Causes and consequences of blood parasite infections in birds

University dissertation from Martin Stjernman, Ecology building, S-223 62, Lund, Sweden

Abstract: Parasites are ubiquitous and can cause significant fitness reductions to their hosts. Therefore, selection for the evolution of host resistance should be strong. However, resistance may be costly and should be traded-off against other fitness related traits. Parasites could therefore have a significant impact on the evolution of fitness related characters of their hosts. It has been suggested that the workload put into reproduction is negatively related to the ability to resist parasites and that this trade-off could explain the reduction in future reproduction as a result of current reproductive effort – a trade-off termed the cost of reproduction. I studied whether blood parasites could mediate reproductive costs by examining if altered reproductive effort affected infection levels of a blood parasite (Haemoproteus) and concomitant survival in the blue tit (Parus caeruleus). I found a negative relationship between altered reproductive effort and survival and a positive relationship between reproductive effort and parasite intensity. However, since parasite intensities were not related to survival when controlling for other factors related to the experiment, these parasites could not mediate the reproductive costs found. An alternative way of verifying costs of resistance may be to study selection patterns since the presence of such fitness costs should manifest as stabilising selection on resistance. That is, fitness is not only reduced if hosts are unable to control the parasites, but also if resistance comes with a fitness cost. Indeed, I found that individuals with intermediate parasite intensities had highest survival. I also found that individuals with intermediate immune responsiveness against diphtheria vaccine had highest survival. However, different components of resistance may carry different costs since I found that individuals with the strongest response against another antigen (tetanus) were those that had highest survival. Another finding was that the intensity of infection within one-year-old individuals were significantly related to the rearing conditions experienced during the nestling phase and that the level of infection is repeatable between years. This suggests that parasite resistance is fixed during development and that individuals have limited possibilities to compensate for adverse conditions experienced during the nestling phase. The influence of early development on parasite resistance indicate that maternal effects may be important and one possible route by which the mother could influence offspring immunity may be through the transfer of antibodies via the egg. I found that offspring of mothers that were immunised with a bacterial antigen had higher levels of (and a larger increase in) antibodies at the end of the nestling period compared to offspring of mothers that were not immunised.

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