The frequency of recombination between unlike genotypes is central to understanding the generation of genetic diversity in natural populations of malaria. Here we suggest a way of investigating the problem which could complement conventional biochemical approaches to the population genetics of malaria. Sex allocation theory is one of the most successful areas of evolutionary biology. A well-supported prediction is that progressively less female-biased sex ratios are favoured with more outcrossing; equal numbers of males and females being evolutionarily stable in randomly mating outbred populations. We present a simple game theory model to support the idea that outcrossing rates in malaria will be correlated with the sex ratio of gametocytes in the peripheral blood of vertebrate hosts. Blood films from epidemiological surveys and culture-adapted isolates from Madang Province, Papua New Guinea, were used to estimate average gametocyte sex ratio of Plasmodium falciparum in the area. The geometric mean proportion of males in the population was 0.18 (95% confidence limits: 0.15-0.22). From our model, we estimate that, on average, 36% of zygotes are the result of outcrossing. This estimate assumes that most microgametes released following exflagellation are capable of fertilization. If, on average, fewer than about 70% of microgametes are capable of fertilization (as is the case in at least one other species of Plasmodium), the observed sex ratio would be consistent with between zero and 36% of zygotes being the result of outcrossing. These estimates suggest that there is usually a numerically dominant genotype in the gametocyte population in a blood meal, and that a considerable amount of selfing is occurring in P. falciparum populations in the Madang region, even though it is an area of intense year-round transmission.
Active community and self-reporting surveillance techniques have been used to describe the dynamics of febrile illness and associated malaria infection in children aged 2 to 15 years from a rural area of Madang Province, Papua New Guinea (PNG). Both history of fever and fever in association with parasitaemia appeared to be reliable indicators of malaria morbidity in this endemic area. Parasite density was observed to be a major determinant of mild malarial disease at both the population level and within an individual. Age-specific prevalence of febrile illness correlated with age-specific patterns of parasite density but not of parasite prevalence. Seasonal changes in fever incidence correlated with parasite density. The transition from afebrile to febrile state within an individual was generally associated with an increase in parasite density. Surveillance and self-reported febrile cases (which differ in severity on the basis of the perceived need for treatment) could be distinguished on the basis of parasite density. Thus surveillance techniques divide clinical malaria in rural PNG into 'mild' and 'very mild' forms. The age-specific pattern of decline of prevalence of malaria-associated febrile illness and parasite density is best explained by induction of strain-specific anti-disease immunity upon infection with a given strain of Plasmodium falciparum. The fever threshold in self-reporting febrile cases was seen to decrease with age and can be explained by an age-specific decline in anti-toxic immunity.
Effects of bednet coverage (C) on prevalence of malaria were analysed using data from 1990-92 from 9 Papua New Guinean villages. Effects of coverage varied by age, resulting in a shift in age ofpeakprevalence from 4.7 (C = 0%) to 11.6 (C = 100%) years for PZ~smodiumful&pantm, from 3.4 to 4.9 years for i? vivax and from 11.0 to 16.8 years for l? malaldae. In small areas with no bednets the age distribution of P. falciparum parasitaemia was like that of a holoendemic area. Where coverage was complete the pattern corresponded to mesoendemicity. Thus, protracted use of bednets can result in profound changes in the endemicity of malaria even when coverage is incomplete and without insecticide treatment. Average entomological inoculation rates (EIRs) estimated from indoor landing rates on individuals without bednets were 35, 12 and 10 infectious bites per person per annum for I? falcipanrm, I? vivax and P. maluriue, respectively. Logistic regression analyses indicated that the EIR estimate for I? fazciparum was related to prevatence of this species independently of effects of bednet coverage. However, the recent EIR still accounted for much less variation than did the bednets. A similar pattern was seen for P. malariae, while there were no significant relationships between the recent EIR and the parasite positivity for l? uivax. It is concluded that short-term variations in inoculation rate are not important determinants of parasite prevalence in this population.
The burden and duration of asymptomatic malaria infections were measured in residents of the malaria endemic village of Gonoa, Madang Province, Papua New Guinea. Plasmodium falciparum, P. vivax and P. malariae infections in people aged 4 years to adulthood were compared. Frequent sampling at 3-day intervals for up to 61 days allowed assessment of individual episodes of infection. Statistical assessment of P. falciparum detection revealed a periodicity consistent with synchronous replication of this species over periods up to 27 days. The duration of P. falciparum episodes was longer across all age groups than that of P. vivax and P. malariae. A trend for decreasing duration with age was also noted in data from each species. This was most prominent in P. falciparum infections: median duration in 4-year-olds was > 48 days compared with a median between 9 and 15 days in older children and adults. The results are consistent with the slow acquisition of immunity to antigenically diverse Plasmodium populations and suggest a faster rate of acquisition to P. vivax and P. malariae than to P. falciparum.
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