One of the greatest challenges for evolutionary biology is explaining the widespread occurrence of sexual reproduction and the associated process of genetic recombination. A large number of theories have been developed that provide a sufficient short‐term advantage for sex to offset its two‐fold cost. These theories can be broadly classified into environmental (or ecological) and mutation‐based models. Traditionally, the different theories have been viewed as competing, and empirical work has attempted to distinguish between them. Here we highlight the advantages that may be gained from considering that multiple mechanisms (environmental and mutational) may be at work, and that interactions between the theories may be very important.

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Competitive interactions between coinfecting genotypes of the same pathogen can impose selection on virulence, but the direction of this selection depends on the mechanisms behind the interactions. Here, we investigate how host immune responses contribute to competition between clones in mixed infections of the rodent malaria parasite Plasmodium chabaudi. We studied single and mixed infections of a virulent and an avirulent clone and compared the extent of competition in immunodeficient and immunocompetent mice (nude mice and T cell-reconstituted nude mice, respectively). In immunocompetent mice, the avirulent clone suffered more from competition than did the virulent clone. The competitive suppression of the avirulent clone was alleviated in immunodeficient mice. Moreover, the relative density of the avirulent clone in mixed infections was higher in immunodeficient than in immunocompetent mice. We conclude that immune-mediated interactions contributed to competitive suppression of the avirulent clone, although other mechanisms, presumably competition for resources such as red blood cells, must also be important. Because only the avirulent clone suffered from immune-mediated competition, this mechanism should contribute to selection for increased virulence in mixed infections in this host-parasite system. As far as we are aware, this is the first direct experimental evidence of immune-mediated apparent competition in any host-parasite system.

The time between infection and the onset of reproduction (maturation time) is a key determinant of body size, fecundity and generation time in parasitic nematodes. An optimality model for maturation time is developed centred on prematurational growth, the duration of which has opposing consequences for fecundity and for survival to reproductive age. The maturation time favoured by natural selection is found to be inversely proportional to prematurational mortality rate. The product of maturation time and mortality rate is predicted to be an invariant number equal to the allometric slope linking daily fecundity to maturation time. Predictions are tested using comparative data on mammalian gastrointestinal nematode taxa. Half the cross‐species variation in prepatent period (the time from infection until propagules are shed from the host) is accounted for by this adaptive trade‐off hypothesis, even though many biological details are not explicitly modelled. These results are discussed in the light of previous studies and in the context of general models of life history evolution.

If common processes generate size-abundance relationships among all animals, then similar patterns should be observed across groups with different ecologies, such as parasites and free-living animals. We studied relationships among body size, life-history traits, and population intensity (density in infected hosts) among nematodes parasitizing mammals. Parasite size and intensity were negatively correlated independently of all other parasite and host factors considered and regardless of type of analyses (i.e., nonphylogenetic or phylogenetically based statistical analyses, and across or within communities). No other nematode life-history traits had independent effects on intensity. Slopes of size-intensity relationships were consistently shallow, around -0.20 on log-log scale, and thus inconsistent with the energetic equivalence rule. Within communities, slopes converged toward this global value as size range increased. A summary of published values suggests similar convergence toward a global value around -0.75 among free-living animals. Steeper slopes of size-abundance relationships among free-living animals could be related to fundamental differences in ecologies between parasites and free-living animals, although such generalizations require reexamination of size-abundance relationships among free-living animals with regard to confounding factors, in particular by use of phylogenetically based statistical methods. In any case, our analyses caution against simple generalizations about patterns of animal abundance.