In this issue of Arthritis and Rheumatism, Weyand and Goronzy convincingly demonstrate circulating antibodies and proliferative T cell responses to Borrelia buvgdorferi in 18% of patients with reactive arthritis or Reiter's syndrome (RS) who came from an area of the Federal Republic of Germany where Lyme disease is endemic ( I ) . Antibodies to B burgdorferi were found in only 3% each of a well-matched control population and a group of patients with fibromyalgia. Evidence of Chlamydia trachomatis infections was found in 29% of the RS cohort, which is similar to findings of other studies (2,3); however, there was little overlap between patients with presumed sexuallyacquired reactive arthritis and those with evidence of B burgdorferi infection (1 patient only).
The clinical descriptions of these patients, as well as the high incidence of HLA-B27 in this group, strongly support the diagnoses of RS rather than Lyme disease. Although these observations will need to be confirmed in other endemic areas, it appears likely that the spirochete that causes Lyme disease may also trigger a reactive arthritis in the genetically susceptible (HLA-B27 positive) host. Thus, in addition to the previously known gastrointestinal and genitourinary triggers (21, B burgdorferi now joins the human immunodeficiency virus ( 4 3 ) as another recently recognized infectious agent that must be considered in the