Is there a sicker sex? Dose relationships modify male-female differences in infection prevalence.

Throughout the animal kingdom, there are striking differences in the propensity of one sex or the other to become infected. However, precisely when we should expect males or females to be the sicker sex remains unclear. A major barrier to answering this question is that very few studies have considered how the susceptibility of males and females changes across the full range of pathogen doses encountered in nature. Without quantifying this 'dose-susceptibility' relationship, we have likely underestimated the scope for sex differences to arise. Here, we use the Daphnia magnia-Pasteuria ramosa system to reveal that sex differences in susceptibility are entirely dose-dependent, with pathogens having a higher probability of successfully establishing an infection in mature males at low doses, but mature females at high doses. The scope for male-female differences to emerge is therefore much greater than previously appreciated-extending to sex differences in the upper limits to infection success, per-propagule infectivity risks and density-dependent pathogen behaviour. Applying this expanded scope across the animal kingdom will help us understand when and why a sicker sex emerges, and the implications for diseases in nature-where sex ratios, age structure and pathogen densities vary drastically.

Host Sex Modulates the Energetics of Pathogen Proliferation and Its Dependence on Environmental Resources.

AbstractSex differences in immunity are predicted to underlie much of the frequently observed sex differences in the prevalence or severity of infection. We propose the additional hypothesis that differences in the ability of males and females to acquire and use resources will also affect how readily a pathogen can convert host energy into transmission stages, thereby contributing to sex differences in infection dynamics. To test this we manipulated the resource environment of male and female Daphnia magna by altering the availability of food and then exposed hosts to a bacterial pathogen. We measured the production of transmission spores and virulence via the reduction in life span, together with feeding rates and changes in mass-independent metabolic rate, as a measure of the intake and expenditure of energy during infection. When raised in the presence of high resource levels, females more readily allowed for resources in the environment to be translated to pathogen exploitation, as represented by increased spore production, greater virulence, and higher energy use. In contrast, the traits of infected males were robust to changes in resource availability. High food availability thus exaggerated the degree of sexual dimorphism observed between the sexes. It also modified the relationship between host energy use, virulence, and pathogen spore production for each sex. These results suggest that a host's resource environment can affect how a male or female is exploited by a pathogen and may thus be an additional factor driving sex-specific patterns of disease susceptibility or severity.