Seasonal patterns of hormones, macroparasites, and microparasites in wild African ungulates: The interplay between stress, reproduction, and disease

Background/Question/Methods

Stress can modulate the immune system and cause increased disease incidence. Sex hormones and seasonal reproductive status can also influence immune competence, as well as stress hormone secretion. Pathogens can also cause host stress, as well as exploit host niches exposed by stress and reproductive hormone-induced immunomodulation. Therefore, measuring stress and stress-inducing factors concurrently with coinfection issues is important for determining host immune condition and the subsequent potential for contracting other diseases. Using steroid hormone metabolites from fecal samples, we examined seasonal correlations between host stress, reproduction, and gastrointestinal (GI) parasite coinfections in zebra and springbok in Etosha National Park (ENP), Namibia. 

Results/Conclusions

We found strong seasonality of all factors, with infection intensities of all three GI macroparasites examined (strongyle helminths, Strongyloides helminths, and Eimeria coccidia) highest in the wet season, concurrent with the timing of anthrax outbreaks. Parasites also declined with age and with increased acquired immune responses. We found hormonal evidence that both mares and ewes are strongly seasonal breeders in ENP, and that reproductive hormones are correlated with immunosuppression and higher susceptibility to GI parasite and ectoparasite infections. While stress hormones exhibit seasonality in both zebra and springbok, stress hormones largely peak in the dry season when parasite infection intensities are lowest. In fact, peak stress hormone levels are mostly driven by dry season environmental challenges and host reproductive status, rather than by pathogen prevalence or infection intensity in this system. Given the evidence that GI parasites are capable of causing host pathology, causing immunomodulation and immunosuppression, and controlling population age structures, the fact that these parasites persist in ENP hosts without causing chronic stress responses supports the hypothesis that hosts are tolerant of their parasites. Such tolerance would help explain the ubiquity of these pathogens in ENP herbivores, even in the face of their immunomodulatory trade-offs with anti-anthrax immunity.