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Bacillary Angiomatosis and Bacillary Splenitis in Immunocompetent Adults

Jordan W. Tappero, MD, MPH; Jane E. Koehler, MD; Timothy G. Berger, MD; Clay J. Cockerell, MD; Tzong-Hae Lee, PhD; Michael P. Busch, MD, PhD; Daniel P. Stites, MD; Janet Mohle-Boetani, MD; Arthur L. Reingold, MD; and Philip E. LeBoit, MD
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From the University of California, San Francisco, California; the University of California, Berkeley, California; the University of Texas Southwestern Medical Center at Dallas, Texas; the Irwin Memorial Blood Centers, San Francisco, California; the Centers for Disease Control, Atlanta, Georgia. Requests for Reprints: Jordan W. Tappero, MD, MPH, Centers for Disease Control and Prevention, Mail Stop (C09), 1600 Clifton Road, NE, Atlanta, GA 30333. Acknowledgments: The authors thank Drs. Gregory L. Rumore, Francis X. Burch, Merle W. Delmer, Joan King-Angel, Gail Plecash, and Carol E. Wratten for helping to obtain blood and tissue samples and for providing clinical information on Patients 2, 4, and 5. They also thank Lorrie Epling and Thomas McHugh for technical assistance. Grant Support: By a National Research Service Award (AR07175-15) and a Dermatology Foundation Research Fellowship (Dr. Tappero) and by the University of California, San Francisco (UCSF) AIDS Clinical Research Center and the John D. and Catherine T. MacArthur Foundation (Dr. Koehler).

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1993;118(5):363-365. doi:10.7326/0003-4819-118-5-199303010-00007
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Bacillary angiomatosis and bacillary peliosis have been described in patients with human immunodeficiency virus (HIV) infection and drug-induced immunosuppression. Patients with these vascular lesions in the absence of profound immunodeficiency have not been well characterized. We studied five patients with histologically confirmed bacillary angiomatosis or bacillary splenitis without clinical immunodeficiency. Studies to detect HIV infection, immunologic defects, and presence of Rochalimaea species DNA in infected tissues were done. Cell cultures were negative for HIV-1 replication, and HIV-1 DNA was not detected. Results of lymphocyte subsets and activation, neutrophil oxidative burst, skin testing to mumps antigen, and assays for quantitative immunoglobulins and complement were normal. DNA amplification and sequencing confirmed infection by Rochalimaea henselae, even in tissue showing bacillary splenitis without peliosis. Bacillary angiomatosis and bacillary splenitis may occur in the absence of demonstrable immunodeficiency. On the basis of the therapeutic response of these five patients, we recommend treatment with erythromycin or doxycycline for a minimum of 6 weeks.


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Figure 1.
Amplification of Rochalimaea DNA.Rochalimaea henselaeR. henselae

DNA was extracted from formalin-fixed, paraffin-embedded, or frozen biopsy specimens from Patients 2 and 4, and amplified followed by electrophoresis on a 1.5% agarose gel and amplification. Lanes 1 and 8 contain DNA size standards. The DNA template added for each polymerase chain reaction tube: lane 2, ; lane 3, complete reaction mixture without DNA template; lane 4, DNA extracted from frozen skin biopsy tissue of Patient 4 when bacillary angiomatosis was diagnosed; lane 5, DNA from frozen skin biopsy of a Kaposi sarcoma lesion, extracted at the same time as the DNA in lane 4; lane 6, DNA extracted from formalin-fixed, paraffin-embedded splenic tissue of Patient 2 at the time of bacillary splenitis diagnosis; and lane 7, DNA from formalin-fixed, paraffin-embedded, control splenic tissue, extracted at the same time as the DNA in lane 6. A fragment of approximately 300 base pairs was amplified from reference strain DNA and from the DNA extracted from both the frozen and paraffin-embedded tissue specimens of Patients 2 and 4. There was no similar amplification from the control tubes without added DNA, from the Kaposi sarcoma specimen, or from the control spleen specimen. Numbers at the right and left indicate the number of base pairs of the DNA standards.

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