Lyme disease was first reported in 1977, following an unusual cluster of adults and children with oligoarticular arthritis in a certain neighborhood of Lyme, Connecticut. Subsequently, a multisystem disease was described and attributed to the spirochete Borrelia burgdorferi. Lyme disease manifests as a spectrum of skin, musculoskeletal, cardiac, and neurologic findings. It is a vector-borne disease following the bite of an Ixodes tick—usually the black-legged Ixodes scapularis, commonly known as the deer tick. The species Ixodes includes additional subspecies (eg, I. pacificus, I. dammini, and I. ricinus) that contribute to a worldwide distribution of the disease and is known to be endemic in North and South America, Europe, Asia, Africa, and Australia. Prenatal exposure to B. burgdorferi and the development of gestational borreliosis can result in maternal Lyme disease with placentitis and transplacental infection of the fetus and newborn.
In 2009, more than 38,000 cases of Lyme disease were reported to the Centers for Disease Control and Prevention. In the United States, 44 continental states reported cases of Lyme disease, with an incidence of 12.71 in 100,000 nationwide. No specific data for the number of pregnancy-related Lyme disease is available. Estimates for active infection after exposure to a deer-tick bite are only 1–3%. Presumably the number of infected pregnant women in the United States is small.
Transmission. The Ixodes tick lives a 2-year life cycle consisting of 3 life stages: larval, nymph, and adult. The preferred reservoirs for the larval and nymph tick are the white-footed field mouse and for the adult tick it is the white-tailed deer. The larval stage emerges from eggs in early summer and feeds on previously infected mice from which they acquire the B. burgdorferi spirochete. The infected nymph stage emerges the next spring and is the most likely source of human infection because the activity of the feeding nymph corresponds to the outdoor activity of humans in spring and summer. The adult tick may infect before laying eggs in summer and dying soon after.
Human spirochetemia. Following the tick bite, the incubation period of the spirochetes is 1–32 days with a median of 11 days, followed by the first clinical signs of disease. The disease is characterized by “early” and “late” manifestations. Early disease is in 2 stages. Spirochete dissemination is presumed to be facilitated by the surface of the organism binding to human plasminogen and subsequently binding to integrins, matrix glycosaminoglycans, and extracellular matrix proteins. These complexes may explain the propensity of the spirochetes to localize to collagen fibrils in the extracellular matrices of the heart, nervous system, and bone joints. Late Lyme disease occurs months to a year or more after dissemination.
Placentitis and transplacental disease. Before 1990, a number of case reports had confirmed the transplacental passage of B. burgdorferi by way of identification of spirochetes in placental tissues, ...
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