Description
Borrelia burgdorferi is a spirochete that causes Lyme disease. The organism is transmitted by ticks of the genus Ixodes. In endemic areas, these ticks are commonly found on vegetation and animals such as deer, mice, dogs, horses, and birds.
B. burgdorferi infection shares features with other spirochetal infections (diseases caused by three genera in humans: Treponema, Borrelia, and Leptospira). Skin is the portal of entry for B. burgdorferi and a characteristic rash called erythema migrans (EM) develops around the tick bite in 60% to 80% of patients. Spirochetemia occurs early with wide spread dissemination through tissue and body fluids. Lyme disease occurs in stages, often with intervening latent periods and with different clinical manifestations.
In Lyme disease there are generally three stages of disease often with overlapping symptoms. Symptoms vary according to the sites affected by the infection such as joints, skin, central nervous system, heart, eye, bone, spleen, and kidney. Late disease is most often associated with arthritis or CNS syndromes. Asymptomatic subclinical infection is possible and infection may not become clinically evident until the later stages. Patients with early infection produce IgM antibodies during the first few weeks after onset of EM and produce IgG antibodies more slowly. Although IgM only may be detected during the first month after onset of illness, the majority of patients develop IgG antibodies within one month. Both IgG and IgM antibodies can remain detectable for years. Isolation of B. burgdorferi from skin biopsy, blood, and spinal fluid has been reported. However, these direct culture detection methods may not bepractical in the large scale diagnosis of Lyme borreliosis. Serological testing methods for antibodies to B. burgdorferi include Indirect Fluorescent Antibody (IFA) staining, Immunoblotting, and Enzyme Immunoassay (EIA). B. burgdorferi is antigenically complex with strains that vary considerably. Early antibody responses often are to flagellin, which has cross-reactive components. Patients in early stages of infection may not produce detectable levels of antibody. Also, early antibiotic therapy after EM may diminish or abrogate good antibody response. Thus, serological tests for antibodies to B. burgdorferi are known to have low sensitivity and specificity, and because of such inaccuracy, these test cannot be relied upon for establishing a diagnosis of Lyme disease.
In 1994, the Second National Conference on Serological Diagnosis of Lyme disease recommended a two-steptesting system toward standardizing laboratory serologic testing for B. burgdorferi.Because ELISA and IFA methods were not sufficiently specific to support clinical diagnosis, it was recommended that positive or equivocal results from a sensitive ELISA or IFA (first step) should be further tested, or supplemented, by using a standardized Western-blot method (second step) for detecting antibodies to B. burgdorferi (Western-blot assays for antibodies to B. burgdorferi are supplemental rather than confirmatory because their specificity is less than optimal, particularly for detecting IgM). Two-step positive results provide supportive evidence of exposure to B. burgdorferi, which could support a clinical diagnosis of Lyme disease but should not be used as a criterion for diagnosis. Antibody detection methods do not provide definitive results for establishing or ruling out a diagnosis of Lyme disease in that the predictive value of positive results will be low when specimens are tested from patients with diagnoses that are not supported by history of exposure, symptoms, signs, and laboratory data