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THE RISK OF MALARIAL INFECTIONS AND DISEASE IN PAPUA NEW GUINEAN CHILDREN

In a treatment re-infection study of 206 Papua New Guinean school children, we examined risk of reinfection and symptomatic malaria caused by different Plasmodium species. Although children acquired a similar number of polymerase chain reaction–detectable Plasmodium falciparum and P. vivax infections in six months of active follow-up (P. falciparum = 5.00, P. vivax = 5.28), they were 21 times more likely to develop symptomatic P. falciparum malaria (1.17/year) than P. vivax malaria (0.06/year). Children greater than nine years of age had a reduced risk of acquiring P. vivax infections of low-to-moderate (>150/µL) density (adjusted hazard rate [AHR] = 0.65 and 0.42), whereas similar reductions in risk with age of P. falciparum infection was only seen for parasitemias > 5,000/µL (AHR = 0.49) and symptomatic episodes (AHR = 0.51). Infection and symptomatic episodes with P. malariae and P. ovale were rare. By nine years of age, children have thus acquired almost complete clinical immunity to P. vivax characterized by a very tight control of parasite density, whereas the acquisition of immunity to symptomatic P. falciparum malaria remained incomplete. These observations suggest that different mechanisms of immunity may be important for protection from these malaria species.

Received December 3, 2006. Accepted for publication February 1, 2007.

Acknowledgments: We thank the children for participating in the study; the guardians, teachers, and support staff at Mugil and Megiar schools for their support; Livingstone Tavul, Mary Goroti, and Mugil health centre staff for assistance with the field work; and Kay Baea, Lina Lorri, and Moses Lagog for reading the blood films and David T. McNamara for technical assistance with LDR-FMA.

Financial support: This study was supported by the National Health and Medical Research Council of Australia (NHMRC; grants 215201 and 406601), the National Institutes of Health (grant AI063135), and the United States Veterans Association. Peter A. Zimmerman was supported by the National Institutes of Health (grants AI-46919 and AI-52312). Jennifer L. Cole-Tobian was supported by grant AI07024. Louis Schofield is an International Research Scholar of the Howard Hughes Medical Institute. James G. Beeson was supported by an NHMRC Career Development Award and a Miller Fellowship of the Walter and Eliza Hall Institute.

^* Address correspondence to Ivo Mueller, Papua New Guinea Institute of Medical Research, PO Box 378, Madang, MAD 511, Papua New Guinea. E-mail: pngimr_ivo{at}datec.net.pg

Authors’ addresses: Pascal Michon, Elijah Dabod, Jennifer Igu, Melinda Susapu, Nandao Tranogka, John C. Reeder, and Ivo Mueller, Papua New Guinea Institute of Medical Research, PO Box 378, Madang, MAD 511, Papua New Guinea. Jennifer Cole-Tobian, Peter A. Zimmerman, and Christopher King, Center for Global Health and Diseases, Case Western Reserve University School of Medicine, Wolstein Research Building, 4-125, Cleveland, OH 44106-7286. Sonja Schoepflin, Swiss Tropical Institute, Socinstrasse, 4002 Basel, Switzerland, James G. Beeson and Louis Schofield, Walter and Eliza Hall Institute, 1G Royal Parade, Parkville, Victoria 3050, Australia.

Reprint requests: Ivo Mueller, Papua New Guinea Institute of Medical Research, PO Box 378, Madang, MAD 511, Papua New Guinea, Telephone: 675-8522909, Fax: 675-852-3289, E-mail: pngimr_ivo{at}datec.net.pg.

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