Testing the immunocompetence handicap hypothesis (ICHH) in both sexes in wild brown mouse lemurs (Microcebus rufus)


Meeting Abstract

23.6  Tuesday, Jan. 4  Testing the immunocompetence handicap hypothesis (ICHH) in both sexes in wild brown mouse lemurs (Microcebus rufus). ZOHDY, Sarah*; TECOT, Stacey; WRIGHT, Patricia C.; JERNVALL, Jukka; University of Helsinki, Helsinki, Finland; University of Arizona, Tucson; Stony Brook University, Long Island; University of Helsinki, Helsinki, Finland sarah.zohdy@helsinki.fi

Testosterone is thought to be the underlying cause for immunosuppression in males with elaborate ornamentation, as it results in costly secondary sexual characteristics which compete for resources with the immune system. This is widely known as the immunocompetence handicap hypothesis (ICHH) and has been examined extensively (with conflicting results)on numerous organisms in both captive and wild conditions. Yet the studies testing the ICHH have only examined the parasitic response to testosterone in males. We have previously found that female brown mouse lemurs (Microcebus rufus) have comparable or higher levels of testosterone than males in the wild. Here we test to see if the ICHH holds true in both sexes, using the unique situation of elaborate secondary sexual characteristics in males during the breeding season and high testosterone in females and comparing these values to ecto and endoparasite intensities. Data was collected from August 2008 through November 2009, samples were analyzed for fecal testosterone(n=541) at the Wisconsin National Primate Research Center using enzyme linked immunoassays. Our results show a direct correlation between ectoparasite load and an increase in testicular volume, but no correlation between fecal testosterone and ecto or endo parasite load. Similarly, fecal testosterone in females shows no significant trend that would support the ICHH. We find evidence that supports the idea that elaborate secondary sexual characteristics may be related to immunosuppression, but our data fails to support testosterone as the primary underlying cause of this mechanism. We suggest, rather, a much more complex cause of decreased immunocompetence in sexually elaborate males.

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