INTRODUCTION

Lyme disease is a tick-borne illness caused by three pathogenic species of the spirochete Borrelia burgdorferi sensu lato. B. burgdorferi is the sole cause of the disease in the United States. All three pathogenic species, B. burgdorferi, B. afzelii and B. garinii, occur in Europe, and the latter two species have been identified in Asia. Lyme disease has a broad spectrum of clinical manifestations, and it also varies in severity due, in part, to differences in the infecting species.

Lyme disease was first described in 1977 as "Lyme arthritis" in studies of a cluster in Connecticut of children who were thought to have juvenile rheumatoid arthritis [1]. The multisystem nature of the infection became clear as involvement of other systems was subsequently identified [2,3].

The clinical manifestations of Lyme disease in adults will be reviewed here. Issues related to bacteriology, epidemiology, diagnosis, and therapy, and more detailed descriptions of the various clinical manifestations of Lyme disease, are discussed separately in the appropriate topic reviews. The clinical manifestations of Lyme disease in children are reviewed separately. (See "Lyme disease: Clinical manifestations in children".)

Other tick-borne diseases are reviewed elsewhere. (See "Clinical manifestations and diagnosis of Rocky Mountain spotted fever" and "Human ehrlichiosis and anaplasmosis" and "Southern tick-associated rash illness (STARI)" and "Clinical manifestations, diagnosis, treatment, and prevention of babesiosis".)

CLINICAL STAGES

The clinical manifestations of Lyme disease can generally be divided into three phases: early localized, early disseminated, and late disease (table 1). However, the clinical features of each stage can overlap and some patients present in a later stage of Lyme disease without a history of prior signs or symptoms suggestive of earlier Lyme disease [4]: