[Lyme borreliosis: underdiagnosed?--overtreated?].
Lyme borreliosis is a tick-borne mediated systemic inflammatory disorder caused by a newly recognized spirochete, Borrelia burgdorferi. Its clinical hallmark is an early expanding skin lesion, erythema chronicum migrans (ECM) which may be followed weeks to months later by neurological, cardiac, or joint abnormalities. Symptoms may be associated with any of these systems alone or in combination. All stages of Lyme borreliosis may respond to antibiotics, but treatment of early disease is the most successful. Foci of Lyme borreliosis are widely distributed within the USA and Europe and the disorder appears to be worldwide. Although there are some variations in clinical expression between the USA and Europe, the various syndromes, Erythema migrans (Afzelius), Meningopolyneuritis [Garin-Bujadoux, Bannwarth (MPN)] are now generally subsumed under the name Lyme borreliosis. B. burdorferi is also responsible for an early skin lesion, Borrelia lymphozytom [Lymphadenosis cutis benigna (LCB)], and for a late one, Acrodermatitis chronica atrophicans (ACA), both seen primarily in Europe. In the USA joint abnormalities are the leading abnormalities in the later manifestation of the disease. Lyme borreliosis grew up in the last ten years as a new nosologic entity with some aspects for an infectious etiology of rheumatic disease.
Universitäts-Kinderklinik Freiburg.
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W
Peuckert
D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D015748:Borrelia burgdorferi Group / Q000276:immunology; D002648:Child; D003937:Diagnosis, Differential; D005500:Follow-Up Studies; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis; D008193:Lyme Disease / Q000175:diagnosis* / Q000188:drug therapy
D000900:Anti-Bacterial Agents; D007074:Immunoglobulin G; D007075:Immunoglobulin M
Lyme-Borreliose: unterdiagnostiziert?--übertherapiert?