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Biology of infection with Borrelia burgdorferi

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W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.idc.2007.12.013

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  1. Intramural NIH HHS [Z99 AI999999] Funding Source: Medline
  2. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [Z01AI000917] Funding Source: NIH RePORTER

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The spirochete Borrelia burgdorferi is a tick-borne obligate parasite whose normal reservoir is a variety of small mammals [1]. Although infection of these natural hosts does not lead to disease, infection of humans can result in Lyme disease as a consequence of the human immunopathologic response to B burgdoferi [2,3]. Consistent with the pathogenesis of Lyme disease, bacterial products that allow B burgdorferi to replicate and survive, rather than true virulence factors, seem to be primarily what is required for the bacterium to cause disease in a susceptible host. In support of this idea, the genome sequence of 1331, the type strain of B burgdorferi sensu stricto [4,5], revealed that the bacterium lacks factors common to many bacterial pathogens, such as lipopolysaccharide, toxins, and specialized secretion systems. In this article, the authors describe the basic biology of B burgdorferi and review some of the bacterial components required for infection of and survival in the mammalian and tick hosts.

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