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Lyme disease is a zoonotic infection and 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 that follows the bite of an Ixodes tick, usually the black-legged Ixodes scapularis, commonly known as the deer tick. Lyme disease has a worldwide distribution and is known to be endemic in the Americas, 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 possible transplacental infection of the fetus and newborn.


In 2017, a total of 42,743 cases of Lyme disease were reported and confirmed by the Centers for Disease Control and Prevention with an incidence of 106.6 cases per 100,000 nationwide. No specific data on pregnancy-related Lyme disease is available; however, the number of infected pregnant women in the United States is presumably small. Estimates for active infection after exposure to a deer-tick bite are only 1% to 3%.


  1. Transmission. The Ixodes tick lives a 2-year life cycle consisting of 3 stages: larval, nymph, and adult. The preferred reservoirs are the white-footed field mouse for the larval and nymph tick and the white-tailed deer for the adult tick. 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 in the next spring and is the most likely source of human infection as its activity corresponds to outdoor human activities in spring and summer. The adult tick may infect before laying eggs in summer and dying soon after.

  2. Human spirochetemia. After the tick bite, the incubation period of the spirochetes is 1 to 32 days, with a median of 11 days. The disease is characterized by “early” and “late” manifestations. Early disease occurs in 2 stages (early localized and early disseminated). 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 joints. Late Lyme disease occurs months to a year or more after dissemination.

  3. Placentitis and transplacental disease. Before 1990, a number of case reports had confirmed the transplacental passage of B burgdorferi by identifying spirochetes in placental tissues, umbilical vessels, fetal brain, heart, spleen, kidneys, bone marrow, liver, and adrenal glands. However, several recent clinical, serologic, and epidemiologic studies have failed to confirm a causal association between Lyme disease in ...

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