Study Provides Greater Understanding of Lyme Disease-Causing Bacteria

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Lyme disease in the U.S. is caused by the tickborne bacteria Borrelia burgdorferi and usually begins with a skin lesion, after which the bacteria spread throughout the body to the nervous system, heart or joints. About 60 percent of untreated individuals develop arthritis, which affects the knees in particular. Lyme disease usually responds well to antibiotic therapy, but in rare cases arthritis can persist for months or years after treatment, a rare condition known as antibiotic-refractory Lyme arthritis. Joint fluid usually tests negative for B burgdorferi after treatment, indicating that joint inflammation may persist even after the bacteria has been eradicated.

Two genetic marker systems are used to correlate the variation of this bacterial strain with clinical outcomes: OspC typing divides B burgdorferi strains into 21 types, while the ribosomal RNA intergenic spacer type (RST) system divides them into just three groups, with certain RST groups corresponding uniquely to specific OspC types.

A new study led by Allen Steere of Massachusetts General Hospital and Harvard Medical School analyzed joint fluid samples from 124 patients with Lyme arthritis who were seen over a 30-year period. It identified B. burgdorferi strains in the joints of patients with Lyme arthritis and found that the genotype frequencies in joints reflected those in skin lesions. However, RST1 strains were the most frequent in patients with antibiotic-refractory arthritis. The study was published in the July issue of Arthritis & Rheumatism.

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