Female great tits do not alter their yolk androgen deposition when infested with a low-transmittable ectoparasite

In birds as in many other taxa, parasites can have deleterious effects on offspring development. Therefore, avian mothers have evolved responses to counteract parasite virulence in offspring via transgenerational defense mechanisms that is the transfer of immune-enhancing substances such as antibodies to their eggs. Another maternal pathway is suggested by the finding that infested great tit mothers produced eggs with lower androgens, since these yolk androgens are immunosuppressive and potentially affect parasite susceptibility of the nestlings. However, whether this pathway is a specific adaptation to infestation with parasites that affect the offspring or an epiphenomenon of lower androgen production in the female due to the parasite effects on the mother itself is as yet unclear. In this study we infested female great tits (Parus major) with sheep ticks (Ixodes ricinus), which are nonnidicolous ectoparasites with low vertical transmission capability, and evaluated the effects on yolk androgen deposition. Tick-infested females did not significantly reduce their deposition of androgens (androstenedione (A₄) and testosterone) compared to tick-reduced females, which is in contrast to a previous study showing a lowered deposition of A₄ and testosterone when females were exposed to the nidicolous hen flea. Thus, females alter their hormone deposition, and thus likely offspring phenotype, when exposed to parasites that also form the parasitic environment of their offspring, but not when temporarily infested with the field-dwelling sheep ticks with low transmission capability. This suggests that selection favored the evolution of an adaptive transgenerational effect by acting mainly on the parasite-induced maternal effect.