Although descriptions of infections caused by Bartonella (formerly Rochalimaea), such as Oroya fever, trench fever, and cat-scratch disease (CSD), have existed for more than 50 years, much of the current understanding of Bartonella-associated infections has resulted from the AIDS epidemic. In 1983, Stoler et al(94) provided the first report of a Bartonella-associated infection in an HIV-infected individual. This report described an AIDS patient from New York who developed multiple subcutaneous vascular nodules that contained numerous bacillary organisms visualized by electron microscopy. Additional reports in the late 1980s described patients with similar cutaneous lesions, and these vascular proliferative lesions became known as bacillary angiomatosis (BA).(52) During this time, however, investigators could not cultivate an organism from these lesions, and the cause remained unidentified. In a December 1990 issue of the New England Journal of Medicine, separate groups of investigators respectively described three key new findings: (1) the close relationship of a DNA sequence from the bacillus in BA tissue to the agent of trench fever, Rochalimaea quintana; (2) the isolation of a small, fastidious, gramnegative rod from patients with relapsing bacteremia; and (3) the association of a small bacillus with the unusual histopathologic entity of peliosis hepatis in the livers of HIV-infected patients.(76, 81, 88) These three research groups soon realized that their separate findings involved the same organism. This newly-recognized bacillary organism, which was subsequently named Rochalimaea henselae,(79 102) was initially presumed to be the sole agent of BA. In 1992, however, Kcehler et al(47) became the first group to isolate organisms from BA lesions, and in this process demonstrated that either R. quintana or R. henselae can cause BA. The four species belonging to the genus of Rochalimaea were moved to the genus of Bartonella in 1993 after genetic studies showed the close relationship between the Rochalimaea species and B. bacilliformis, the original member of the genus Bartonella.(14) More recently, the genus of Grahamella was merged with the genus of Bartonella, and at present, nine cultivated species belong to the genus Bartonella.(11) Four of these species, B. bacilliformis, B. henselae, B, quintana, and B. elizabethne, have been documented to be pathogenic in humans. Four species, B. vinsonii, B. grahamii, B, taylorii, and B. doshine, were isolated from small wild mammals, and B. clarridgeiae was isolated from a domestic cat.(3, 10, 26, 51) In addition, one group recently isolated a subspecies of B. vinsonii from a dog with endocarditis.(13) The spectrum of diseases caused by Bartonella has rapidly expanded to include BA(47, 81) bacillary peliosis,(76, 102) relapsing bacteremia,(59, 88) endocarditis,(28, 33) (90, 91) and "urban trench fever."(92) Moreover, in 1995 Regnery et al(80) demonstrated antibodies to Bartonella species in a panel of banked sera from immunocompetent patients with a clinical diagnosis of CSD, thus contradicting the initial belief that Afipia felis was the causative agent of CSD. Subsequently, B. henselae was isolated from the lymph nodes of two patients with apparent CSD and B. henselae DNA was detected by polymerase chain reaction (PCR) in specimens from patients with CSD.(2, 31) In addition, the domestic cat was identified as the major reservoir for B. henselae.(45) Taken together, these data from 1992 to 1994 convincingly identified B. henselae, not A. felis, as the predominant causative organism of CSD. Bartonella species represent a fascinating group of emerging pathogens. This article presents a summary of the manifestations of human Bartonella infections identified at present in North America and in Europe, but will not discuss B. bacilliformis, an infection predominantly limited to South America. Although considerable knowledge of Bartonella-associated infections has been gained, much data remain to be gathered to better define disease spectrum, prevalence, maintenance, and mode of transmission.