Identifying the hosts responsible for the majority of disease transmission and the mechanisms that cause them to be "super-spreaders" are central questions in disease ecology. The male-super-spreader hypothesis proposes several mechanisms creating empirically observed male-biased transmission in mammals, including greater parasite intensity, higher prevalence, greater reproductive output per parasite, and greater behavioral-mediated spread of infective stages from males compared to females. The goals of our study were to, 1. test the male-super-spreader hypothesis of white-footed mice (Peromyscus leucopus) transmission of an intestinal nematode parasite (Pterygodermatites peromysci) with a trophically-transmitted life-cycle and, 2. to determine the mechanisms generating this transmission pattern. We performed a longitudinal field experiment where intestinal nematode parasites of male or female white-footed mice were removed with anthelminthic treatment. We monitored the responses of nematode infective stages in the intermediate cricket hosts (Ceuthophilus pallidipes) and subsequent transmission to the non-treated sex of the mouse host. If males drive transmission, we predicted intermediate hosts and female mice would have lower infection rates on male-dewormed sites compared to controls. We also dissected a cross-sectional sample of hosts and compared the prevalence, intensity, and fecundity of intestinal parasites between host sexes to examine potential mechanisms for male-biased transmission.

Results/Conclusions

Removing parasites from either definitive host sex reduced the prevalence and mean intensity of infection in the intermediate host, with male-deworming producing 25% lower intensity of infective stages. This effect translated through the parasite life-cycle and resulted in lower infection rates among female mice in male-treated sites compared to females in control sites.  We detected no effect of female-deworming on transmission in male mice.  We found no difference in prevalence, intensity, or fecundity of P. peromysci parasites in the cross-sectional sample of mice. Our field experiment confirmed that male white-footed mice are responsible for driving transmission of a parasitic nematode, even with a complex life-cycle. Further, without male-biased prevalence, intensity, or parasite fecundity, we concluded that physiological differences between male and female hosts are unlikely to be creating male-biased transmission.