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Current Trends Update: Lyme Disease -- United States

Lyme disease (LD) is a systemic, tick-borne illness that usually occurs during the summer. It was first recognized in 1975 in Connecticut (1). With the tick season approaching, public health officials and practitioners should be aware of recent advances in the microbiology, epidemiology, and treatment of this disease.

LD is characterized by a distinctive skin lesion, erythema chronicum migrans (ECM), often accompanied by nonspecific constitutional symptoms, such as fever, headache, myalgias, and arthralgias. ECM begins as a red macule or papule that expands to become an annular lesion, reaching up to 70 cm in diameter (2). Multiple skin lesions may occur. Some patients subsequently develop arthritic, neurologic, or cardiac complications weeks to months after the initial lesion. The arthritis is intermittent and usually involves large joints. Neurologic manifestations include Bell's palsy, meningoencephalitis, and peripheral neuritis; cardiac manifestations include myocarditis and atrioventricular conduction defects. Patients with the B-cell alloantigen, DR2, often have more severe and frequent late manifestations.

Early epidemiologic work suggested that LD's etiologic agent was transmitted by Ixodes ticks; subsequent studies confirmed that the distribution of known U.S. vectors--I. dammini ticks in the Northeast and Midwest and I. pacificus ticks in the West--parallels the distribution of U.S. cases. In 1982, a spirochete was isolated from an I. dammini tick (3). Subsequently, spirochetes were isolated from ECM skin lesions, blood, and spinal fluid of patients with LD (4,5). The spirochete has recently been classified taxonomically as a Borrelia (6,7).

LD diagnosis is primarily based on clinical criteria, and in endemic areas, the diagnosis can usually be made based on the characteristic ECM lesion and associated symptoms. However, atypical cases, cases presenting with only late manifestations, or cases occurring outside previously recognized endemic areas may be difficult to diagnose. Several laboratories have developed serologic tests for LD that can aid in the diagnosis. Laboratories at CDC and elsewhere currently use an indirect immunofluorescence assay (IFA) to measure antibodies against the spirochete. A titer of 256 or higher is considered positive, and the IFA appears to be highly specific, although patients with treponemal infections (syphilis, yaws, and pinta) may have false-positive titers. These latter patients have positive treponemal reagin tests, while patients with LD do not. The sensitivity of the LD test varies with the stage of the disease. When only ECM is present, as few as 50% of patients may have positive tests, while with complicated disease (when neurologic, arthritic, or cardiac symptoms are present), almost all patients will have positive tests (8).

Early treatment with tetracycline, penicillin, or erythromycin was previously shown to shorten the duration of ECM and to prevent or ameliorate late complicated disease. Recently, oral tetracycline 250 mg four times a day for 10 days has been suggested as the preferred therapy for patients with ECM (9). Longer or higher dose therapy or parenteral penicillin may be necessary for patients with more severe disease. The role of antibiotic therapy for the late arthritic phase of the disease is still being studied.

With the cooperation of state health departments, LD cases for 1980, 1982, and 1983 were reported to CDC. In 1980 and 1982, 226 and 487 cases, respectively, were reported (10,11). A review of the still incomplete 1983 surveillance data indicates that over 500 cases occurred last year. Whether the increase in number of reported cases is due to increased recognition and interest in the disease or to a real increase in the incidence is unclear.

LD has been reported primarily from states in the three recognized endemic areas: the coastal areas of the Northeast (Connecticut, Delaware, Maryland, Massachusetts, New Jersey, New York, Pennsylvania, Rhode Island); in the Midwest (Minnesota, Wisconsin); and in the West (California, Nevada, Oregon, Utah). These states are within the known range of recognized tick vectors. Additional isolated cases, clinically compatible with LD, have been reported from states outside the range of I. dammini or I. pacificus: Arkansas, Florida, Georgia, Indiana, Kentucky, Montana, North Carolina, Tennessee, Texas, and Virginia. For the moment, it may be prudent not to consider these states as endemic until additional cases are identified in these areas. The confirmation of cases in these areas, however, will suggest either previously unrecognized vectors or spread of Ixodes ticks to new areas. The recent isolation of the spirochete from Ambylomma americanum collected in New Jersey, indicates that ticks other than Ixodes may be vectors for LD (12).

To better define the geographic distribution and the incidence of LD, state and territorial epidemiologists and CDC are collecting information on suspected cases of LD occurring in the United States each year. Health-care providers are encouraged to report suspected cases to appropriate local and state health departments. Serologic testing of sera from suspected cases of LD is available at some state health departments or CDC. All sera should be submitted to the appropriate state health department with patients' clinical histories.

References

  1. Steere AC, Malawista SE, Syndman DR, et al. Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three Connecticut communities. Arthritis Rheum 1977;20:7-17.

  2. Steere AC, Bartenhagen NH, Craft JE, et al. The early clinical manifestations of Lyme disease. Ann Intern Med 1983;99:76-82.

  3. Steere AC, Grodzicki RL, Kornblatt AN, et al. The spirochetal etiology of Lyme disease. N Engl J Med 1983;308:733-40.

  4. Burgdorfer W, Barbour AG, Hayes SF, Benach JL, Grunwaldt E, Davis JP. Lyme disease--a tick-borne spirochetosis? Science 1982;216:1317-9.

  5. Benach JL, Bosler EM, Hanrahan JP, et al. Spirochetes isolated from the blood of two patients with Lyme disease. N Engl J Med 1983;308:740-2.

  6. Schmid GP, Steigerwalt AG, Johnson S, et al. DNA characterization of the spirochete that causes Lyme disease. J Clin Microbiol (in press).

  7. Hyde FW, Johnson RC. Genetic relationships of Lyme disease spirochetes to Borrelia, Treponema and Leptospira. J Clin Microbiol (in press).

  8. Russell H, Sampson JS, Schmid GP, Wilkinson HW, Plikaytis B. Enzyme-linked immunosorbent assay and indirect immunofluorescence assay for Lyme disease. J Infect Dis 1984;149:465-70.

  9. Steere AC, Hutchinson GJ, Rahn DW, et al. Treatment of the early manifestations of Lyme disease. Ann Intern Med 1983;99:22-6.

  10. CDC. Lyme disease--United States, 1980. MMWR 1981;30:489-92, 497.

  11. Schmid GP, Hightower A, Steere AC, et al. Lyme disease surveillance in the United States, 1982 (Abstract). Interscience Conference on Antimicrobial Agents and Chemotherapy. October 1983.

  12. Schulze TA, Bowen SG, Bosler EM, et al. Ambylomma americanum; a potential vector of Lyme disease in New Jersey. Science 1984;224:601-3.



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