Abstract

Bacillary angiomatosis (BA) was first described by Stoler and colleagues in 1983 in an HIV-infected patient with multiple subcutaneous nodules. Numerous bacilli were observed by Warth in-Starry staining of the biopsicd nodules, and the subcutaneous masses resolved during erythromycin therapy. Subsequently, the BA bacilli visualized using the Warthin-Stilrry silver stain werc noted to have an appearance similar to that of the cat scratch disease (CSD) bacillus.:!') The BA bacillus remained refractory to isolCltion attempts for many years, impeding identification efforts. Studies of bacterial DNA extracted from BA lesions subsequently identified the bacillus as closely related to Bartollclla (Rochalimaea) qllinlmza,4 and after isolation of the bacillus from the blood of hvo HIV-infected patients without SA,' the organism was further characterized and named B. !Iel/selae in 1992.'; The Bartol1ella genus has expanded from a single species in 1993 to >20 species. The BA bacillus was directly cultivated from cutaneous BA lesions for the first time in 1992, which led to the identification of two species of the genus Bartol/tila as causative agents of SA: B. IU!Jlsdae or B. quiutlJJla.· To date, the Bartoella species causing BA has been identified in more than 60 AIDS patients; in all these cases, only two species have been found to cause BA or bacillary peliosis hepatis.M,9 Interestingly, the two different species differ in the predilection to form a specific type of lesion. Bartouella hel/selae, but never B. quilltaua, has been associated with peliosis of the liver or spleen, or both.'} Bartoella htllselnc illso is ilssociilted with lymphadenopathy, and B. quilltal1a with subcutilneous nodules in late stage HIV infection.':I In patients with severe immunosuppression due to HIV infection, organ transplantation or chemotherapy, infection with B. hcnse/ac or B. quintal/a can produce unique vascular proliferative lesions known as BA.IO,1l BA occurs as a late manifestation of HIV infection; in a study of 42 patients with BA, the medirm CD4 lymphocyte count was 21 cells/mm~.12 These vtlsculnr proliferative lesions cnn form in many different organs, including skin, bone, brain parenchyma, lymph nodes, bone marrow and gastrointestinal and respiratory tract. A histopathologically different vascul<lr proliferative response to Bartvl/dla infection, known as bacillary peliosis hep<ltis (BP), is seen in the liver and spleen. One notable aspect of focal Barlolldla infection, especially cutaneous BA, is the chronic, indolent nature of the disease: lesions may be present for as long <IS 1 year before a dielgnosis is made.M,I:! HIV-infected individuals also can develop manifesteltions of Barto1lella infection other than vascular proliferation. Bacteremia with 14 or without• endocarditis has been reported in HIV-infected individuals, in the absence of focal BA or BP involvement. Patients with higher CD4 cell counts can develop focal necrotizing infections due to B. Irellsdac in lymph nodes, liver or spleen that have an appearance similar to that of CSD in immunocompetent individuals. Rarely, HIV-infccted individuals with CD4 cell counts <50 can manifest this necrotizing lymph<ldenitis without vascular proliferation. ls A celse-control study comparing clinical findings of 42 patients with BA and/or BP compared \vith 84 control patients found that case-patients were

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