CDC Lyme Disease Introduction: Lyme disease was named in 1977 when arthritis was observed in a cluster of children in and around Lyme, Connecticut.	Borrelia burgdorferi are helical shaped bacteria about 10-25µm long. (View enlarged image.)	NEWS & HIGHLIGHTS MMWR Update: Lyme Disease in the United State, 2001-2002. May 2004
Other clinical symptoms and environmental conditions suggested that this was an infectious disease probably transmitted by an arthropod.
Further investigation revealed that Lyme disease is caused by the bacterium, Borrelia burgdorferi. These bacteria are transmitted to humans by the bite of infected deer ticks and caused more than 23,000 infections in the United States in 2002.

From left to right: The deer tick (Ixodes scapularis) adult female, adult male, nymph, and larva on a centimeter scale. (View enlarged image.)

Vector: Black-legged ticks (Ixodes scapularis) are responsible for transmitting Lyme disease bacteria to humans in the northeastern and north-central United States. On the Pacific Coast, the bacteria are transmitted to humans by the western black-legged tick (Ixodes pacificus). Ixodes ticks are much smaller than common dog and cattle ticks. In their larval and nymphal stages, they are no bigger than a pinhead. Ticks feed by inserting their mouths into the skin of a host and slowly take in blood. Ixodes ticks are most likely to transmit infection after feeding for two or more days.

National Lyme disease risk map with four categories of risk. (View enlarged image.)

Risk: In the United States, Lyme disease is mostly localized to states in the northeastern, mid-Atlantic, and upper north-central regions, and to several counties in northwestern California. In 2002, 23,763 cases of Lyme disease were reported to the Centers for Disease Control and Prevention (CDC) (MMWR 52(31):741-750). Ninety-five percent of these cases were from the states of Connecticut, Delaware, Rhode Island, Maine, Maryland, Massachusetts, Minnesota, New Jersey, New Hampshire, New York, Pennsylvania, and Wisconsin.

Individuals who live or work in residential areas surrounded by tick-infested woods or overgrown brush are at risk of getting Lyme disease. Persons who work or play in their yard, participate in recreational activities away from home such as hiking, camping, fishing and hunting, or engage in outdoor occupations, such as landscaping, brush clearing, forestry, and wildlife and parks management in endemic areas may also be at risk of getting Lyme disease.

Prevention and Treatment: Prevention measures can be effective in reducing your exposure to infected ticks, and most people can be successfully treated with antibiotic therapy when diagnosed in the early stages of Lyme disease.

Visit the links below for more information on the following topics:

• Prevention and Control
• Symptoms
• Treatment
• Questions and Answers

Other Tick-Borne Diseases: Information about other tick transmitted illnesses like Southern tick-associated rash illness (STARI), Babesia infection, and ehrlichiosis can be found at CDC Health Topics A-Z.

More on the History of Lyme Disease: Early in the 20th century, European physicians observed patients with a red, slowly expanding rash (called erythema migrans or EM), associated this rash with the bite of ticks, and postulated that it was caused by a tick-borne bacterium. Then in the 1940s, similar tick-borne illness was described that often began with EM and developed into multi-system illness. Later that decade, spirochete-like structures were observed in skin specimens leading to the use of penicillin for treatment.

Aware of these findings, a physician in Wisconsin diagnosed a patient with EM and successfully treated it with penicillin in 1969. In the mid-1970s, physicians observed clusters of children with arthritis in and around Lyme, Connecticut. Other clinical symptoms and environmental conditions suggested that this was a distinct illness probably transmitted by an arthropod. Researchers linked the presence of EM rash lesions to preceding tick bites and determined that early treatment with penicillin not only shortened the duration of EM but also reduced the risk of subsequent arthritis.

In 1982, spirochetes were identified in the midgut of the adult deer tick, Ixodes dammini (referred herein by its original name, the black-legged tick, Ixodes scapularis) and given the name Borrelia burgdorferi. Finally, conclusive evidence that B. burgdorferi caused Lyme disease came in 1984 when spirochetes were cultured from the blood of patients with EM, from the rash lesion itself, and from the cerebrospinal fluid of a patient with meningoencephalitis and history of prior EM. CDC began surveillance for Lyme disease in 1982 and the Council of State and Territorial Epidemiologists (CSTE) designated Lyme disease as a nationally notifiable disease in January 1991.

References:

Barbour AG. Lyme Disease: The Cause, the Cure, the Controversy. 1996. The Johns Hopkins University Press, Baltimore, MD.

Benach JL, Bosler EM, Hanrahan JP, et al. Spirochetes isolated from the blood of two patients with Lyme disease. N Engl J Med. 1983;308:740-742.

Burgdorfer W. How the discovery of Borrelia burgdorferi came about. Clin Dermatol. 1993 Jul-Sep;11(3):335-338.

Burgdorfer WA, Barbour AG, Hayes SF, et al. Lyme disease - a tick-borne spirochetosis? Science. 1982;216:1317-1319.

Centers for Disease Control and Prevention. Notice to Readers: Final 2002 Reports of Notifiable Diseases. MMWR. 8 August 2003; 5(31):741-750.

Centers for Disease Control and Prevention. Appendix Methods Used for Creating a National Lyme Disease Risk Map. MMWR. 4 Jun 1999;48(RR07);21-24.
(Also available in PDF format [742 KB, 39 pages].)

Centers for Disease Control and Prevention. Lyme Disease—United States, 1999. MMWR. 16 Mar 2001;50(10):181-185.
(Also available in PDF format [1.47 MB, 20 pages].)

Hellerstrom S. Erythema chronicum migrans Afzelius with meningitis. Southern Med J. 1950;43:330-335.

Nadelman RB and Wormser GP. Lyme borreliosis. Lancet. 1998;352:557-565.

Orloski KA, Hayes EB, Campbell GL, Dennis DT. Surveillance for Lyme disease--United States, 1992-1998. Mor Mortal Wkly Rep CDC Surveill Summ. 2000 Apr 28;49(3):1-11.

Rahn DW, Evans J eds. Lyme Disease. 1998. American College of Physicians, Philadelphia, PA.

Scrimenti RJ. Erythema chronicum migrans. Arch Dermatol. 1970;102:104-105.

Sood SK, Salzman MB, Johnson BJ, Happ CM, Feig K, Carmody L, Rubin LG, Hilton E, Piesman J. Duration of tick attachment as a predictor of the risk of Lyme disease in an area in which Lyme disease is endemic. J Infect Dis. 1997 Apr;175(4):996-999.

Steere AC. Lyme disease. N Engl J Med. 1989 Aug 31;321(9):586-596.

Steere AC. Lyme disease. N Engl J Med. 2001 Jul 12;345(2):115-125.

Steere AC, Grodzicki RL, Kornblatt AN, et al. The spirochetal etiology of Lyme disease. N Engl J Med. 1983;308:733-740.

Steere AC, Malawista SE, Hardin JA, et al. Erythema chronicum migrans and Lyme arthritis: the enlarging clinical spectrum. Ann Intern Med. 1977;86:685-698.

Steere AC, Malawista SE, Newman JH, et al. Antibiotic therapy in Lyme disease. Ann Intern Med. 1980;93:1-8.

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

Wang G, van Dam AP, Schwartz I, Dankert J. Molecular typing of Borrelia burgdorferi sensu lato: taxonomic, epidemiological, and clinical implications.Clin Microbiol Rev. 1999 Oct;12(4):633-653.

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