Infections in Animals
West Nile fever results from infection by the West Nile virus, a mosquito-borne arbovirus in the genus Flavivirus, family Flaviviridae. Two genetic lineages exist; viruses in lineage 1 but not lineage 2 have been definitely linked to human disease. The strain found in the United States may have originated in the Middle East. It appears to be related to a lineage 1 virus found in Israel from 1997 to 2000.
West Nile fever has been seen in Africa, Eastern Europe, the Mediterranean region, the Rhone River delta of France, Russia, west and central Asia and the Middle East. Since 1999, the West Nile virus has also been found in the United States. The first infections were seen in New York; the virus has now spread along the East Coast and into the Midwest and South
The West Nile virus is transmitted by mosquitoes. At least 29 species of North American mosquitoes are susceptible to infection. Culex pipiens, Culex restuans, and Culex salinarius appear to be the most important maintenance vectors in the United States. Infections have also been documented in ticks in Asia and Russia, but their role in transmission is uncertain.
Birds are the primary reservoir hosts. In endemic regions, West Nile virus is maintained in an enzootic cycle between culicine mosquitoes and birds. When environmental conditions favor high viral amplification, significant numbers of "bridge vector" mosquitoes (mosquitoes that feed on both birds and mammals) become infected in the late summer and can spread the virus to humans, horses and other incidental hosts. Migratory birds may carry West Nile virus into new areas. Direct transmission between animals has not been seen in experimentally infected chickens or turkeys, but has been documented in geese. Infected humans and horses do not seem to spread the virus to other mammals.
Little or no information has been published on the susceptibility of West Nile virus to disinfectants; however, related flaviviruses (St. Louis encephalitis, yellow fever and dengue viruses) are destroyed by many disinfectants including 1% sodium hypochlorite, 2% glutaraldehyde and 70% ethanol.
The incubation period is currently estimated to be 3 to 14 days.
Most cases of West Nile fever are mild and flu-like, with fever, headache and body aches. Weakness, malaise, anorexia, lymphadenopathy, nausea and vomiting may also be seen. An erythematous macular, papular, or morbilliform skin rash occasionally develops on the neck, trunk, arms or legs. Most uncomplicated infections resolve in 3 to 6 days.
Yes. C. jejuni is found in the feces and can be shed for as long as 2 to 7 weeks in untreated infections; however, humans rarely become chronic carriers. C. fetus subsp. fetus is communicable for several days to several weeks.
In more severe cases, there may be signs of encephalitis, meningoencephalitis or meningitis; the symptoms may include a high fever, headache, neck stiffness, stupor, disorientation, tremors, convulsions, severe muscle weakness, flaccid paralysis and coma. Ataxia, cranial nerve abnormalities, myelitis, eye pain, polyradiculitis, and seizures have also been seen. In some outbreaks, myocarditis, pancreatitis, and fulminant hepatitis occur.
In humans, West Nile fever can be diagnosed by a rising titer or by finding IgM in serum or cerebrospinal fluid, using an IgM antibody-capture ELISA. A plaque reduction neutralization test, indirect immunofluorescence and hemagglutination inhibition tests are also available. Cross-reactions may be seen with other flaviviruses, including yellow fever, Japanese encephalitis, St. Louis encephalitis or dengue. False positive reactions may be clarified with the plaque reduction neutralization test but the results may still be ambiguous.
The West Nile virus, viral antigens or nucleic acids may also be detected in cerebrospinal fluid, tissue, blood and other body fluids. Virus isolation from cerebrospinal fluid and brain tissue is often negative. Polymerase chain reaction assays may also be available.
Treatment and Vaccination
No specific treatment, other than supportive care, is available. Intensive care and mechanical ventilation may be required in some cases. Ribavirin and interferon are effective in vitro. Human vaccines are not yet available but are in development.
Morbidity and Mortality
Most human infections appear to be asymptomatic. In 1999, a survey found that 20% of seropositive individuals in New York reported symptoms consistent with West Nile fever; approximately half had visited a physician at the time of the illness. Neurologic disease is more likely to develop in those over 50 years old and to be more serious in this group. An estimated one in 140 to one in 320 infections are thought to result in meningitis or encephalitis.
The case fatality rate in outbreaks ranges from 4 to 14%. The mortality rate is higher among older patients. Case fatality rates of 15 to 29% have been seen in those over 70 years old. There is some evidence that concurrent disease such as diabetes or immunosuppression increases the risk of death. There is also evidence that seriously ill patients may suffer substantial long-term morbidity after recovery. In New York, 67% of hospitalized patients had continued fatigue one year after discharge; memory loss was seen in 50%, difficulty walking in 49%, muscle weakness in 44% and depression in 38%.
Wild birds are the main reservoir hosts. Many birds carry the virus without clinical signs, but symptomatic infections can be seen in crows, ravens, jays, pigeons, domestic geese and some other avian species. Among mammals, neurologic disease has been seen mainly in horses and humans. Infections have also been documented in gray squirrels, chipmunks, skunks, domestic rabbits, cats, dogs, a wolf, sheep, goats, bats, an alpaca, a fox squirrel and a mountain goat. Mice, hamsters and rhesus monkeys can be infected experimentally.
The incubation period in horses appears to be 5 to 15 days. The incubation period for other species is unknown.
Infections in Birds
Infections in many birds appear to be asymptomatic, but high mortality can be seen in crows, ravens and jays. Affected wild birds are usually found dead and the clinical signs in these species have not been well described. In some cases, myocarditis and encephalitis are found post-mortem. Naturally or experimentally infected chickens and turkeys are asymptomatic. Domestic geese can show clinical signs; in natural and experimental infections, the symptoms may include weight loss, decreased activity, depression, myocarditis and neurologic signs including torticollis, opisthonos and rhythmic side-to-side head movements. Infections in geese can be fatal.
Infections in Mammals
In horses, West Nile virus causes neurologic disease. The clinical signs may include anorexia, depression, ataxia, muscle twitches, partial paralysis, impaired vision, head pressing, teeth grinding, aimless wandering, convulsions, circling and an inability to swallow. Attitudinal changes including depression, somnolence, listlessness, apprehension or periods of hyperexcitability may be seen. Weakness, usually in the hind limbs, is sometimes followed by paralysis. Coma and death may occur. Fever has been seen in some but not all cases. Fatal hepatitis developed in one donkey with neurologic signs in France.
There is limited evidence of pathogenicity in other species. Recently, deaths were reported in an infected 3-month old wolf and an 8-year old dog in the United States. The dog was suffering from an immune-mediated disease. There are few reports of experimental infections; however, in one study, two of three experimentally infected dogs developed a mild recurrent myopathy. West Nile virus has also been recovered from the brain of a cat with neurologic signs, two other fatally ill cats and dead squirrels. Fatal encephalitis is seen in experimentally infected mice, hamsters and rhesus monkeys.
Horses, chickens and turkeys do not seem to infect other animals by direct contact. Experimentally infected geese may be able to spread the virus without a mosquito vector.
West Nile fever can be diagnosed by virus isolation. Virus can be recovered from the brain, spinal cord, blood and other tissues of infected horses, and the brain, heart, kidney and intestines of geese. Vero cells are often used for isolation. A reverse transcription- polymerase chain reaction (RT-PCR) test and immunohistochemical staining can detect viral RNA and antigens, respectively.
Serology may also be helpful. Assays include a plaque-reduction neutralization test (PRNT) and an IgM-capture enzyme-linked immunosorbent assay (ELISA). A fourfold increase in titer should be seen in the PRNT test. There is some evidence that IgM may be low or undetectable in some recently infected horses. The efficacy of serologic tests has not been determined in cats; this species does not develop antibodies in response to some flaviviruses.
Treatment and Vaccination
No specific treatment is available but animals may recover on their own if they are given supportive care. Mild cases have, in some cases, recovered without treatment. A vaccine has been conditionally approved for horses and is available from Fort Dodge Laboratories.
Morbidity and Mortality
Birds are the main reservoir host and can infected asymptomatically. In endemic areas, the prevalence of infection in wild birds ranges from 10 to 53%. Mammals can also be infected without disease. Antibodies have been found in normal dogs, horses, donkeys and mules in endemic regions, including the United States. In some cases, the prevalence of infection may be high. In 1959, 54% of the horses, donkeys and mules in Egypt were seropositive. More recently, West Nile antibodies were found in 37% of dogs in the highveld region of South Africa.
Estimates of the morbidity rates in horses vary. During outbreaks, 20 to 43% of infected horses appear to develop acute neurologic signs. Experimental studies have been equivocal. In one recent study, only one of 12 horses experimentally infected by mosquito vectors developed encephalitis. The other 11 horses seroconverted but remained asymptomatic. Higher rates of encephalitis and fever have been seen when foals and horses were infected subcutaneously and intravenously; 4 of 9 animals in two studies became ill.
The case fatality rate in horses has varied from 25 to 45% in different outbreaks. In the current epidemic in the United States, the case fatality rate is approximately 35 to 45%. Deaths have also been seen in squirrels in endemic areas, although West Nile virus has not been proven to be the cause.
Severe myocarditis and encephalitis have been found post-mortem in some but not all wild birds. Geese may be dehydrated and in poor condition, with subcutaneous hemorrhages around the joints, pale lungs, a pale beak, and petechial hemorrhages in the splenic capsule. An enlarged gall bladder, severe thymic and cloacal bursa atrophy and excess cerebrospinal fluid have also been seen in this species.
In horses, a moderate to severe meningoencephalitis, associated with hemorrhages, may be seen in the central nervous system. The lesions are most often found in the brainstem and ventral horns of the lumbo-sacral spinal cord. Few abnormalities are seen in the brain and cerebellum.
|Centers for Disease Control and Prevention (CDC)|
|Articles on West Nile Virus
Emerging Infectious Diseases Vol. 7, No. 4 (Jul–Aug 2001)
|West Nile Virus
USDA Animal and Plant Health Inspection Service (APHIS)
|West Nile Virus Guidelines for Horse Owners
Nebraska Cooperative Extension
|West Nile Virus: A Primer for the Clinician
Annals of Internal Medicine
|What you should know about West Nile virus.
American Veterinary Medical Association
|USDA APHIS West Nile Index|
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