This report investigates Lyme disease, with a focus on anatomic and physiological aspects, stages of the disease with bodily effects, how the disease mimics other diseases, and treatments. Lyme disease (LD) has a history of more than 100 years in the Old World. In the 1970s, LD was the adopted term for the multisystem nature of Lyme arthritis. Lyme arthritis was described in 1975 as a juvenile rheumatoid arthritis, usually preceded by a distinctive skin rash, erythema chronicum migrans (ECM, now called erythema migrans, EM). Spirochete, isolated from Ixodes dammini ticks, was associated with the spread of the disease in 1982.
The cause of the disease was established as the spirochete and named Borrelia burgdorferi (Bb). Three species of Borrelia cause LD: Borrelia burgdorferi sensu stricto (United States and Europe), Borrelia garinii, and Borrelia afzelii (Europe). A syndrome consisting of lymphocytic meningitis, radiculitis, and cranial nerve palsy was described by Garin-Bujadoux and Bannwarth. This syndrome is related to a preceding ECM and bite by Ixodes ricinus; it was called tick-borne meningopolyneuritis (Gannwarth syndrome). The bacterial pathogen suspected is now called Bb (Sigal, 1997).
LD is a zoonotic infection occurring in enzootic cycles among wildlife; it affects humans when they are bitten by an infected tick. LD affects all age groups and may involve the skin, joints, nervous system, and heart. Most human cases of LD in the United States are found in the hyperendemic mid-Atlantic and northeastern regions. I. scapularis (blacklegged tick) is a polytypic species with a widespread distribution in eastern North America. Numbers of reported cases have declined from 1994 (13,043) to 1995 (11,603) (Hutcheson, Oliver, Houck, & Strauss, 1995; Oliver, 1996). Tick vectors of LD require a vertebrate blood meal during developmental stages; adult ticks are primarily dependent on deer for feeding and reprodu...