BORRELIOOSITUTKIMUS 2004

[Bb]

Lähettäjä: Soijuv Lähetetty: 19.4.2004 7:57

J. Clin. Invest. 113:1093-1101 (2004). doi:10.1172/JCI200421681.
Copyright ©2004 by the American Society for Clinical Investigation
The emergence of Lyme disease
Allen C. Steere, Jenifer Coburn and Lisa Glickstein

Abstract

Since its identification nearly 30 years ago, Lyme disease has continued to spread, and there have been increasing numbers of cases in the northeastern and north central US. The Lyme disease agent, Borrelia burgdorferi, causes infection by migration through tissues, adhesion to host cells, and evasion of immune clearance. Both innate and adaptive immune responses, especially macrophage- and antibody-mediated killing, are required for optimal control of the infection and spirochetal eradication. Ecological conditions favorable to the disease, and the challenge of prevention, predict that Lyme disease will be a continuing public health concern.

In the late 20th century, Lyme disease, or Lyme borreliosis, was recognized as an important emerging infection (1). It is now the most commonly reported arthropod-borne illness in the US and Europe and is also found in Asia (2). Since surveillance for Lyme disease was begun in the US by the Centers for Disease Control and Prevention, the number of reported cases has increased steadily, and in the year 2000, more than 18,000 cases were reported (3).

Lyme disease was recognized as a separate entity in 1976 because of geographic clustering of children in the Lyme, Connecticut, area who were thought to have juvenile rheumatoid arthritis (4, S1 [http://www.jci.org/cgi/content/full/113/8/1093/DC1]). It then became apparent that Lyme arthritis was a late manifestation of an apparently tick-transmitted, multisystem disease, of which some manifestations had been recognized previously in Europe and America (S2?S6 [http://www.jci.org/cgi/content/full/113/8/1093/DC1]). In 1981, Burgdorfer and colleagues discovered a previously unidentified spirochetal bacterium, called Borrelia burgdorferi, in a nymphal Ixodes scapularis (also called Ixodes dammini) tick (S7 [http://www.jci.org/cgi/content/full/113/8/1093/DC1]). This spirochete was then cultured from patients with early Lyme disease, and patients? immune responses were linked conclusively with that organism, proving the spirochetal etiology of the infection (S8, S9[http://www.jci.org/cgi/content/full/113/8/1093/DC1]).

Based on genotyping of isolates from ticks, animals, and humans, the formerly designated B. burgdorferi has now been subdivided into multiple Borrelia species, including three that cause human infection. In the US, the sole cause is B. burgdorferi (S10 [http://www.jci.org/cgi/content/full/113/8/1093/DC1]). Although all three species are found in Europe, most of the disease there is due to Borrelia afzelii or Borrelia garinii, and only these two species seem to be responsible for the illness in Asia (S11, S12 [http://www.jci.org/cgi/content/full/113/8/1093/DC1]). During the 20th century, conditions evolved in the northeastern US that were especially favorable for enzootic B. burgdorferi infection (5). In this setting, Lyme disease continues to flourish and spread.

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