West Nile virus (WNV) is an enveloped single‑stranded RNA virus of the Flaviviridae family. It is transmitted by a variety of mosquitoes and has so far been discovered in more than 40 different mosquito species and in several tick species. Birds represent the vertebrate reservoir. Acting as incidental hosts, mammals can also become infected when bitten by an infected mosquito.
Other than humans, usually only horses become ill after natural infection. After an incubation period of three to fifteen days, most horses show a short period of viraemia with low virus titers. Generally, humans and horses are considered as dead‑end hosts owing to the low‑level viraemia. Only around 10 % of infected horses show clinical symptoms. The first symptoms are mostly unspecific and include fever, depression, loss of appetite and colic. When the infection proceeds, neurological disorders often follow, leading to lameness and ataxia or even paresis, which are considered as predominant clinical symptoms. In rare cases, problems of the facial nerves, photosensitivity and blindness, subsultus as well as general sensitivity and personality changes are observed.
In horses with a mild course of the disease, recovery usually takes two to seven days. In severe infections, recovery may take 20 days or several weeks. 20 % of horses with past severe infection show long‑term sequelae such as weight loss, lethargy, ataxia and cerebral nerve problems. In non‑vaccinated horses, the infection is fatal in 24 % to 45 % of clinical cases. Intensive medical care is the only possibility to positively influence the illness. A vaccine with formalin‑inactivated WNV is available for horses.
Diagnosis of WNV infection can be established by means of direct virus detection or detection of specific antibodies. Owing to the short viraemic phase, direct detection of the virus in living animals is often unsuccessful. The virus can be detected post mortem in the brain or spinal cord of horses, e.g. using reverse transcriptase polymerase chain reaction (RT-PCR). For these reasons, the serological detection of specific anti-WNV antibodies by means of ELISA or IIFT is of major importance. Specific IgM antibodies can be detected in equine serum after seven to ten days and generally persist for one to two months, sometimes even for much longer. Persisting IgM antibodies can therefore complicate the diagnosis of acute WNV infections. Additionally, the determination of IgM antibodies is often problematic since alongside the persistence, further disturbing factors such as weak, no, or delayed IgM formation or unspecific IgM formation due to B cell stimulation may occur. Investigating low-avidity antibodies of class IgG is offering an additional parameter that significantly enhances serological analyses of fresh WNV infections. Anti-WNV IgG antibodies can be detected for at least 15 months after infection.
Differential diagnosis includes further arbovirus-caused encephalitides (e.g. equine encephalomyelitis, Japanese encephalitis and tick-borne encephalitis), equine herpesvirus 1, Borna disease and rabies. As the degree of antigenic similarity within the Flavivirus genus is high, antibody cross reactions can occur. Therefore, positive results should be confirmed using a different test system, e.g. neutralisation test, which is considered as gold standard in human diagnostics.
|Method||Substrate||Diagnostic application||Order number|
|ELISA||Recombinant glycoprotein E of WNV||IgG ELISA; high sensitivity and|
specificity; reduced cross reactivity with antibodies against TBE virus
|EI 2662-9601 GE|
|ELISA Avidity||Recombinant glycoprotein E of WNV||ELISA-based avidity determination of WNV-specific IgG antibodies; alternative principle for the detection of fresh infections (no influence from persisting IgM antibodies)||EI 2662-9601-1 GE|