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Applied and Environmental Microbiology, August 2008, p. 5008-5014, Vol. 74, No. 16
0099-2240/08/$08.00+0 doi:10.1128/AEM.00479-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Gary P. Wormser,2 and
Ira Schwartz1
Department of Microbiology and Immunology, New York Medical College, Valhalla, New York 10595,1 Division of Infectious Diseases, Department of Medicine, New York Medical College, Valhalla, New York 105952
Received 22 February 2008/ Accepted 24 May 2008
Lyme borreliosis, the most commonly reported vector-borne disease in North America, is caused by the spirochete Borrelia burgdorferi. Given the extensive genetic polymorphism of B. burgdorferi, elucidation of the population genetic structure of the bacterium in clinical samples may be relevant for understanding disease pathogenesis and may have applicability for the development of diagnostic tests and vaccine preparations. In this investigation, the genetic polymorphism of the 16S-23S rRNA (rrs-rrlA) intergenic spacer and ospC was investigated at the sequence level in 127 clinical isolates obtained from patients with early Lyme borreliosis evaluated in suburban New York City. Sixteen distinct rrs-rrlA and 16 distinct ospC alleles were identified, representing virtually all of the genotypes previously found in questing Ixodes scapularis nymphs in this region. In addition, a new ospC group was identified in a single patient. The strong linkage observed between the chromosome-located rrs-rrlA and plasmid-borne ospC genes suggests a clonal structure of B. burgdorferi in these isolates, despite evidence of recombination at ospC.
Published ahead of print on 6 June 2008.
Present address: School of Medicine, St. George's University, Bayshore, NY 11706.
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