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Epidemiologic Notes and Reports Western Equine Encephalitis -- United States and Canada, 1987

CDC has received reports of 37 western equine encephalitis (WEE) cases among humans and 132 cases among horses in the Plains and Rocky Mountain states thus far this year. This outbreak is the largest in the United States since 1977, when 41 cases among humans were reported. Active, hospital-based surveillance in Colorado has identified 29 cases, including one fatality. Passive surveillance has revealed three cases in Nebraska, two in Texas, two in North Dakota, and one in Montana. Colorado, Iowa, Nebraska, and North Dakota also reported sporadically occurring cases of St. Louis encephalitis (SLE), concurrently with the WEE epidemic. The diffuse character of the outbreak has made it difficult to assign a denominator to the human population at risk. However, the crude attack rate in Colorado, where there is evidence of statewide virus transmission, is 1.0/100,000.

The first WEE cases among humans were reported from Texas and Colorado; both had onset during the first week in July (Figure 1). The sex and age distribution of human patients follows the typical pattern of WEE outbreaks--25 are male, and 16 of these are between 15 and 64 years of age. A case-control study has been initiated to investigate behavioral and host factors associated with risk of infection.

Equine cases have been identified in 11 states and Manitoba Province, Canada (Figure 2). The earliest case was reported from south Texas in April. In June, most cases occurred in the Southwest (Texas Panhandle, New Mexico, and Oklahoma). During July, the epizootic spread rapidly across the Plains and Rocky Mountain states, extending as far north as North Dakota and Minnesota. In August, it expanded to Montana and Manitoba in the northwestern and northern reaches of the Great Plains and eastward to Wisconsin. Only four cases were reported from counties west of the Continental Divide.

Routine, seasonal surveillance of sentinel chickens and vector mosquitoes revealed enzootic virus activity in northeastern Utah and in the Imperial Valley and Sacramento Valley of California. However, despite this evidence of intense viral activity, no cases have been recognized among horses or humans in these areas.

The vector mosquito population has been reduced because many municipalities throughout the affected area have applied adulticides as a control measure. In addition, the cessation of host-seeking behavior in Culex tarsalis, the principal mosquito vector, has diminished the risk in most areas. Reported by: WJ Pape, PJ Shillam, RE Hoffman, MD, MPH, State Epidemiologist, Colorado Dept of Health. KL Quickenden, PhD, JK Gedrose, RN, MN, State Epidemiologist, Montana Dept of Health and Environmental Sciences. PA Stoesz, MD, State Epidemiologist, Nebraska Dept of Health. R Hennes, MPH, JL Pearson, DrPH, State Epidemiologist, North Dakota Dept of Health. GR Istre, MD, State Epidemiologist, Oklahoma Dept of Health. JT Taylor, CM Reed, MPH, TG Betz, MD, MPH, State Epidemiologist, Texas Dept of Health. RA French, Acting State Epidemiologist, Kansas Dept of Health and Environment. MT Osterholm, PhD, MPH, State Epidemiologist, Minnesota Dept of Health. TL Brown, MS, M Eidson, DVM, HF Hull, MD, State Epidemiologist, New Mexico Health and Environment Dept. KA Senger, State Epidemiologist, South Dakota Dept of Health. WH Thompson, DVM, PhD, JP Davis, MD, State Epidemiologist, Wisconsin Dept of Health and Social Svcs. HC Crawford, MD, State Epidemiologist, Wyoming Dept of Health and Social Svcs. MV Fast, MD, DTCH, Provincial Epidemiologist, Manitoba Community Health Svcs, Winnipeg, Manitoba. LA Peterson, DVM, JE Pearson, DVM, National Veterinary Svcs Laboratory, US Dept of Agriculture, Ames, Iowa. Immunochemistry Br, Div of Vector-Borne Viral Diseases, Center for Infectious Diseases; Div of Field Svcs, Epidemiology Program Office, CDC.

Editorial Note

Editorial Note: In most years, WEE transmission occurs at a low level in the rural West and principally involves birds and Cx. tarsalis, which constitute the virus' maintenance cycle (1). At such times, infections in humans and equines, which occur outside the maintenance cycle, result in small numbers of sporadically occurring cases (2). However, at intervals of 5 to 10 years and for reasons poorly understood, viral transmission in the maintenance cycle is more intense, and humans and equines become infected at epidemic and epizootic levels.

Outbreaks have often affected wide areas of the western United States and Canada. In 1941, more than 3,400 cases among humans occurred in the northern Plains states and in Canada's Manitoba, Alberta, and Saskatchewan provinces. The attack rate reached 167/100,000 (3). More recently, in 1975, there were 277 reported cases among humans and 281 among equines in an outbreak in the Red River Valley (4,5).

Cx. tarsalis breeds chiefly in waste irrigation water in farmland and pastures in the West (1). Risk of acquiring WEE is associated with residence in rural areas and with agricultural occupations and other outdoor activities that lead to contact with the vector mosquito (2). Attack rates for males are generally twofold greater than for females.

Control of WEE is difficult because major outbreaks occur at unpredictable intervals and because virus activity covers wide and usually sparsely populated areas. The size of vector mosquito populations, the virus infection rates of vectors, the seroconversion rate among sentinel chickens, and the prevalence of cases among equines have been shown to correlate with the appearance of cases among humans (6). These indices are monitored in an attempt to anticipate epidemics and as a guide in planning mosquito control measures. It should be noted, however, that vaccination of horses and underreporting of the disease limit the sensitivity of equine surveillance.

The epizootic this year was remarkable because of the northward progression of cases during the summer. Cx. tarsalis is active year-round in the Rio Grande Valley, and WEE virus has been isolated from winter collections of the mosquito (7). The northward progression of cases during the 1987 season suggests that the epizootic may have originated in the Rio Grande Valley and that WEE virus spread from that area. An alternative explanation is that the northerly spread simply reflects temporal differences in the start of spring and summer activity of Cx. tarsalis and house sparrows, the principal avian host in the maintenance cycle (1).

Contemporaneous SLE and WEE outbreaks in the West have been reported in several instances (1,2,8). While SLE and WEE viruses have common maintenance cycles, SLE virus activity typically peaks several weeks later, and cases among humans occur chiefly in late August and September.


  1. Hayes RO. Eastern and western encephalitis. In: Steele JH, ed. CRC handbook series in zoonoses. Vol I. Boca Raton, Florida: CRC Press, 1981:29-57.

  2. 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. Vol II, 2nd ed. Philadelphia: WB Saunders, 1987:1417-56.

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

  4. 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.

  5. Leech RW, Harris JC, Johnson RM. 1975 encephalitis epidemic in North Dakota and western Minnesota: an epidemiologic, clinical, and neuropathologic study. Minn Med 1981;64:545-8.

  6. Olson JG, Reeves WC, Emmons RW, Milby MM. Correlation of Culex tarsalis population indices with the incidence of St. Louis encephalitis and western equine encephalomyelitis in California. Am J Trop Med Hyg 1979;28:335-43.

  7. CDC. Control of western equine encephalitis. Atlanta: US Department of Health, Education, and Welfare, Public Health Service, 1978. (Vector Topics No. 3.)

  8. Monath TP. Epidemiology. In: Monath TP, ed. St. Louis encephalitis. Washington, DC: American Public Health Association, 1980:239-312.

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