Current Trends Arboviral Infections of the Central Nervous System -- United States, 1987

In 1987, 148 U.S. cases of arboviral encephalitis were reported to CDC (Figure 1). Outbreaks of western equine encephalitis (WEE) and St. Louis encephalitis (SLE) in the Great Plains and Mountain states resulted in 41 WEE cases (one fatal) and 17 SLE cases (1) (Figures 1 and 2). The WEE outbreak led to an epizootic among horses in the same region, producing 173 equine cases. LaCrosse virus, the principal cause of endemic arboviral central nervous system (CNS) infections in the United States, was the etiologic agent in 87 cases (one fatal) reported in 1987. Three sporadic cases of eastern equine encephalitis (EEE) were reported from recognized endemic foci on the Atlantic Coast.

Western equine encephalitis. The WEE outbreak was first recognized in southern Texas with reports of equine cases in April and June (Figure 1). By June, the epizootic had spread through the panhandle of Texas, Oklahoma, New Mexico, and southern Colorado, and by July, equine cases had been reported from as far north as North Dakota (1). From August through October, equine cases were recognized in the northwest and in the eastern plains. Equine cases were reported from 120 counties nationwide (Figure 2).

The epidemic began in early July. Initially, cases were reported from southern Colorado but eventually were recognized in seven western states. Active hospital- based surveillance in Colorado identified cases in 10 counties, for an estimated incidence of 1.63/100,000 in the counties reporting cases and 1.03/100,000 statewide. (Continued on page 513) The incidence in North Dakota, which identified two cases through passive surveillance, was 0.31/100,000.

More than twice as many cases occurred in males (28) as in females (13); one elderly man died. The age- and sex-specific rates in the 10 Colorado counties reporting cases were higher in males in every age group (Figure 3). Risk increased with age for both women and men; however, male infants were also at increased risk.

St. Louis encephalitis. Except for one case reported from California, SLE cases in 1987 occurred in association with the WEE outbreak, although they occurred later in the season. The median date of onset of the SLE cases (September 25) was 6 weeks later than that of WEE cases (August 11). Twelve of the 17 SLE cases were in males.

LaCrosse encephalitis. Cases were reported chiefly from the upper midwest from states where the disease is endemic (Figure 1). In West Virginia, one fatal case and four other cases reported by one Charleston hospital in July prompted an epidemiologic investigation (2). Active surveillance of children hospitalized with CNS infection in a five-county area of southern West Virginia identified 19 laboratory-confirmed cases, for an estimated incidence of 20.4/100,000 children less than 15 years old. A case- control study to examine potential environmental and behavioral risk factors showed that more discarded tires containing water were on the premises of patients than on those of matched controls. Other peridomestic artificial containers or natural sites (treeholes) that could support breeding of Aedes triseriatus, the principal vector of LaCrosse virus, were not implicated as risk factors. Neither mosquitoes nor infection rates in vectors at case and control premises were enumerated.

Eastern equine encephalitis. Cases were reported in a 7-year-old boy from South Carolina, a 4-year-old girl from Georgia, and a 79-year-old woman from Florida. The 7-year-old boy died; EEE virus was isolated from his brain, and immunohistochemical techniques were used for the first time to demonstrate the distribution of EEE viral antigen in infected neurons and mononuclear cells (3). The latter two patients recovered but had significant neurologic sequelae. Reported by: RC Baron, MD, Acting State Epidemiologist, West Virginia State Dept of Health. RD Hoffman, MD, State Epidemiologist, Colorado Dept of Health. Various other state and local health departments. JM Powers, MD, Dept of Neuropathology, Columbia Presbyterian Hospital, New York City, New York. L Peterson, DVM, National Veterinary Diagnostic Laboratory, US Dept of Agriculture, Ames, Iowa. Div of Vector-Borne Viral Diseases, Center for Infectious Diseases; Div of Field Svcs, Epidemiology Program Office, CDC.

Editorial Note

Editorial Note: In the western United States, WEE virus is maintained perennially in a cycle among birds and Culex tarsalis, the principal mosquito vector of WEE (4). In most years, transmission from this enzootic cycle leads to a low level of endemic infection in the human population, but periodically, outbreaks of epidemic proportions occur concurrently with even larger numbers of cases in horses. In 1941, in the largest and most extensive WEE outbreak on record, more than 300,000 cases in horses and 3400 in humans were reported from the northern plains states and neighboring Canadian provinces (5). In 1975, a WEE outbreak that focused in the Red River Valley of North Dakota and Minnesota resulted in 281 equine and 133 human cases (6).

The 1987 WEE outbreak was epidemiologically typical in several respects. Sixty- eight percent of the reported cases were in males; risk of acquiring WEE generally is twofold higher in men than in women, probably because men have a greater level of exposure outdoors to the rural habitat of Cx. tarsalis. An increased risk of WEE with advanced age (seen in the age-specific rates in Colorado in 1987) has been observed in most outbreaks. The biological factors associated with increased susceptibility at the extremes of age remain undefined.

Although the apparent northward advance of epizootic WEE activity observed in 1987 has not been reported in previous WEE outbreaks, a similar pattern occurred in the nationwide SLE epidemic in 1975 and in outbreaks of Japanese encephalitis in Japan in 1965 (7,8). The progression of virus activity from south to north may have reflected a relative delay in the onset of activities of vectors and intermediate hosts with increasing latitude. Alternatively, an epidemic virus strain may have been spread by infected vectors that were carried great distances by northward-moving weather fronts (9).

In the rural western United States, SLE and WEE viruses are transmitted in the same natural cycle among birds and Cx. tarsalis, the principal mosquito vector of both viruses (4). A relative delay in the appearance of SLE cases is characteristic of combined WEE-SLE outbreaks. A slower rate of growth of SLE virus in the vector and a dependence of viral multiplication on higher temperatures may contribute to the slight but consistent difference in seasonality (4).

The upper midwest has been regarded as the principal endemic focus of LaCrosse encephalitis in the United States (10). Population-based epidemiologic studies in Wisconsin and Minnesota in 1978 disclosed an estimated incidence of 31.6/100,000 among children less than 15 years old (11). Although sporadic cases of CNS infection from LaCrosse virus have been recognized previously in southern West Virginia, the area was not regarded as a focus with a high level of transmission. The population-based estimate of incidence in the five-county area near Charleston was similar to that reported from recognized endemic foci in the upper midwest (11,12), suggesting that the incidence of LaCrosse virus infection of the CNS may be underestimated in other areas of the eastern United States within the range of Ae. triseriatus.

Although discarded tires have been recognized as an important source of Ae. triseriatus, the risks associated with various peridomestic natural and artificial containers are unknown (13). The results of the West Virginia study suggest that removing discarded tires may be more important as a control measure than removing other kinds of containers or filling treeholes.

References

1. CDC. Western equine encephalitis--United States and Canada, 1987. MMWR 1987;36:655-9.

2. CDC. La Crosse encephalitis in West Virginia. MMWR 1988;37:79-82.

3. Powers JM, Tsai TF, Garen PD, Tecklenburg F, Seay AR. Eastern equine encephalitis: immunohistochemical and ultrastructural distribution of virus (Abstract). J Neuropathol Exp Neurol 1988;47:304.

4. Tsai TF, Monath TP. Viral diseases in North America transmitted by arthropods or from vertebrate reservoirs. In: Feigin RD, Cherry JD, eds. Textbook of pediatric infectious diseases. 2nd ed. Philadelphia: WB Saunders, 1987;1417-56.

5. Leake JP. Epidemic of infectious encephalitis. Public Health Rep 1941;56:1902-5.

6. Potter ME, Currier RW II, Pearson JE, Harris JC, Parker RL. Western equine encephalomyelitis in horses in the northern Red River Valley, 1975. J Am Vet Med Assoc 1977;170:1396-9.

7. Powell KE, Kappus KD. Epidemiology of St. Louis encephalitis and other acute encephalitides. Adv Neurol 1978;19:197-215.

8. Okuno T, Tsunoda T, Hiraishi K, Matsubara Y, Ishii K, Oya A. Japanese encephalitis surveillance report, 1965. Nihon-iji-Shinpo 1967;2256:17-28.

9. Sellers RF, Pedgley DE. Possible windborne spread to western Turkey of bluetongue virus in 1977 and of Akabane virus in 1979. J Hyg 1985;95:149-58.

10. Kappus KD, Monath TP, Kaminski RM, Calisher CH. Reported encephalitis associated with California serogroup virus infections in the United States, 1963-1981. In: Calisher CH, Thompson WH, eds. California serogroup viruses. New York: Alan R. Liss, 1983;31-41.

11. Hurwitz ES, Schell W, Nelson D, Washburn J, LaVenture M. Surveillance for California encephalitis group virus illness in Wisconsin and Minnesota, 1978. Am J Trop Med Hyg 1983;32:595-601.

12. Beghi E, Nicolosi A, Kurland LT, Mulder DW, Hauser WA, Shuster L. Encephalitis and aseptic meningitis, Olmsted County, Minnesota, 1950-1981: I. epidemiology. Ann Neurol 1984; 16:283-94.

13. Francy DB. Mosquito control for prevention of California (La Crosse) encephalitis. In: Calisher CH, Thompson WH, eds. California serogroup viruses. New York: Alan R. Liss, 1983;365-75.

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