Venezuelan equine encephalitis is caused by the Venezuelan equine encephalitis virus, an Alphavirus belonging to the Togaviridae family. It is characterized by the acute onset of a febrile illness, myalgia, nausea, vomiting and encephalitis. Although there are no recent reports of the disease, it could be a potential biological weapon as it can cause serious nervous system sequelae.
Venezuelan equine encephalitis (VEE) has been associated with epidemics in South and Central America, especially regions of Colombia, although it has not shown a resurgence recently .
The symptoms and signs of the disease resemble those of several other acute, febrile, infectious illnesses like dengue fever. So the diagnosis is often missed in the initial stages of the illness, especially if there are poor awareness and unavailability of special laboratory testing facilities .
Humans acquire the infection following a mosquito bite. The incubation period is between 24 hours to six days after exposure to the virus  . The common symptoms are flu-like with myalgia, fatigue, nausea, vomiting, diarrhea, headache and fever. The symptoms abate after a few days but can recur and in some cases the patients may remain symptomatic for up to 2 weeks.
Between 4 to 14% of cases can develop neurological symptoms 5 to 10 days after exposure. Young adults and children are especially prone to encephalitis due to the Venezuelan equine encephalitis virus. The symptoms include increased sleepiness, confusion, severe headaches, photophobia, neck rigidity, seizures, neurological deficits, coma, and death . Death can be due to encephalitis or gastrointestinal, pulmonary or brain hemorrhage.
Venezuelan equine encephalitis is clinically diagnosed in less than 5% of infected individuals. After obtaining a detailed history and physical examination of the febrile patient, routine laboratory investigations like complete blood count, serum electrolytes, liver function tests, and urinalysis are performed. Usually, the results of these tests are not indicative of any specific infection. However, in patients with encephalitis, the transaminases may be elevated. Thrombocytopenia and lymphopenia may also be present.
The VEE virus can be isolated from either blood or a throat swab obtained 1 to 3 days after symptom onset. In patients with encephalitis, lumbar puncture is performed and cerebrospinal fluid analysis shows normal glucose concentration with marked mononuclear pleocytosis. Enzyme-linked immunosorbent assay (ELISA) is useful to diagnose the causative virus . Polymerase chain reaction (PCR) is another useful technique to detect the virus .
Radiological tests are helpful to diagnose VEE and its complications. Chest radiography typically reveals acute pneumonitis while magnetic resonance imaging (MRI) can establish encephalitis.
Histopathology of affected organs shows congestion, hemorrhage with perivascular and leptomeningeal inflammatory cellular infiltrates and focal necrosis. Basal ganglia, substantia nigra as well as the cerebral cortex and deep white matter involvement has been noted. The findings indicate that the virus targets the human reticuloendothelial and lymphoid system .