BASICS
- WNV is a seasonal and potentially fatal neurotropic disease that has expanded worldwide since 1999 when the lineage 2 neurotropic virus emerged in the USA. Since 2006, WNV lineage 1 has been expanding into Eurasia as a neurotropic infection causing outbreaks in horses.
- At least 11 times more horses develop asymptomatic infection and all horses are dead-end hosts.
- WNV is carried and transmitted by a wide variety of mosquitos, and in North America is principally spread by the very common Culex spp.
- Wild birds are the principal reservoir for WNV.
- WNV enters the body through the bite of an infected mosquito and then multiplies in the hemolymphatics, with multiplication observed in endothelial cells and infection in peripheral blood mononuclear cells. If it crosses the blood–brain barrier, it causes a multifocal poliencephalitis and sometimes death
- Any age, breed, or sex.
- Primarily horses, humans, and birds.
- Older horses have increased risk of severe neurotropic infection.
- Incubation period 9–15 days.
- Signs range from asymptomatic through acutely neurologic.
- Presenting clinical signs are often insidious. Fever is common but is often missed. 1–2 days before presentation, colic, lameness, inappetence, and depression can occur.
- Neurologic signs not pathognomonic.
- Fasciculation is common early disease.
- Ataxia and dysmetria can be present. Spinal deficits primarily lower motor neuron, with symmetric to asymmetric weakness.
- About 30–40% of horses will progress to recumbence.
- Brain signs include a variety of behavioral changes—hyperexcitation, severe obtundation.
- Cranial nerve abnormalities with decreased tongue retraction, vestibular and balance abnormalities, and lack of menace. These can be symmetrical or asymmetrical
- WNV is a member of the genus Flavivirus, family Flaviviridae.
- Risk factor—exposure to infected mosquitos.
- Lack of vaccination
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS