Immune function, parasitization and extended phenotypes in colour polymorphic pygmy grasshoppers

Abstract

Ecological and evolutionary consequences of host–parasite interactions have attracted considerable attention from evolutionary biologists. Previous studies have suggested that immune responsiveness may be genetically or developmentally linked with colour pattern, such that the evolution of animal colour patterns may be influenced by correlated responses to selection for parasite resistance. We studied interactions between the endoparasitic fly Leiophora innoxia (Meigen) (Diptera: Tachinidae) and its colour polymorphic pygmy grasshopper host Tetrix undulata (Sow.) (Orthoptera: Tetrigidae) to test for morph-specific differences in parasitization and immune defence, and host-induced variation in parasite phenotypes. Our results revealed that c. 2 and 30% of adult grasshoppers collected from the same natural population in two subsequent years, respectively were parasitized. Parasite prevalence was independent of host sex and colour morph. Pupae were larger if the parasite had developed in a female than in a male host, possibly reflecting host resource value or a physical constraint on larval growth imposed by host body size. Pupal size was also associated with host colour morph, with individuals that had developed in dark morphs being smaller at pupation compared to those that developed in paler morphs. However, immune defence, measured as the encapsulation response to a novel antigen, did not differ among individuals belonging to alternative colour morphs or sexes. Darker morphs warm up more quickly and prefer higher body temperatures than paler ones. Encapsulation was not influenced by maintenance temperature (15 vs. 30 °C), however, suggesting that indirect effects of coloration on parasite resistance mediated via differential body temperature are unlikely. The dependence of parasite body size on host colour morph may thus reflect plasticity of growth and development of the larvae in response to differential host body temperature, rather than variable host immune defence.