Chapter 260 Arboviral Encephalitis outside North America
The principal causes of arboviral encephalitis outside North America are Venezuelan equine encephalitis (VEE) virus, Japanese encephalitis (JE) virus, tick-borne encephalitis (TBE), and West Nile (WN) virus (Table 260-1).
260.1 Venezuelan Equine Encephalitis
The VEE virus was isolated from an epizootic in Venezuelan horses in 1938. Human cases were first identified in 1943. Hundreds of thousands of equine and human cases have occurred over the past 70 yr. During 1971, epizootics moved through Central America and Mexico to southern Texas. After 2 decades of quiescence, epizootic disease emerged again in Venezuela and Colombia in 1995.
Etiology
VEE is an alphavirus of the family Togaviridae. VEE circulates in nature in 6 subtypes. Virus types I and III have multiple antigenic variants. Types IAB and IC have caused epizootics and human epidemics.
Epidemiology
The majority of epizootics resulting from types IAB and IC have occurred in Venezuela and Colombia. The virus resides in ill-defined sylvatic reservoirs in the South American rain forests. Known hosts include rodents and aquatic birds with transmission by Culex melaconion species. Vectors for horse-to-horse and horse-to-human transmission include Aedes taeniorhynchus and Psorophora confinnis. Epizootics move rapidly, up to several miles per day. Human cases are proportional to and follow epizootic occurrences. Viremia levels in human blood are high enough to infect mosquitoes. Because virus can be recovered from human pharyngeal swabs, and household attack rates are often as high as 50%, it is widely believed that person-to-person transmission occurs, although direct evidence is lacking. Virus types II-VI are restricted to relatively small foci; each has a unique vector-host relationship and rarely results in human infections.
Clinical Manifestations
The incubation period is 2-5 days, followed by the abrupt onset of fever, chills, headache, sore throat, myalgia, malaise, prostration, photophobia, nausea, vomiting, and diarrhea. In 5-10% of cases, there is a biphasic illness; the 2nd phase is heralded by seizures, projectile vomiting, ataxia, confusion, agitation, and mild disturbances in consciousness. There is cervical lymphadenopathy and conjunctival suffusion. Cases of meningoencephalitis may demonstrate cranial nerve palsy, motor weakness, paralysis, seizures, and coma. Microscopic examination of tissues reveals inflammatory infiltrates in lymph nodes, spleen, lung, liver, and brain. Lymph nodes show cellular depletion, necrosis of germinal centers, and lymphophagocytosis. The liver shows patchy hepatocellular degeneration, the lungs demonstrate a diffuse interstitial pneumonia with intra-alveolar hemorrhages, and the brain shows patchy cellular infiltrates.
Diagnosis
The etiologic diagnosis of VEE is established by testing an acute-phase serum collected early in the illness for the presence of virus-specific immunoglobulin (Ig) M antibodies or, alternatively, demonstrating a fourfold or greater increase in IgG antibody titers by testing paired acute and convalescent sera. The virus can also be identified by polymerase chain reaction (PCR).
Treatment
There is no specific treatment for VEE. The treatment is intensive supportive care (Chapter 62), including control of seizures (Chapter 586).
Prognosis
In patients with VE meningoencephalitis, the fatality rate ranges from 10% to 25%. Sequelae include nervousness, forgetfulness, recurrent headache, and easy fatigability.
Prevention
Several veterinary vaccines are available to protect equines. VEE virus is highly infectious in laboratory settings, and biosafety level 3 containment should be used. An experimental vaccine is available for use in laboratory workers.
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