An outbreak of Venezuelan equine encephalitis (VEE) that began in northwestern Venezuela in April 1995 has spread westward to the Guajira peninsula and to Colombia (Figure_1), resulting in an estimated minimum of 13,000 cases in humans and an undetermined number of equine deaths. Governments of both countries have initiated efforts to control the spread of this outbreak by quarantining and vaccinating equines and applying insecticides. This report summarizes the ongoing investigation of the outbreak in Colombia.

During the first week of September, rural health clinics in the towns of Mayapo, Manaure, and El Pajaro in the municipality of Manaure in La Guajira state reported an increased number of patients seeking care for acute febrile illnesses characterized by intense headache, muscle pain, prostration, and vomiting. Illness in some patients was complicated by convulsions and other neurologic symptoms.

As of September 28, a total of 8320 persons with acute febrile illness compatible with VEE had been treated at public hospitals and clinics in La Guajira, and large outbreaks had been reported from the towns of Manaure, Riohacha, El Pajaro, Mayapo, Uribia, and Meicao. Based on a random survey of 250 residents of Manaure, a recent history of acute illness compatible with VEE was present in 57% of respondents (Figure_2); 4% reported associated convulsions, and one person died (case-fatality rate=0.7%). All age groups were equally affected. In Manaure, the epidemic peaked on September 19, and malathion spraying was initiated on September 21.

In Riohacha, the state capitol, hospital visits for acute febrile illness increased steadily in September, reaching 143 visits on September 24 with no evidence of a decline. A similar pattern occurred in Uribia. Based on interviews and physical examinations of 23 inpatients at local hospitals on September 27-28, prominent manifestations included fever (100%); convulsions (98%); headache (56%); photophobia (56%); myalgias (56%); and chills, vomiting, and diarrhea (48% each). Ten associated deaths were reported statewide. Unidentified viral isolates have been recovered from four of 18 human blood samples submitted to the Colombian National Institute of Health.

Because of a prolonged rainy season (the heaviest in 20 years in La Guajira), mosquito abundance has increased dramatically. Aedes aegypti house indices increased in August to 70% in Manaure and to 22% in Riohacha. Entomologic surveys in Manaure detected large numbers of Psorophora confinnis and Ae. taeniorhynchus breeding in estuarine waters in the town's vicinity. The equine population in La Guajira consists of approximately 70,000 unvaccinated horses, donkeys, and mules owned by native Wayuu people, who constitute approximately 35% of the inhabitants of Riohacha. Control measures instituted by the government of Colombia include vaccination of equines in La Guajira, restriction of equine movement from and within the state, large-scale application of insecticides, public education and community mobilization campaigns to eradicate mosquito breeding sites, issuance of guidelines on case-management and referral, and surveillance of humans and equines.

Reported by: E Daza, V Frias, A Alcola, I Lopez, I Bruzon, La Guajira Health Dept; JT Montero, G Alvarez, MA Garcia, R Rodriguez, Colombia Ministry of Health; J Boschell, F de la Hoz, F Rivas, V Olano, LA Diaz, FM Caceras, G Aristizabal, V Cardenas, Colombian National Institute of Health, Colombia. J Cuellar, Pan American Health Organization, Colombia. E Gonzalez, Pan American Health Organization, Venezuela. A Ruiz, F Pinheiro, R Gusmao, Pan American Health Organization, Washington, DC. S Weaver, R Tesh, Univ of Texas Medical Br, Galveston, Texas. R Ricco-Hesse, Yale Arbovirus Research Unit, Yale Univ, New Haven, Connecticut. Div of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Major epizootics and concurrent epidemics of VEE have occurred periodically in northern areas of South America, resulting in hundreds of thousands of human and equine cases. The current epidemic is the largest in the region since 1962-1971, when outbreaks affected Colombia, Ecuador, Peru, Venezuela, all the countries of Central America (except Panama), Mexico, and Texas (1,2). No major outbreaks had been recognized since the outbreak that occurred on La Guajira peninsula in 1973, suggesting that epizootic viral strains (subtypes IAB and IC) had become extinct. However, based on recent molecular phylogenetic studies, these strains may have evolved from enzootic ID strains maintained in silent cycles of rodent-mosquito transmission. This hypothesis predicts that strains with epidemic and epizootic potential will continue to emerge periodically from enzootic reservoirs (1,3,4). Partial nucleotide sequencing and antigenic analysis of three human isolates from the current epidemic indicates they are related to the IC epizootic strain of VEE virus isolated during a large outbreak in Venezuela and Colombia during 1962-1964 (S. Weaver, University of Texas, and R. Ricco-Hesse, Yale University, personal communications, 1995) and to a strain isolated from a mosquito pool in Venezuela in 1983 (1).

Although conditions leading to the emergence of VEE epidemics have not been clearly defined, previous outbreaks also were associated with heavy rains and flooding in arid rural areas, especially during the dry season. During epidemics and epizootics, VEE virus is transmitted rapidly among equines and from equines to humans by a variety of mosquito species. Horses are the principal amplifying hosts in epidemic transmission because they develop and sustain high levels of viremia and attract large numbers of biting mosquitoes. Cases among humans generally occur 2 weeks after epizootic infections in horses, and epidemic transmission ceases after susceptible horses have been either infected or vaccinated. Because the total number of horses and other equines in South America has declined since the last major outbreaks in 1971, the current outbreak suggests a possible role of human and other animal infections in sustaining the epidemic cycle. VEE virus levels in human blood are sufficiently high to infect mosquitoes, and virus has been isolated from the pharynx of ill persons, indicating the virus could be transmitted between humans by mosquitoes or by close direct contact (5).

The clinical features of cases in the current outbreaks are consistent with those reported in previous VEE epidemics in which neurologic symptoms developed in 4% of cases, primarily among children and the elderly (6). VEE infections during pregnancy may result in fetal infection and malformations. VEE outbreaks have the potential for substantial social impact: for example, during the 1967 outbreak in Colombia, an estimated 220,000 human cases immobilized villages and local clinics (7).

The Pan American Health Organization coordinates a surveillance system for equine encephalitis in the Americas and is assisting countries of Latin America and the Caribbean in strengthening their diagnostic capacity. Equine vaccination with the live attenuated TC-83 vaccine provides rapid immunity and, when combined with restriction of equine movements, may limit the spread of epizootics and prevent their emergence (1).

No commercially licensed human VEE vaccine is available. Persons who cannot defer travel to these areas should use insect repellents, stay in air-conditioned or well-screened accommodations when possible, and wear long-sleeved shirts and long pants. The incubation period for VEE is 2-5 days. Health-care providers who suspect VEE in ill returned travelers can refer clinical specimens through state health departments to CDC for diagnosis.

References

1. Weaver SC, Belew LA, Rico-Hesse R. Phylogenetic analysis of alphaviruses in the Venezuelan equine encephalitis complex and identification of the source of epizootic viruses. Virology 1992; 191:282-90.

2. Walton TE, Grayson MA. Venezuelan equine encephalomyelitis. In: Monath TP, ed. The arboviruses: epidemiology and ecology. Boca Raton, Florida: CRC Press, 1989;203-32.

3. Ricco-Hesse R, Weaver SC, deSiger J, Medina G, Salas RA. Emergence of a new epidemic/epizootic Venezuelan equine encephalitis virus in South America. Proc Natl Acad Sci U S A 1995;92:5278-81.

4. Kinney RM, Tsuchiya KR, Sneider JM, Trent DW. Genetic evidence that epizootic Venezuelan equine encephalitis (VEE) viruses may have evolved from enzootic VEE subtype I-D virus. Virology 1992;191:579-80.

5. Bowen GS, Calisher CH. Virological and serological studies of Venezuelan equine encephalomyelitis in humans. J Clin Microbiol 1976;4:22-7.

6. Briceno-Rossi AL. Rural epidemic encephalitis in Venezuela caused by a group A arbovirus (VEE). Prog Med Virol 1967;9:176-203.

7. Sanmartin C, Mackenzie RB, Trapido H, et al. Equine encephalitis in Colombia, 1967. Bol Oficina Sanit Panam 1973;74:108-37.

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