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Article
September 1997

Borrelia burgdorferi DNA and Borrelia hermsii DNA Are Not Associated With Morphea or Lichen Sclerosus et Atrophicus in the Southwestern United States

Author Affiliations

Houston, Tex

4.112 McCullough Bldg, G-83 University of Texas Medical Branch Galveston, TX 77555-0783

Arch Dermatol. 1997;133(9):1174. doi:10.1001/archderm.1997.03890450126024
Abstract

Borrelia burgdorferi, the causal agent of Lyme disease, has been implicated as the causative agent for some types of morphea by serologic (enzyme-linked immunosorbent assay) and Western blot analyses. Furthermore, spirochetal organisms have been found in lesions of morphea and lichen sclerosus et atrophicus (LSA) by histological methods.1Borrelia burgdorferi also has been reported2 as the causative agent of morphea and LSA using the polymerase chain reaction technique of DNA amplification.

Methods.  In this study, we analyzed 27 paraffinembedded skin biopsy specimens of patients from south-eastern Texas with morphea (n=13), LSA (n=13), and morphea-LSA overlap (n=1) for B burgdorferi DNA using polymerase chain reaction. Eleven paraffin-embedded biopsy specimens of inflammatory dermatoses and 2 snap-frozen fresh samples of normal skin served as negative controls. DNA samples obtained from B burgdorferi and Borrelia hermsii (American Type Culture Collection, Rockville, Md) at a density of 10 000 spirochetes per milliliter (determined

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