The Risk of Malarial Infections and Disease in Papua New Guinean Children

Abstract

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/microL) 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/microL (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.

Naturally acquired Duffy-binding protein-specific binding inhibitory antibodies confer protection from blood-stage Plasmodium vivax infection

“…Overall, however, children in this age group from this study area were protected against high levels of P. vivax parasitemia and clinical vivax malaria (13). This suggests that by the time children have reached school age, most have acquired protection against P. vivax disease by immune mechanisms directed against an array of bloodstage antigens, including PvDBPII.…”

“…vivax and P. falciparum infections detected in the first 6 weeks posttreatment by LDR-FMA were genotyped for the highly polymorphic PvDBPII alleles and P. falciparum merozoite surface protein two alleles, respectively, to identify treatment failures (13). Only one P. vivax infection detected in the first 6 weeks posttreatment by LDR-FMA had the same P. vivax PvDBPII genotype as observed at baseline, suggesting a possible treatment failure.…”

“…At enrollment and before treatment, all four human malaria species were detected in the study children (n ϭ 206), with 33.9% and 9.8% infected with P. vivax by PCR and light microscopy (LM), respectively, at baseline, as described in detail (13). All children in the study were treated with a 7-day course of artesunate at enrollment to clear blood-stage malaria parasite infections.…”

“…The study population of 206 children (ages 5-14 years) for this treatment reinfection study has been described (13). This study was reviewed and approved by the institutional review boards of the Papua New Guinea Medical Research Advisory Council, the Veteran's Affairs Medical Center (Cleveland), and the Walter and Elisa Hall Institute (Melbourne, Australia); written informed consent was obtained from the parents/guardians of each child, as well as the assent of the children.…”

“…malaria species (13,20). The parasite density of P. vivax was determined by real-time quantitative PCR (14,21), and P. vivax-positive samples were genotyped for the highly polymorphic PvDBPII alleles (22).…”