![]() 10 During this time, it was reported that CSD skin test antigen contained Bartonella nucleic acid sequences. Later, an immunofluorescent antibody serologic test developed for BA was positive in 36 of 41 (88%) serum samples from persons with suspected CSD, compared with only 6% among healthy controls 9 findings soon corroborated among CSD patients in Connecticut. 6 Other reports described morphologically similar-appearing organisms from patients with a vascular abnormality of the liver known as peliosis hepatitis 7 and febrile bacteremia, 8 subsequently noted to be caused by both B. 4, 5 In 1990, molecular probe techniques suggested that BA was caused by a bacterium similar to Bartonella quintana. First, in 1983, Warthin–Starry staining revealed small bacilli among 34 of 39 lymph node samples from patients with CSD and in subcutaneous nodules from a patient with AIDS with a syndrome later recognized as BA. 3 A series of consecutive and sometimes overlapping discoveries were made. It took over 40 years for the etiologic agent of CSD to be identified after its first clinical description in a French boy seen in 1931. These and the continuing descriptions of other clinical syndromes caused by Bartonella extend our current understanding of this genus beyond the previously known trench fever (so named as a complication of trench warfare in World War I) 1 and bartonellosis (a serious febrile illness endemic in the high valleys of the Andes mountains 2). In this time, the widespread use of serology and molecular testing has revealed the ecological and clinical breadth of cat scratch disease (CSD) and of bacillary angiomatosis (BA), an entity seen mainly among the immunocompromised. The Family Bartonellaceae, and its lone genus, Bartonella, has emerged since the 1990s as an instructive example of how the clinical expression of disease can depend substantially on the infecting species, the immune status of the infected, the vector and their interrelationship. No preventive measures have been developed beyond suggestions to avoid at-risk behavior with known vectors. Further, the clinical management for cat scratch disease in particular is quite variable among clinicians, reflecting a poor evidence base. Though not completely understood, it appears that specific immune-modulated interactions between the infecting species and host-related factors play a major role in the observed breadth of human clinical syndromes associated with Bartonellae, the large differences in immunopathologic features of tissue samples among different syndromes and potentially the varied responses to antimicrobial therapy. ![]() A large number of reservoirs and vectors involved with Bartonella propagation and transmission to humans have been identified cats and various arthropods remain the most well-studied to date. ![]() Subsequently, widespread use of modern diagnostic methods revealed the broad ecologic niche of this organism and greatly expanded our knowledge of the epidemiology and clinical presentations associated with this genus. In the 1990s, and in parallel, cat scratch disease and bacillary angiomatosis were definitively linked to Bartonella species. Since the early 1900s, Bartonella species were known only to cause human disease resulting from very restricted geographic (bartonellosis) or environmental influences (“trench fever”).
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