The diagnosis of Lymedisease is made on clinical findings, epidemiologic features, and an elevated antibody response to B burgdorferi. The available laboratory tests (with the exception of a positive culture from an EM lesion) can be unreliable. Serologic testing only should be undertaken when clinical and epidemiologic features suggest Lymediseaseas the diagnosis.
Most patients with B burgdorferi are found to have detectable antibodies when tested with enzyme-linked immunosorbent assay (60-70% within 2-4 weeks of infection and 90% by the disseminated and persistent stages). However, serologic tests lack standardization, their accuracy is often unsubstantiated, and false-positive results are common. IgM antibody appears 2-4 weeks after the EM lesion, peaks at 6-8 weeks, and declines after 4-6 months. IgG antibody appears 6-8 weeks after the EM lesion, peaks at 4-6 months, and remains at low levels despite antibiotic therapy. A fourfold rise in antibody titer would be suggestive of recent infection. Western blot analysis is used to confirm results obtained by enzyme-linked immunosorbent assay.
Lyme disease is a bacterial disease caused by Borrelia burgdorferi. The bacterium is transmitted to humans via a tick bite. Within 1 to 2 weeks after being infected, a “bull’s-eye” rash can develop at the tick bite site accompanied by fever, headache, and muscle or joint pain. Some people may have Lymedisease and not have any early symptoms. However, others can have a fever and other “flu-like” symptoms without a rash.
The first sign of Lyme disease in 70-80% of patients is a red circular rash, called an erythema migrans, around the puncture mark made where the tick pierced the skin. This rash appears after a 3-30 day delay. The most common shape of the rash is an oval 2-3 inches in diameter that usually lasts about 4 weeks. The center of the rash occasionally will lighten resulting in a bull’s-eye appearance. The rash does not itch but may feel warm to the touch. Flu-like symptoms may also develop that often include aches, fever, fatigue, muscle pain, joint pain, and headache. Arthritis, cardiac disease, and neurologic disorders may develop if the disease is not properly or promptly treated. Sometimes these more serious symptoms develop without the individual ever having had a rash.
The primary vector of Lyme disease in the U.S. is the black-legged deer tick (Ixodes scapularis) . Other Ixodes ticks are also known to transmit the disease. Lyme disease is maintained in wild rodent populations, on which the larval and nymphal ticks develop. These immature ticks pick up the disease organism when they suck the blood of infected rodents. The nymphal and adult ticks then seek a larger host, such as deer or humans, to obtain their final blood meal and transmit the disease when they feed.