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Arboviral Disease -- United States, 1991

During 1991, state and local health departments reported 122 cases of human arboviral encephalitis to CDC. More than half (69) of the cases resulted from outbreaks of St. Louis encephalitis (SLE) in Arkansas and Texas. In addition, an epizootic of eastern equine encephalitis (EEE) extending from the Atlantic and Gulf coasts into the upper midwest caused sporadic human cases and a substantial loss of livestock. This report summarizes the reported cases of arboviral encephalitis in the United States during 1991 and underscores the continuing need for arbovirus surveillance and control.

St. Louis encephalitis. SLE activity in the United States during 1990-1991 was at the highest level since 1976 (Figure 1). From July through September 1991, 25 laboratory-confirmed SLE cases occurred in Pine Bluff, Arkansas, and 41 SLE cases occurred in Harris County (Houston), Texas, resulting in annual incidence rates of 44 and 1.5 cases per 100,000 population, respectively. Additional sporadic SLE cases were confirmed from Arkansas (three), California (three), Florida (one), Louisiana (one), North Carolina (one), Texas (two) and Washington (one). Travel histories suggest that two of the three California patients and the Washington patient contracted SLE during visits to Arizona and New Mexico.

LaCrosse encephalitis. In 1991, 38 laboratory-confirmed cases of LaCrosse encephalitis (LAC) were reported from Illinois (13), Minnesota (four), North Carolina (one), Pennsylvania (one), and Wisconsin (19). Although LAC is generally the predominant cause of arboviral encephalitis in the United States, it is often undiagnosed and underreported.

Eastern equine encephalitis. In 1991, an EEE epizootic occurred among horses in states along the southeastern seaboard, with intense transmission occurring in Florida, Georgia, and South Carolina. The epizootic also extended into the midwestern states, causing deaths among horses in Ohio and Michigan. A cluster of five laboratory-confirmed human EEE cases occurred in northeastern Florida in June and July 1991, resulting in two deaths (1). Six additional human cases occurred in Georgia (two), Michigan (two), Louisiana (one), and South Carolina (one). For the first time, EEE virus was isolated from Aedes albopictus mosquitoes collected at a tire depot in central Florida (2,3).

Western equine encephalitis. In 1991, one laboratory-confirmed human case of western equine encephalitis (WEE) occurred in Colorado. Since 1980, zero to 40 human cases of WEE have been reported annually, primarily from the western United States.

Reported by: Participating state epidemiologists, veterinarians, and vector-control directors. Div of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: The isolation of EEE from a potential new mosquito vector (Ae. albopictus) and the increasing trend in human SLE cases that began in 1990 indicate the continuing need for arboviral surveillance and control in 1992 (2-4).

The last nationwide SLE epidemic in 1975 resulted in 1815 human cases in 31 states. This epidemic was preceded by an increase in cases in 1974, particularly in the southeastern United States. SLE virus is transmitted by the mosquito Culex quinquefasciatus in the south-central and southeastern United States, except in Florida, where it is transmitted by Cx. nigripalpus. Virus activity generally peaks in August and September. The 1991 SLE outbreak in Pine Bluff was the first reported from that community but was similar to outbreaks occurring in the Midwest in 1975 (5). During 1991, seroepidemiologic studies indicated that 10% of residents in Pine Bluff had antiflaviviral IgG (CDC, unpublished data, 1991), indicating unrecognized SLE transmission in this area.

Control measures that may reduce the risk for SLE infection include targeting vector-control efforts at open storm drains near housing developments, eliminating water-holding containers on premises, and reducing exposure to the vector mosquito at dusk and during the evening hours by staying indoors and using insect repellents. For those who must be outdoors in the evening, long-sleeved shirts and long pants reduce exposure to mosquito bites. Light-colored clothing is less attractive than dark clothes to most mosquitoes. Residents of areas where SLE is epizootic should repair window and door screens and avoid sitting on unscreened porches at dusk. In particular, prevention efforts should be aimed at elderly persons (greater than 60 years old), who have the highest age-specific SLE attack rates during outbreaks (6). Although precise prediction of SLE epidemics is not possible, the increased level of SLE activity in the southern and southeastern United States during 1990-1991 suggests that continued SLE activity is likely in 1992.

LAC encephalitis, caused by an arbovirus of the California serogroup transmitted by Ae. triseriatus, is most common among young children. LAC virus is prevalent primarily in midwestern states; however, serosurveys and active surveillance programs have demonstrated this virus has a wide geographic distribution in the United States. LAC may be underreported in many areas and should be considered in the differential diagnosis of pediatric viral encephalitis in states where hardwood forests and woodlots are common.

Although fewer than 10 human cases of EEE are reported annually in the United States, this virus is associated with a high case-fatality rate. An effective equine vaccine is licensed in the United States and is recommended for livestock in areas where EEE transmission is known to occur. However, revaccination during a single transmission season may be necessary. Specific control measures to prevent human EEE cases are difficult to implement because the disease is rare, even during a major equine epizootic.

The recent detection of Ae. albopictus in the United States has prompted concern because of its potential for transmission of EEE virus. This mosquito was imported from Asia to Texas, where it was discovered in 1985, and has since become widespread in the central and southern United States (7). Ae. albopictus is an aggressive biter that thrives in both forest and suburban habitats. This species, therefore, potentially could serve as an important bridging vector for EEE virus from swamp habitats into populated areas, although there is no evidence to indicate this has occurred.

Clinicians should be encouraged to obtain acute and convalescent arboviral antibody titers on all suspected cases of arboviral encephalitis. Patients with arboviral encephalitis should be reported promptly to state and local public health authorities.


  1. CDC. St. Louis encephalitis outbreak -- Arkansas, 1991. MMWR 1991;40:605-7.

  2. CDC. Eastern equine encephalitis virus associated with Aedes albopictus -- Florida, 1991. MMWR 1992;41:115,121.

  3. Mitchell CJ, Niebylski ML, Smith GC, et al. Isolation of eastern equine encephalitis virus from Aedes albopictus in Florida. Science 1992;257:526-7.

  4. CDC. Update: St. Louis encephalitis -- Florida and Texas, 1990. MMWR 1990;39:756-9.

  5. CDC. Eastern equine encephalitis -- Florida, eastern United States, 1991. MMWR 1991;40:533-5.

  6. Luby JP, Miller G, Gardner P, Pigford CA, Henderson BE, Eddins D. The epidemiology of St. Louis encephalitis in Houston, Texas, 1964. Am J Epi 1967;83:584-97.

  7. Moore CG, Francy DB, Eliason DA, Monath TP. Aedes albopictus in the United States: rapid spread of a potential disease vector. J Am Mosq Control Assoc 1988;4:356-61.

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