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EFFECT OF COTRIMOXAZOLE PROPHYLAXIS TAKEN BY HUMAN IMMUNODEFICIENCY VIRUS (HIV)–INFECTED PERSONS ON THE SELECTION OF SULFADOXINE-PYRIMETHAMINE–RESISTANT MALARIA PARASITES AMONG HIV-UNINFECTED HOUSEHOLD MEMBERS

The purpose of this prospective cohort study was to assess the effect of cotrimoxazole prophylaxis taken by human immunodeficiency virus (HIV)–infected persons on the selection of sulfadoxine-pyrimethamine (SP)–resistant malaria parasites among HIV-uninfected household members. A total of 2,567 HIV-uninfected persons from 605 households were followed and blood specimens were collected each time an episode of Plasmodium falciparum malaria was diagnosed. Study participants were living in households where HIV-infected persons were either taking (exposed) or not taking (unexposed) cotrimoxazole prophylaxis. From all malaria episodes diagnosed, 50% of the specimens were randomly selected and tested for the presence of five key mutations known to mediate resistance to SP (dihydrofolate reductase [dhfr] Asn-108, Ile-51, and Arg-59, and dihydropteroate synthase [dhps] Gly-437 and Glu-540). Plasmodium falciparum isolates were recovered from 163 specimens in the exposed households and 113 specimens in the unexposed households, with similar proportions containing the dhfr triple mutant (37% versus 45%; P = 0.18), the dhps double mutant (64% versus 62%; P = 0.81), and the dhfr/dhps quintuple mutant (30% versus 32%; P = 0.74). The HIV-uninfected persons living with HIV-infected household members taking cotrimoxazole prophylaxis had a lower incidence of malaria (incidence rate ratio [IRR] = 0.64, 95% confidence interval [CI] = 0.50–0.83, P = 0.001) and fewer malaria episodes due to parasites containing the dhfr/dhps quintuple mutant (IRR = 0.61, 95% CI = 0.41–0.91, P = 0.014). Cotrimoxazole prophylaxis taken by HIV-infected persons did not select for SP-resistant malaria parasites among HIV-uninfected household members, and was associated with a lower overall incidence of SP-resistant malaria among household members.

Received February 13, 2006. Accepted for publication March 28, 2006.

Acknowledgement: We thank the staff and clients of TASO, the Uganda Virus Research Institute-CDC laboratory, and the staff of CDC-Uganda for participating in the study.

Financial support: This study was supported by the Fogarty AIDS International Training and Research Program/University of California, Berkeley (1-D43-TW00003), the Fogarty International Center/ National Institutes of Health (TW00007), and the Centers for Disease Control and Prevention.

^* Address correspondence to Samuel S. Malamba, Division of Epidemiology, School of Public Health, University of California, 1918 University Avenue, Fourth Floor, Berkeley, CA 94720 and Centers for Disease Control and Prevention–Uganda, Global AIDS Program, National Center for HIV, STD and TB Prevention, c/o Uganda Virus Research Institute, PO Box 49, Entebbe, Uganda. E-mails: malambas{at}berkeley.edu and zcq2{at}ug.cdc.gov

Authors’ addresses: Samuel S. Malamba, Division of Epidemiology, School of Public Health, University of California, 1918 University Avenue, Fourth Floor, Berkeley, CA 94720 and CDC-Uganda, Global AIDS Program, National Center for HIV, STD and TB Prevention, c/o Uganda Virus Research Institute, PO Box 49, Entebbe, Uganda, Telephone: 256-41-320776, 256-752-790145, or 510-643-4922, Fax: 256-41-321457 or 510-643-4927, E-mails: zcq2{at}ug.cdc.gov and malambas{at}berkeley.edu. Jonathan Mermin, John R. Lule, Robert Downing, Ray Ransom, and Aminah Kigozi, Centers for Disease Control and Prevention–Uganda, Global AIDS Program, National Center for HIV, STD and TB Prevention, PO Box 49, Entebbe, Uganda. Arthur Reingold and Alan Hubbard, Division of Epidemiology, School of Public Health, University of California, Berkeley, CA 94720. Ben M. Hunt, Philip J. Rosenthal, and Grant Dorsey, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, CA 94110.

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