Infection Dynamics of Plasmodium Mexicanum, A Malarial Parasite of Lizards

Abstract

A mark—recapture technique was used to evaluate variation in the course of infection of the malarial parasite, Plasmodium mexicanum, in its natural host, the western fence lizard (Sceloporus occidentalis) during the warm season in northern California, USA. These data were used to examine the hypothesis that the parasite modifies its reproductive schedule during the year to meet the challenges of a seasonal environment. Infections first became evident in the blood at various times during the warm season (May—September), then rose exponentially before leveling off to a constant parasite load. Parasite levels (parasitemia) declined during the winter, but rebounded rapidly the next spring,apparently once again to a steady level. Most infections studied were older ones remaining at a relatively constant level throughout the warm season. Exponential growth rate of rising infections varied over a fourfold range, and chronic infections varied greatly in parasitemia (over two orders of magnitude). The end of exponential growth, and the ultimate parasitemia level reached, were related to the timing of production of gametocytes (nondividing sex cells.) Gametocytes appeared very early in an infection, then increased so that they eventually dominated the parasite population. The rate of increase of gametocytes varied greatly among infections, but was not clearly related to host age or to date the infection originated. Weak evidence suggests that the rate of asexual proliferation was more rapid in infections originating late in the warm season. Neither host sex nor age was associated with rate of parasite increase in growing infections. Maximum parasitemia was independent of sex or starting date of the infection, but was higher in juveniles than in adults. We conclude that during the warm season, the schedule of reproductive activities of P. mexicanum does not follow precisely the time of year or host quality, perhaps because of the developmental mechanism driving gametogenesis.