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Am. J. Trop. Med. Hyg., 73(3), 2005, pp. 520-522
Copyright © 2005 by The American Society of Tropical Medicine and Hygiene

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SHORT REPORT


ASYMPTOMATIC CRYPTOSPORIDIUM HOMINIS INFECTION AMONG HUMAN IMMUNDEFICIENCY VIRUS–INFECTED PATIENTS IN TANZANIA

ERIC R. HOUPT*, OLUMA Y. BUSHEN, NOEL E. SAM, ANITA KOHLI, AMON ASGHARPOUR, CHERIE T. NG, DAVID P. CALFEE, RICHARD L. GUERRANT, VENANCE MARO, SENDUI OLE-NGUYAINE, AND JOHN F. SHAO
Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, Virginia; Kilimanjaro Christian Medical Centre, Moshi, Tanzania; Division of Infectious Diseases, Mount Sinai School of Medicine, New York, New York

 

ABSTRACT

Few data exist on the relative importance of individual Cryptosporidium species in acquired immunodeficiency syndrome cryptosporidiosis. We characterized 127 inpatients infected with human immunodeficiency virus (HIV) in Tanzania for their CD4 cell count and by stool analysis, including Cryptosporidium immunofluorescence and polymerase chain reaction-restriction fragment length polymorphism. Cryptosporidium was detected in patients both with and without diarrheal symptoms (defined as ≥ 3 liquid stools/day, 11 of 61 versus 11 of 66; P = not significant) and was a marker for low CD4 cell count (median = 124/µL versus 212/µL in Cryptosporidium-negative patients; P < 0.04). Cryptosporidium hominis was the predominant species in this region and was associated with a longer duration of symptoms, a higher rate of asymptomatic infection, and a lower CD4 cell count versus C. parvum-infected patients (P < 0.05). This study suggests there may be important differences in the natural history of Cryptosporidium infection in HIV-infected persons depending on parasite species.

Received June 23, 2004. Accepted for publication November 11, 2004.

Acknowledgments: We thank Edward Mushi, Sr., Ruwaichi Uiso, and the other nurses involved in this study; Stanislaus Siriwa, Richard Tarimo, and Eline Ngomuo and the other clinical laboratory technicians; and all the patients who participated in this work. We also thank Dr. William Petri (University of Virginia) for helpful discussions and David Lyerly (Techlab, Inc.) for the E. histolytica II ELISA kits.

Financial support: This study was supported by the National Institutes of Health (grant U19 AI056872-01) and the Virginia Commonwealth Technology Research Fund.

Disclosure: None of the authors has a commercial or other association that might pose a conflict of interest.

* Address correspondence to Eric R. Houpt, Division of Infectious Diseases and International Health, University of Virginia, PO Box 801340, MR4 Building Room 2144, Charlottesville, VA 22908-1340. E-mail: erh6k{at}virginia.edu

Authors’ addresses: Eric R. Houpt, Oluma Y. Bushen, Anita Kohli, Amon Asgharpour, Cherie T. Ng, and Richard L. Guerrant, Division of Infectious Diseases and International Health, University of Virginia, PO Box 801340, MR4 Building Room 2144, Charlottesville, VA 22908-1340, Telephone: 434-243-9326, Fax: 434-924-0075, E-mails: erh6k{at}virginia.edu, ob3d{at}vurginia.edu, ak7t{at}virginia.edu, aa3z{at}virginia.edu, ctn8d{at}virginia.edu, and rlg9a{at}virginia.edu. Noel E. Sam, Venance Maro, Sendui Ole-Nguyaine, and John F. Shao, Kilimanjaro Christian Medical Centre, Moshi, Tanzania, E-mails: nsam{at}kcmc.ac.tz, venmaro{at}yahoo.co.uk, solengudr{at}yahoo.com, and jshao{at}kcmc.ac.tz. David P. Calfee, Division of Infectious Diseases, Mount Sinai School of Medicine, New York, NY 10029, E-mail: David.Calfee{at}msnyuhealth.org.




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