Lyme disease was first documented in 1909 in Europe. It was not until 1970s that Lyme disease was reported in the United States. In 1975 major attention was drawn to the disease when an unusual number of children in Lyme, CT were diagnosed with juvenile rheumatoid arthritis. The disease was initially called Lyme arthritis and when dermatologic cardiac and neurologic component were recognized the name was broadened to Lyme disease.
Lyme disease (LD) is caused by Borrelia burgdorferi a spirochetal bacterium transmitted by the bite of Ixodes scapularis (black-legged deer tick) and Ixodes pacificus (western black-legged deer tick). The deer tick has a two-year life cycle, which begins when the mother tick lays her eggs on the ground in a wooded area in early spring. Several weeks later the eggs hatch into larval stage. The larvae attach most commonly to the white-footed mouse, and feeds for 2-3 days. During this feeding the spirochete infects the tick larvae. Although the white-footed mouse carries the spirochete it shows no symptoms of infection. The larvae go into a resting phase for the remaining summer, fall and winter. In the spring the six-legged larva molts into an eight-legged nymph, which is no larger than the head of a pin. The nymph then feeds again on the white-footed mouse or any other warm-blooded host. The spirochete, stored in the gut of the larva now migrates up to the salivary glands of the nymph and is injected into the nymph’s host as it feeds. During late spring and early summer nymph phase tick is most likely to attach to human and transmit the spirochete. I n the fall the nymphs become mature adults and feed again. The adult tick can and will feed on human and transmit the spirochete.
Today, LD is the most common vector-borne disease in North America. In 1999, over 16,000 cases of human LD were reported in the United States by the Centers for disease Control and Prevention (CDC), representing an overall incidence of 6.0 per 100,000 persons. The annual incidence rate of LD in CT is 54.6 or 9 times that of the national average. It is thought that many more cases probably go unreported.
The signs and symptoms of LD occur in stages and involve a variety of tissues and organs, including the skin, joints, heart, and nervous system. Early infection (stage 1) consists of primary erythema migrans (EM), an annular skin rash that begins days to weeks after a tick bite. Hematogenous dissemination of spirochetes over subsequent days to weeks (stage 2) can result in multiple skin lesions (secondary EM), as well as meningitis, radiculoneuritis, atrioventricular block, myocarditis, and oligoarticular arthritis. Persistent infection (stage 3) occurs months to years after the initial exposure and can be associated with varying degrees of encephalopathy and encephalomyelitis, and persistent arthritis and rarely acrodermatitis chronica atrophicans.
Over the years, several laboratory tests have been developed and clinicians have a wide array of options for the direct detection of organisms in tissues, serologic detection of immune responses, and molecular detection of specific nucleic acid sequences and antigens. All of the various testing methodologies have their inherent advantages and limitations. Culture isolation of B. burgdorferi from clinical specimens is time consuming and requires long incubation period. In fact, isolation of B. burgdorferi from sites, such as cerebrospinal fluid (CSF) and synovial fluid is uncommon in part due to the small number of viable organisms present in these anatomic locations. Serologic test are by far the most common means of diagnosing LD. CDC recommends that all serum specimens for LD diagnosis be evaluated in a two-step process. The first step employs a sensitive serologic test, such as EIA. Specimens found to be negative are not tested further. All specimens with positive or equivocal results are tested by immunoblotting, using standardized criteria for interpretation. Most LD patients will seroconvert within 4-weeks of exposure. Clinical Laboratory Partners offers a highly sensitive and automated ELISA test that is based on C6 peptide derived from the VisE protein, which has been shown to be highly specific and immunogenic. All ELISA positive samples are retested with supplemental IgG and IgM western blots that are interpreted using the latest interpretive guidelines recommended by CDC.
References:
- Barbour, A. G. 1998. Fall and rise of Lyme disease and other Ixodes tick-borne
- Centers for Lyme Disease Control and Prevention. 2001 Lyme Disease—United States 1999. Morb. Mort. Wkly. Rep. 50:181-185.
- Willis Dawn 1991. Lyme Disease J. Neuroscience Nursing 23:211-219.
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