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Epidemiologic Notes and Reports Outbreak of Relapsing Fever -- Grand Canyon National Park, Arizona, 1990

On June 21, 1990, 11 days after returning from the Grand Canyon North Rim (GCNR), a 61-year-old California resident developed an acute illness lasting 2 days, characterized by fever, shaking chills, headache, myalgias, and drenching sweats. During the next 2 weeks, he had three febrile relapses and was hospitalized. Physical examination and laboratory studies were nondiagnostic. However, during a fourth recurrence of fever and prostration, examination of a peripheral blood smear revealed spirochetes, consistent with the diagnosis of relapsing fever. The patient was treated with tetracycline and recovered.

One additional confirmed case with onset July 5 and one suspected case with onset July 12 were reported in Arizona residents. All three patients had stayed overnight in cabins at the GCNR.

Beginning July 6, 1990, visitors to the GCNR were notified of the risk for exposure to tickborne relapsing fever (TBRF). A survey of 244 employees at the GCNR identified two persons who had had recurrent febrile symptoms compatible with TBRF. One had been hospitalized with meningismus and cerebrospinal fluid pleocytosis. A retrospective mail and telephone survey of 6993 visitor groups, representing more than 10,000 persons who stayed in park cabins during the 1990 season, identified 14 cases of laboratory-confirmed (four cases) or clinically defined (10 cases) relapsing fever* in park visitors from nine states, Canada, and Germany. Seven of the 14 patients had been hospitalized.

An environmental investigation revealed rodent nests likely to harbor vector ticks above the ceilings and below the floors of many of the cabins at the GCNR. During August, all cabins were sprayed with acaricides. National Park officials plan to inspect all buildings, remove rodent nests, and make structural changes to prevent rodent access and nesting in attics and crawl spaces before the park opens for the 1991 season. Reported by: D Lakin, MD, Scottsdale Memorial Hospital, Scottsdale; J Wurgler, MD, C Brickley, Grand Canyon Clinic, Grand Canyon Village; C Levy, MS, LK Sands, DO, SJ Englender, MD, State Epidemiologist, Arizona Dept of Health Svcs. California Dept of Health Svcs. J Bartzatt, National Park Svc, US Dept of the Interior. Div of Vector-Borne Infectious Diseases, Center for Infectious Diseases; Div of Field Epidemiology, Epidemiology Program Office, CDC.

Editorial Note

Editorial Note:

This outbreak is the first recognized occurrence of TBRF at GCNR since 1973, when an interstate outbreak of 62 confirmed or suspected cases occurred in employees or visitors who had stayed in cabins at GCNR (1). TBRF is endemic throughout much of the western United States; sporadic cases occur each summer and fall. The disease is caused by infection with the spirochetes Borrelia hermsii or B. turicatae; B. hermsii was identified in 1973 at the GCNR (1). The soft ticks of the genus Ornithodoros, which transmit the illness, usually feed on rodents and frequently infest rodent nesting material (2). The ticks are reclusive, usually feeding at night for only 5-20 minutes. Their bites are painless and frequently go unnoticed (3). Most infections with B. hermsii are acquired by persons vacationing in mountain cabins where rodents have nested (1-7).

Because onset of illness occurs 4-18 days after infection, patients infected with TBRF in tourist areas where the disease is endemic often develop symptoms after they have returned to areas where TBRF is not suspected. TBRF that is undiagnosed and untreated may cause recurrent febrile illness for weeks to months before the illness resolves. Neurologic sequelae, such as aseptic meningitis and cranial nerve palsy, occur in a small proportion of patients. Serologic testing by enzyme-linked immunosorbent assay is available at CDC's Division of Vector-Borne Infectious Diseases, Center for Infectious Diseases, through state health departments and may aid with a diagnosis when symptoms are suggestive of TBRF but laboratory results are equivocal. Following infection, paired serum specimens often demonstrate diagnostic levels of antibody to B. hermsii or B. turicatae.

The 1973 outbreak was associated with epizootic plague (2,4), which caused a marked decrease in rodent populations that serve as the usual hosts for the vector tick and resulted in increased feeding of ticks on humans. Recent observations suggest that a decline in rodent populations occurred in 1990, which may similarly have increased the risk for human exposure.

Prevention strategies for TBRF focus on avoiding tick bites and preventing rodents from nesting in human shelters in areas where TBRF is endemic. "Rodent proofing"--structural changes that prevent rodent access to the foundations or attics of homes and vacation cabins--reduces human contact with ticks that transmit the disease.

References

  1. Boyer KM, Munford RS, Maupin GO, et al. Tick-borne relapsing fever: an interstate outbreak originating at Grand Canyon National Park. Am J Epidemiol 1976;105:469-79.

  2. Burgdorfer W. The enlarging spectrum of tick-borne spirochetoses: R.R. Parker Memorial Address. Rev Infect Dis 1986;8:932-40.

  3. Southern PM, Sanford JP. Relapsing fever: a clinical and microbiological review. Medicine 1969;48:129-49.

  4. Burgdorfer W. The epidemiology of relapsing fevers. In: Johnson RC, ed. The biology of parasitic spirochetes. New York: Academic Press, 1976:389-94.

  5. CDC. Common source outbreak of relapsing fever--California. MMWR 1990;39:579,585-6.

  6. Horton JM, Blaser MJ. The spectrum of relapsing fever in the Rocky Mountains. JAMA 1985;145:871-5.

7. Thompson RS, Burgdorfer W, Russell R, et al. Outbreak of tick-borne relapsing fever in Spokane County, Washington. JAMA 1969;210:1045-50.

  • A confirmed case was defined as illness occurring within 3

weeks of exposure in any person who had been a resident or overnight visitor at the GCNR from May 15 through August 15, 1990, from whom spirochetes were visualized on a Wright- or Giemsa-stained blood smear, or in whom antibody to Borrelia hermsii was demonstrated by enzyme-linked immunosorbent assay. A clinical case was defined as illness in a resident or visitor during the same dates who had fever and three of four characteristic symptoms (chills, sweats, myalgias, or headache) and in whom a history of clinical remission followed by relapse was reported.

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