Clinical Information

Lyme disease is caused by the spirochete Borrelia burgdorferi. The spirochete is transmitted to humans through the bite of Ixodes species ticks. Endemic areas for Lyme disease in the United States (US) correspond with the distribution of 2 tick species, Ixodes dammini (Northeastern and Upper Midwestern US) and Ixodes pacificus (West Coast US). In Europe, Ixodes ricinus transmits the spirochete.

 

Lyme disease exhibits a variety of symptoms that may be confused with immune and inflammatory disorders. Any of the following clinical manifestations may be present in patients with Lyme disease: skin lesions or cardiac or neurological disease. In the first stage of disease, inflammation around the tick bite causes skin lesions, erythema chronicum migrans (ECM)-a unique expanding skin lesion with central clearing that results in a ring-like appearance. Culture of skin biopsies obtained near the margins of ECM are frequently positive. Neurologic and cardiac symptoms may appear with stage 2 and arthritic symptoms with stage 3 of Lyme disease. In some cases, a definitive distinction between stages is not always seen. Further, secondary symptoms may occur even though the patient does not recall a tick bite or rash.

 

The presence of antibodies to Borrelia burgdorferi in cerebrospinal fluid (CSF) is suggestive of neurologic Lyme disease (Lyme neuroborreliosis). PCR testing also may be used to confirm late-stage neurologic disease. However, the sensitivity of PCR is low when testing CSF.

 

According to the manufacturer’s package insert, early antibiotic treatment of Lyme disease can resolve clinical symptoms and prevent progression of the disease to later stages. However, the early administration of antibiotics may suppress the antibody response to levels that are undetectable by current laboratory tests.(1)