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Primary Cutaneous B-Cell Lymphoma and Borrelia burgdorferi Infection in Patients From the Highlands of Scotland

Goodlad, John R. M.D.; Davidson, Marilyn M. F.R.C.Path.; Hollowood, Kevin M.D.; Ling, Claire M.Sc.; MacKenzie, Carol M.N.C.; Christie, Irene M.N.C.; Batstone, Paul J. B.Sc.; Ho-Yen, Darrel O. M.D.

The American Journal of Surgical Pathology: September 2000 - Volume 24 - Issue 9 - p 1279-1285
Original Articles

Although a link beteen primary cutaneous B-cell lymphoma (PCBCL) and Borrelia burgdorferi infection has long been suspected, previous studies have not demonstrated a significant association. The authors looked for evidence of B. burgdorferi in 20 cases of PCBCL from the Scottish Highlands, an area with endemic Lyme disease, and compared their findings with those in 40 control patients (20 undergoing wide reexcision at sites of malignant melanoma and 20 biopsies of inflammatory dermatoses). All studies were performed on formalin-fixed, paraffin-embedded tissues. The cases of PCBCL were classified according to criteria described by the European Organization for Research and Treatment of Cancer Cutaneous Lymphoma Project Group using a combination of morphology, immunohistochemistry, and seminested polymerase chain reaction (PCR) for immunoglobulin heavy chain gene rearrangement. A nested PCR was performed on deoxyribonucleic acid (DNA) extracts from the lymphoma and control cases using primers to a unique conserved region of the B. burgdorferi flagellin gene. B. burgdorferi-specific DNA was detected in seven of 20 lymphoma cases (five of 12 marginal zone lymphomas, one of five primary cutaneous follicle center cell lymphomas, one of three diffuse, large B-cell lymphomas of the leg) and in one melanoma reexcision patient of 40 control subjects. The relationship between B. burgdorferi and PCBCL was significant when compared with the control groups separately (p <0.05) or in combination (p <0.01). These results provide strong evidence to support the concept of B. burgdorferi-driven lymphomagenesis in the skin.

From the Departments of Pathology (J.R.G., C.M., I.C., P.J.B.) and Microbiology (M.M.D., C.L., D.O.H.-Y.), Raigmore Hospital, Inverness, Scotland; and the Department of Cellular Pathology (K.H.), The John Radcliffe Hospital, Oxford, U.K.

Supported by a grant from the Research and Development Committee Endowment Fund, Raigmore Hospital, Inverness, Scotland.

Address correspondence and reprint requests to John R. Goodlad, MD, Department of Pathology, Raigmore Hospital, Highland Acute Hospitals NHS Trust, Old Perth Road, Inverness, IV2 3UJ Scotland; e-mail:

© 2000 Lippincott Williams & Wilkins, Inc.