Arboviral Encephalitides, Part 3

by CDC

(Page 3 of 3)

Venezuelan Equine Encephalitis

Like EEE and WEE viruses, Venezuelan equine encephalitis (VEE) is an alphavirus and causes encephalitis in horses and humans and is an important veterinary and public health problem in Central and South America. Occasionally, large regional epizootics and epidemics can occur resulting in thousands of equine and human infections. Epizootic strains of VEE virus can infect and be transmitted by a large number of mosquito species. The natural reservoir host for the epizootic strains is not known. A large epizootic that began in South America in 1969 reached Texas in 1971. It was estimated that over 200,000 horses died in that outbreak, which was controlled by a massive equine vaccination program using an experimental live attenuated VEE vaccine. There were several thousand human infections. A more recent VEE epidemic occurred in the fall of 1995 in Venezuela and Colombia with an estimated 90,000 human infections. Infection of man with VEE virus is less severe than with EEE and WEE viruses, and fatalities are rare. Adults usually develop only an influenza-like illness, and overt encephalitis is usually confined to children. Effective VEE virus vaccines are available for equines.

Enzootic strains of VEE virus have a wide geographic distribution in the Americas. These viruses are maintained in cycles involving forest dwelling rodents and mosquito vectors, mainly Culex (Melanoconion) species. Occasional cases or small outbreaks of human disease are associated with there viruses, the most recent outbreaks were in Venezuela in 1992, Peru in 1994 and Mexico in 1995-96.

Other Arboviral Encephalitides

Many other arboviral encephalitides occur throughout the world. Most of these diseases are problems only for those individuals traveling to countries where the viruses are endemic.

Japanese Encephalitis

Japanese encephalitis (JE) virus is a flavivirus, related to SLE, and is widespread throughout Asia. Worldwide, it is the most important cause of arboviral encephalitis with over 45,000 cases reported annually. In recent years, JE virus has expanded its geographic distribution with outbreaks in the Pacific. Epidemics occur in late summer in temperate regions, but the infection is enzootic and occurs throughout the year in many tropical areas of Asia. The virus is maintained in a cycle involving culicine mosquitoes and waterbirds. The virus is transmitted to man by Culex mosquitoes, primarily Cx. tritaeniorhynchus, which breed in rice fields. Pigs are the main amplifying hosts of JE virus in peridomestic environments.

The incubation period of JE is 5 to 14 days. Onset of symptoms is usually sudden, with fever, headache and vomiting. The illness resolves in 5 to 7 days if there is no CNS involvement. The mortality in most outbreaks is less than 10%, but is higher in children and can exceed 30%. Neurologic sequelae in patients who recover are reported in up to 30% of cases. A formalin-inactivated vaccine prepared in mice is used widely in Japan, China, India, Korea, Taiwan and Thailand. This vaccine is currently available for human use in the United States, for individuals who might be traveling to endemic countries.

Tick-Borne Encephalitis

Tick-borne encephalitis (TBE) is caused by two closely related flaviviruses which are distinct biologically. The eastern subtype causes Russian spring-summer encephalitis (RSSE) and is transmitted by Ixodes persulcatus, whereas the western subtype is transmitted by Ixodes ricinus and causes Central European encephalitis (CEE). The name CEE is somewhat misleading, since the condition can occur throughout much of Europe. Of the two subtypes, RSSE is the more severe infection, having a mortality of up to 25% in some outbreaks, whereas mortality in CEE seldom exceeds 5%.

The incubation period is 7 to 14 days. Infection usually presents as a mild, influenza-type illness or as benign, aseptic meningitis, but may result in fatal meningoencephalitis. Fever is often biphasic, and there may be severe headache and neck rigidity, with transient paralysis of the limbs, shoulders or less commonly the respiratory musculature. A few patients are left with residual paralysis. Although the great majority of TBE infections follow exposure to ticks, infection has occurred through the ingestion of infected cows' or goats' milk. An inactivated TBE vaccine is currently available in Europe and Russia.

West Nile Encephalitis

WNV is a flavivirus belonging taxonomically to the Japanese encephalitis serocomplex that includes the closely related St. Louis encephalitis (SLE) virus, Kunjin and Murray Valley encephalitis viruses, as well as others. WNV was first isolated in the West Nile Province of Uganda in 1937 The first recorded epidemics occurred in Israel during 1951-1954 and in 1957. Epidemics have been reported in Europe in the Rhone delta of France in 1962 and in Romania in 1996. The largest recorded epidemic occurred in South Africa in 1974.

An outbreak of arboviral encephalitis in New York City and neighboring counties in New York state in late August and September 1999, was initially attributed to St. Louis encephalitis virus based on positive serologic findings in cerebrospinal fluid (CSF) and serum samples using a virus-specific IgM-capture enzyme-linked immunosorbent assay (ELISA). The outbreak has been subsequently confirmed as caused by West Nile virus based on the identification of virus in human, avian, and mosquito samples. See also Outbreak of West Nile-Like Viral Encephalitis -- New York, 1999. MMWR, 1999:48(38);845-9 and Update: West Nile-Like Viral Encephalitis -- New York, 1999. MMWR, 1999:48(39);890-2. A recent outbreak WN encephalitis occurred in Bucharest, Romania in 1996.

The virus that caused the New York area outbreak has been definitively identified as a strain of WNV. The genomic sequences identified to date from human brain, virus isolates from zoo birds, dead crows, and mosquito pools are identical. SLE and West Nile viruses are antigenically related, and cross reactions are observed in most serologic tests. The isolation of viruses and genomic sequences from birds, mosquitoes, and human brain tissue permitted the discovery of West Nile virus in North America and prompted more specific testing. The limitations of serologic assays emphasize the importance of isolating the virus from entomologic, clinical, or veterinary material.

Although it is not known when and how West Nile virus was introduced into North America, international travel of infected persons to New York or transport by imported infected birds may have played a role. WNV can infect a wide range of vertebrates; in humans it usually produces either asymptomatic infection or mild febrile disease, but can cause severe and fatal infection in a small percentage of patients. Within its normal geographic distribution of Africa, the Middle East, western Asia, and Europe, WNV has not been documented to cause epizootics in birds; crows and other birds with antibodies to WNV are common, suggesting that asymptomatic or mild infection usually occurs among birds in those regions. Similarly, substantial bird virulence of SLE virus has not been reported. Therefore, an epizootic producing high mortality in crows and other bird species is unusual for either WNV or SLE virus. For both viruses, migratory birds may play an important role in the natural transmission cycles and spread. Like SLE virus, WNV is transmitted principally by Culex species mosquitoes, but also can be transmitted by Aedes, Anopheles, and other species. The predominance of urban Culex pipiens mosquitoes trapped during this outbreak suggests an important role for this species. Enhanced surveillance for early detection of virus activity in birds and mosquitoes will be crucial to guide control measures.

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