Résumé
Parasites are a fundamental component of wild animal populations, often inducing sub-lethal chronic effects that impact host fitness and demography. However, the factors determining variation in infection burden are often poorly understood in wild systems. Environmental conditions can determine exposure to infection and the resources required to respond, but exhibit strong temporal variation. As environmental conditions are predicted to become more variable, it is crucial to understand how these conditions shape burden to predict the downstream effects on host populations. Early-life conditions can shape responses to infection, potentially leading to delayed effects of environmental variation on fitness. The extent to which these are mediated by resources and later-life conditions remains unclear and may vary between the sexes, who often differ in exposure risk and resource requirements. Here, we examine how differences in hatching and breeding conditions influence parasite burden throughout life. We utilise data from a long-term population study of European shags (Gulosus aristotelis) on the Isle of May, Scotland, in which there is substantial variation in the timing of breeding within and between years, and nematode parasite burden can be measured in vivo using endoscopy. We show that adult parasite burden is influenced by seasonal and annual differences in current and early life conditions, but different patterns were observed in adult males and females. Burdens increased across the season in chicks and adult females but not in adult males. Instead, early life effects better explained burden in adult males, with those hatching later and in productive years displaying lower burdens. This suggests that early life may shape behaviour, immunity, or physiological development, impacting subsequent infection. Our findings reveal complex temporal effects on parasitism in species breeding in fluctuating environments. Incorporating seasonal and sex-specific responses to parasitism is crucial to understanding how predicted environmental shifts could impact disease dynamics.