D68)

In Romania in 1996 the clinical case definition used in the investigation of the epidemic was "acute aseptic meningitis, encephalitis, or meningoencephalitis of suspected viral etiology, with a CSF pleocytosis. Out of those patients meeting the clinical case criteria, 84% were subsequently laboratory confirmed with WNV infection or were considered probable, based on the presence of anti-WN virus IgM antibodies in CSF or serum samples collected in the first week of illness. It was also noted that cases were confirmed in individuals hospitalised with fever and headache, presenting with non-specific febrile illness, and in individuals with clinical respiratory infection. (J93.38.w5)

For the purposes of West Nile virus surveillance in the USA, definitions have been agreed on "confirmed" and "probable" cases for human infections. (D67, D72, D147).

The most recent (2002) CDC definition for WN Fever gives the following case classification (text copied directly) (D147):

CASE DEFINITION
Case Description

A non-specific, self-limited, febrile illness caused by infection with WNV, a mosquito-borne flavivirus. Clinical disease generally occurs 2-6 days (range, 2-15 days) following the bite of an infected mosquito. Typical cases are characterized by the acute onset of fever, headache, arthralgias, myalgias, and fatigue. Maculopapular rash and lymphadenopathy generally are observed in less than 20% of cases. Illness typically lasts 2-7 days.

Case Classification

A clinically compatible illness, plus:

Confirmed:

1) Fourfold or greater change in WNV-specific serum antibody titer;

2) Isolation of WNV from or demonstration of specific WN viral antigen or genomic sequences in tissue, blood, CSF, or other bodily fluid; or

3) WNV-specific IgM antibodies demonstrated in serum by antibody-capture enzyme immunoassay and confirmed by demonstration of WNV-specific serum neutralizing antibodies in the same or a later specimen.

Probable:

1) WNV-specific serum IgM antibodies detected by antibody-capture enzyme immunoassay but with no available results of a confirmatory test for WNV-specific serum neutralizing antibodies in the same or a later specimen.

(Note: Some WN fever cases progress to WN meningitis or encephalitis. Cases meeting the more restrictive case definition of WN encephalitis/meningitis should be reported as such and only once, using event code 10056 for “WN Encephalitis or Meningitis”.)

  • NOTE: it can be impossible to distinguish clinically between WN fever and dengue fever, therefore a recent travel history and appropriate serological testing, to distinguish between closely-related flaviviruses, are very important. (D147 - Appendix D)

The most recent (2004) CDC definition for neuroinvasive and non-neuroinvasive arboviral disease gives the following case classification (text copied directly) (D344, W170.12May08.wnv6) [Full text included]:

Clinical criteria for diagnosis 

Cases of arboviral disease are classified either as neuroinvasive or non-neuroinvasive, according to the following criteria: 

Neuroinvasive disease requires the presence of fever and at least one of the following, as documented by a physician and in the absence of a more likely clinical explanation: 
  • Acutely altered mental status (e.g., disorientation, obtundation, stupor, or coma), or 
  • Other acute signs of central or peripheral neurologic dysfunction (e.g., paresis or paralysis, nerve palsies, sensory deficits, abnormal reflexes, generalized convulsions, or abnormal movements), or 
  • Pleocytosis (increased white blood cell concentration in cerebrospinal fluid [CSF]) associated with illness clinically compatible with meningitis (e.g., headache or stiff neck). 

Non-neuroinvasive disease requires, at minimum, the presence of documented fever, as measured by the patient or clinician, the absence of neuroinvasive disease (above), and the absence of a more likely clinical explanation for the illness. Involvement of non-neurological organs (e.g., heart, pancreas, liver) should be documented using standard clinical and laboratory criteria.

Laboratory criteria for diagnosis

Confirmed case : 

  • Four-fold or greater change in virus-specific serum antibody titer, or 
  • Isolation of virus from or demonstration of specific viral antigen or genomic sequences in tissue, blood, CSF, or other body fluid, or 
  • Virus-specific immunoglobulin M (IgM) antibodies demonstrated in CSF by antibody-capture enzyme immunoassay (EIA), or 
  • Virus-specific IgM antibodies demonstrated in serum by antibody-capture EIA and confirmed by demonstration of virus-specific serum immunoglobulin G (IgG) antibodies in the same or a later specimen by another serologic assay (e.g., neutralization or hemagglutination inhibition).
  • Probable case : 

    Stable (less than or equal to a two-fold change) but elevated titer of virus-specific serum antibodies, or 
  • Virus-specific serum IgM antibodies detected by antibody-capture EIA but with no available results of a confirmatory test for virus-specific serum IgG antibodies in the same or a later specimen. 

Case definition 

A case must meet one or more of the above clinical criteria and one or more of the above laboratory criteria. 

Further details are provided in: Human Surveillance for West Nile Virus

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Similar Diseases The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.

In birds (Aves - Birds (Class)):

  • The differential diagnosis for encephalitis and myocarditis in birds should include eastern equine encephalitis (EEE), avian influenza and Newcastle’s disease. Other cause of nervous signs include avian encephalomyelitis virus infection, botulism and listeriosis.

(J26.37.w1, B32.31.w14, B36.20.w20, B36.21.w21, B36.22.w22, W43.Jan04.wnv6)

In horses (Equus caballus - Domestic horse):

  • Diseases which may cause similar signs in horses include the other arboviral encephalitides (Western Equine Encephalitis, Eastern Equine Encephalitis, Venezuelan Equine Encephalitis), Equine herpes virus 1 (EHV-1), central nervous system protozoal infections, encephalopathy due to diseases of other organ systems (e.g. hepatic encephalopathy), various toxicities including botulism, focal spinal cord lesions, Wobbler syndrome and, most importantly, rabies. 

(J4.218.w2, J14.44.w1, J89.16.w1, W43.Jan04.wnv4)

In humans (Homo sapiens - Human):

  • For clinical signs of typical West Nile Fever, diseases such as typhus fever, infectious mononucleosis, leptospirosis, dengue, measles, rubella, exanthemata due to ECHO and Coxsackie viruses, a wide variety of arthropod-borne viral infections such as dengue, sandfly fever, chikungunya and o'nyong-nyong fever, and unidentified summer fevers must be considered.
  • In cases of West Nile Virus encephalitis, other viral encephalitides must be considered (Eastern equine encephalitis (EEE), Western equine encephalitis (WEE), St. Louis encephalitis (SLE), California encephalitis, Venezuelan equine encephalitis (VEE), Japanese B encephalitis (JE)) as well as aseptic meningitis, lymphocytic choriomeningitis, and nonparalytic poliomyelitis; severe forms from cerebrovascular accidents, brain tumours, brain abscess and intoxications and a variety of other viral and toxic causes of encephalitis.
  • In individuals with acute flaccid paralysis, differentiation must be made from Guillain-Barré syndrome, poliomyelitis, stroke and myopathy.

(J84.9.w13, J101.64.w1, J129.42.w1, J214.267.w9, B240.14.w14, B252.32.w32, P39.4.w3, P31.6.w1)

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Treatment and Control

Specific Medical Treatment (Antiserum, Antidote, Anti-(viral/bacterial/fungal) etc.)

Specific Medical Treatment The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.

ANTISERUM

  • Treatment with intravenous immunoglobulins (IVIG) has been used in humans, sometimes with a marked positive effect.
  • Experimentally IVIG from Israeli donors, but not from USA donors, was shown to have a protective effect against WNV infection in mice; the difference was presumed to be related to a higher level of natural immunity in the Israeli donors, since WN virus has been endemic in the Middle East for many years.
  • A clinical trial of IVIG (Omr-IgG-am ™) for use in certain cases of WNV infection started September 2003 in the USA [data from January 2004]. (W483.Jan04.wnv1)
  • Administration of neutralizing antibodies to hamsters (Mesocricetus auratus - Golden Hamster) was shown to give protection against subsequent subcutaneous inoculation with WN virus.
  • Administration of human WN virus-immune gamma globulin to mice post-inoculation provided a significant degree of protection and in wild-type mice, but not in immunodeficient mice, some protection was shown even when therapy was initiated after virus would have reached the CNS.
  • Two products, one plasma-based (from Lake Immunogenics, Inc.) and one serum-based (from Novartis Animal Health), have been granted conditional licences for use in horses in the USA. 

ANTIVIRAL DRUGS

  • Antiviral drugs to date have not proved useful for the treatment of Flaviviridae (Virus Family) infections. Some protective and therapeutic effects results have been seen with interferon alpha-2b in vitro and with ribavirin in a mouse model and in at least one in vitro model. Ribavirin has been used in the treatment of human patients but no controlled studies have been completed for the use of ribavirin or interferon alpha-2b in humans. Other drugs have been tested for their efficacy in vitro.

(J19.68.w1, J64.19.w1, J80.77.w3, J84.7.w31, J84.8.w2, J100.182.w1, J100.188.w1, J100.188.w2, J106.55.w2, J221.86.w1, J128.13.w1, J133.951.w29, J258.326.w1, J259.2.w1, J280.55.w1, B244.w1, D67, W170.Aug02.WNV1, W479.Jan04.wnv3, W479.Jan04.wnv4, W483.Jan04.wnv1)

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  • No specific techniques described

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General Nursing and Surgical Techniques

Nursing and Supportive Care The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.
  • General supportive care is indicated to limit inflammation and pain.
  • In patients with central nervous system signs symptomatic and supportive treatment should be given as for other viral encephalitides.
  • Intravenous nutrient and fluid support may be required if the affected individual is unable to eat.
  • Respiratory support may be required.
  • In horses, specific consideration should be given to the prevention of self-inflicted injury and the provision of physical (sling) support for severely ataxic individuals.

(J4.218.w2, J4.222.w1, J5.36.w8, J64.19.w1, J14.45.w1, J84.7.w27, J89.16.w1, J89.22.w1, J101.64.w1, J123.31.w1, J215.24.w1, J257.168.w3, J258.326.w1, J259.2.w1, J484.35.w1, B100, B222.34.w34, B240.14.w14, B243.31.w1, B249.11.w1, P51.48.w1, P51.49.w3, W170.Nov01.WNV2, W170.Aug02.WNV1) 

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Surgical Treatment
  • Not applicable for this disease.

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Vaccination & Prophylactic Treatment

Vaccination The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.
  • Research into vaccines has progressed rapidly over the last few years.
  • Four vaccines have been given USDA approval for use in horses in the USA; three are commercially available, and have also been licensed for use in Canada:
    • 1) A killed virus product (West Nile - Innovator, Fort Dodge Animal Health) for use in horses, requiring an initial course of two injections, has been developed and was given a full licence by USDA in February 2003.This vaccine also has been used in other species.
      • The reported vaccine efficacy in properly vaccinated horses is 94%.
      • The vaccine has been shown to be immunogenic in llamas and alpacas.
      • In birds, variable seroconversion has occurred following extralabel use of this vaccine.
    • 2) A recombinant vaccine (RECOMBITEK® Equine West Nile Virus vaccine, Merial Animal Health Ltd.) for use in horses, expressing WN virus prM/E genes in a canarypox vector, with a primary course of two injections, was granted a full license by USDA in December 2003.
    • 3) A Flavivirus chimera vaccine, for use in horses, (PreveNile, Intervet) containing West Nile virus pre-membrane (prM) and envelope (E) genes (from the NY99 strain) in a backbone of yellow fever (YF) 17D vaccine virus), was granted a full license by USDA in August 2006.
    • 4) A DNA vaccine for use in horses (from Fort Dodge Animal Health) was given a full licence by USDA in 2005 but is not commercially available.
  • A killed virus requiring a course of two injections has been used to protect goslings in commercial flocks in Israel.
  • A live attenuated vaccine has been used experimentally in mice and geese with apparent success.
  • Recombinant and DNA vaccines are under development.
    • Work is progressing on the development of chimeric vaccines combining West Nile structural protein genes with a dengue type 4 virus or a yellow fever virus. In mice these chimeric vaccines have provided effective protection against challenge with WN virus. In baboons the yellow fever chimeric vaccine has been shown to result in the development of high levels of neutralising antibodies. In rhesus monkeys the WN/DEN4 chimeras have been shown to result in development of moderate-to-high levels of neutralising antibodies and protection against challenge with wild-type WN virus. 
    • Work has been carried out on the use of DNA vaccines, with initial results a) using a recombinant plasmid expressing the WN virus prM and E structural proteins showing that neutralizing antibodies can be elicited, and protection from challenge, and b) with a vaccine encoding the WV virus capsid protein (WNVCp) showing development of antibody (IgG) response and also cellular immune responses.
    • Protection has been shown for Corvus ossifragus - Fish crow vaccinated once intramuscularly with a DNA vaccine, but not for these crows vaccinated once orally or for Corvus brachyrhynchos - American Crow vaccinated once intramuscularly or orally.
    • Protection (lower viraemia) has been shown in Buteo jamaicensis - Red-tailed hawk following vaccination with a DNA-plasmid vaccine.
    • Good immune responses have been seen in condors inoculated with DNA-plasmid vaccine.
    • A recombinant envelope (E) protein vaccine has been shown to give protection against experimental infection with WN virus in mice.
  • It is possible that in some cases individuals who have been vaccinated against other flavivirus infections may have a degree of immunity to disease caused by WNV infection.
  • Vaccination could be useful in a situation in which large numbers of nonimmune humans were moving into an area known to have a very high rate of transmission of WN virus and for protection of people in known "at risk" groups (e.g. the elderly and people living in areas with evidence of high rates of virus transmission).
  • Note: until recently there was apparently no need for a vaccine against West Nile virus. Within the historical range of WNV, most infections were subclinical or resulted in mild febrile disease; the incidence of infections involving neurological complications and fatal infections were very low in humans while outbreaks of encephalitic infection in horses were rare.

(J1.40.w9, J2.36.w4, J2.38.w1, J2.40.w3, J4.225.w2, J4.225.w3, J4.225.w5, J4.225.w6, J4.226.w1, J5.47.w1, J13.65.w2, J20.314.w1, J64.19.w1, J70.23.w5, 70.25.w7, J80.75.w1, J84.7.w12, J84.8.w1, J84.8.w14, J84.9.w15, J87.39.w3, J90.1999.w2, J91.66.w1, J91.66.w2, J91.67S2.w2, J91.67S2.w3, J100.184.w1, J115.13.w2, J133.951.w5, J133.951.w26, J133.951.w27, J135.99.w1, J215.24.w1, J216.167.w1, J219.14.w2, J258.326.w1, J259.2.w1, J484.38.w1, J489.28.w1, J490.5.w1, B240.14.w14, B241.49.w49, B243.31.w1, B244.w1, P9.2004.w12, P39.3.w3, P39.3.w10, P39.4.w4, P51.49.w2, P51.52.w1, P51.51.w1, P87.10.w2, P503.1.w8, P507.2005.w8, W27.06Feb02.wnv1, W27.17Sept02.wnv1, W30.Nov01.WNV3, W30.28Jan04.WNV2, W348.20Jan03.wnv1, W479.Jan04.wnv2, D148, D149, D150)

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Prophylactic Treatment The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.

Antiviral drugs:

  • No prophylactic treatment is available for this disease, although both human recombinant interferon alpha-2b and ribavirin, applied prior to infection of cells with the virus, have been shown to protect Vero cells in vitro.

(J84.8.w2, J128.13.w1)

Passive immunisation:

  • Injection of WN virus-immune serum 24 hours prior to infection has been shown to protect hamsters (Mesocricetus auratus - Golden Hamster) challenged with the virus.
  • Injection of either mouse WNV-immune serum or human WN virus-immune gamma globulin has been shown to provide protection in mice although in immuno-deficient mice this effect was time-limited depending on the initial dose of immune serum. (i.e. antibodies alone were not sufficient to eliminate infection)

(J80.77.w3, J84.8.w14)

Personal protective measures:

  • Personal protective measures, including the use of DEET insect repellent and general avoidance of mosquitoes are effective for reducing risk of WNV infection and are particularly important for the elderly and immunocompromised, who have the greatest risk of severe infection. 

(J257.168.w3, J258.326.w1, P48.4.w9)

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Environmental and Population Control Measures

General Environment Changes, Cleaning and Disinfection The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.
  • The most effective long-term control strategies are likely to involve the reduction of vector breeding by habitat management.
  • Larvicides control mosquitoes before they become dispersed and may keep mosquito populations at low levels, reducing the risk of transmission of arboviruses.
  • During an epidemic, use of adulticides may be required to reduce the population of vector mosquitoes.

(B240.14.w14, B241.49.w49, B243.31.w1, B244.w1, J115.13.w2, P32.1.w3, P32.1.w8, P48.4.w14, D67, D71, D73, W175.Nov01.wnv21)

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Population Control Measures

The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.

  • Due to the feeding behaviour of the mosquito vectors and the migratory habits of species likely to be acting as reservoir hosts, it is unlikely that population control measures directed against host species would be effective.
  • The most effective long-term control strategies are likely to involve the reduction of vector breeding by habitat management.
  • Biological control measures, larvicides and adulticides may also be used as part of an integrated mosquito management programme.
  • Adulticides may be important to control adult vector mosquitoes and thus provide protection in the face of an epidemic.

(B244.w1, J84.7.w35, J115.13.w2, P32.1.w8, P48.4.w14, D67, D71, D73, W477.Jan04.wnv2, W478.Jan04.wnv1)

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Isolation and Quarantine The following editorial comment summarises detailed information given within the LITERATURE REPORTS. Links to the LITERATURE REPORTS are provided at the bottom of this box.
  • Normal quarantine measures appropriate for species being moved to a new area should be observed.
  • Animals should be free of ectoparasites.
  • Normal precautions should be taken to prevent the unwitting translocation of mosquito larvae and eggs through the importation of artificial containers which could provide suitable transport and a breeding habitat.
  • Within the USA, discussions have been held at state and federal levels regarding measures to prevent future importation of WNV infection, for example in birds or amphibians "no testing, evaluation, screening, embargo or other program has yet been devised to control the spread of the virus geographically by animal movement."
  • One case has been reported of a horse diagnosed with WNV infection while in quarantine.

(W187.Nov01.WNV4, W27.04Oct02.wnv2)

BLOOD TRANSFUSIONS:

  • Following occurrence in the USA in 2002 of several cases of transfusion-related WNV infection a system was set up to screen blood donations in the USA for presence of the virus, using highly sensitive nucleic acid-amplification tests, with quarantine of blood products from a reactive sample, and further testing. Similar measures have been implemented in Canada. (N7.52.w1, W181.28Jan04.WNV4)
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Authors & Referees

Authors Debra Bourne MA VetMB PhD MRCVS (V.w5)
Referee Suzanne I. Boardman (V.w6); Becki Lawson (V.w26); Dr Robert G. McLean (V.w42)

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