Natural Parasite Infection Affects the Tolerance but Not the Response to a Simulated Secondary Parasite Infection

Parasites deplete the resources of their host and can consequently affect the investment in competing traits (e.g. reproduction and immune defence). The immunocompetence handicap hypothesis posits that testosterone (T) mediates trade-offs between parasite defence and reproductive investment by suppressing immune function in male vertebrates while more recently a role for glucocorticoids (e.g. cortisol (C)) in resource allocation has been suggested. These hypotheses however, have not always found support in wild animals, possibly because most studies focus on a single parasite species, whereas infections with multiple parasites are the rule in nature. We measured body mass, T- and C-levels of wild male highveld mole-rats (Cryptomys hottentotus pretoriae) naturally uninfected or infected with a cestode (Mathevotaenia sp.) right after capture. Subsequently, we injected animals subcutaneously with a lipopolysaccharide (LPS) to simulate a bacterial infection and recorded changes in body mass, food intake, haematological parameters and hormone levels. As a control, animals were injected with saline. Natural infection neither affected initial body mass nor C-levels, whereas infected males had significantly reduced T-levels. We observed significant reductions in food intake, body mass and T in response to LPS but not saline while C increased. However, this response did not vary with infection status. In contrast, final body mass and some haematological parameters were significantly lowered in infected males. Our results suggest that naturally infected males are able to compensate for resource depletion by physiological adjustments. However, this leaves them less tolerant to the challenges of a secondary infection.