PUB - Publikationen an der Universität Bielefeld

Short after coming to life, young vertebrates face many new challenges. How early-life adversity is dealt with during this critical developmental period primes a spectrum of long-term consequences for host fitness, that may ultimately regulate population dynamics. In this thesis, I intend to address aspects of this fundamental arc at increasing organizational scales, from gene, tissue, individual to population. I use multiple approaches such as transcriptomic, blood chemistry, physiology, and survival analyses, to assess host defence abilities and consequences of endoparasite infections during host nestling phase. I show that in a long-lived raptor, the common buzzard (Buteo buteo), nestlings infected with the blood parasite Leucocytozoon toddi display low transcriptional response to increasing parasitemia (density of parasite per host cells), moderate signs of parasite-induced tissue damages in the blood, disease symptoms only at the highest parasitemia level, and ultimately no effect of early-life infection on medium- to long-term survival. Additionally, through a combination of genotyping, whole genome and RNA sequencing we reveal that this nestling population presents a higher MHC allele diversity than previously thought. Antimalarial medication successfully reduced Leucocytozoon parasitemia in these young hosts but did not clear infections in most cases. Interestingly, treated nestlings did not show blood chemistry changes and physiological improvements compared with control nestlings. Altogether, this thesis emphasizes that Leucocytozoon parasites reside on the lower side of parasitic virulence spectrum. They appear to induce minor consequences to young long-lived hosts, at various organizational levels, although we show that nestlings already possess functional antiparasitic defences. This may provide the opportunity for growing hosts to rely on moderate defence responses, sometimes leading to disease symptoms during the harshest of infections and potentially impairing fitness of some particularly susceptible nestlings. Long-lived altricial nestlings and low-burden parasites may have co-evolved these traits, enabled by the naïve and immature host phase as a stable host-parasite evolutionary playground.