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.

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The regulation of helminth populations tends to occur primarily as a result of limitations imposed on the build up of parasite subpopulations within individual hosts (Anderson & May, 1979; May & Anderson, 1979). Considering the relevance of these factors to the success or otherwise of intestinal helminth control programmes, it is perhaps surprising that more information is not yet available concerning the particular mechanisms which may be responsible, and in particular, the population consequences of the immune responses which such parasites may precipitate. Density-dependence in a single rate parameter, if operative over the naturally observed numerical range, is sufficient to regulate parasite population flow throughout the life-cycle, whether direct or indirect (Anderson, 1976). For the genera given in Table 1, this could be provided by the observed pattern of parasite mortality and/or fecundity. It is of interest to note, however, that circumstantial evidence cited in the Table suggests that each of the 6 genera is also potentially able to induce host mortality under certain conditions. Whether this acts in a density-dependent manner in natural infections is almost entirely unknown. Rapid reproduction may be of great selective advantage to intestinal helminths, even if it is necessarily accompanied by pathogenicity (see Anderson, 1981). If the manner in which this pathogenicity acts in any way enhances the stability of the host-parasite interaction, then perhaps it may have contributed to the selection pressures which have led so many genera to continue to break the rules of the ‘well-adapted’ parasite (see, for example, Noble & Noble, 1971).

SUMMARYThe mean parasite burden of a population of Tribolium confusum is shown to rise to a plateau as the exposure density of infective eggs of Hymenolepis diminuta increases. The level of this plateau is shown to be dependent on the nutritional status of the host population, being depressed from approximately 18 cysticercoids/beetle in hosts which have been starved prior to experimentation, to approximately 2 cysticercoids/beetle in satiated hosts. A simple model is used to describe the shape of this infection functional response in terms of the predator–prey interaction between hosts (T. confusum) and parasite infective stages (H. diminuta eggs). The distribution of successful infections/host is shown to be over-dispersed, even when hosts are exposed to infective stages arranged in a uniform spatial pattern. The over-dispersion of parasite numbers/host is shown to become more severe as the spatial pattern of infective stages changes from under-dispersed, through random, to over-dispersed. Experimental results are discussed in relation to the dynamics of parasite–host interactions, in which infection takes place by host ingestion of a free-living infective stage.