Abstract

Forest management is increasingly focused on enhancing structural complexity. An increase in structural complexity is assumed to increase the abundance and diversity of fauna, including vertebrates. This faunal assemblage serves, in turn, as host community for a suite of vectors and their pathogens, so that structural complexity may cascade through a network of interactions in forest ecosystems. Here we use a network of 19 forest plots representing a gradient of structural complexity and dominant tree species (oak, beech, poplar) to test two hypotheses on the effect of structural complexity on the prevalence of tick-borne pathogens. Our first hypothesis is that tick densities will increase with increasing structural complexity, assuming that each life stage has higher chances of finding a suitable host. The second hypothesis is that the pathogen prevalence in ticks and small mammals decreases (cf. dilution hypothesis) or increases (cf. amplification hypothesis) with increasing structural complexity. These expectations are tested through a community-level analysis, looking at twelve pathogens: seven genospecies of Borrelia (B. afzelii, B. bavariensis, B. garinii, B. burgdorferi sensu stricto, B. spielmanii, B. valaisiana and B. miyamotoi), Babesia s.s., Babesia microti, Anaplasma phagocytophilum, Rickettsia helvetica and Spiroplasma ixodetes. We found that more structurally complex forests have a higher density of questing nymphs (in June and July, during the peak of nymph activity). We did not find a clear change in pathogen prevalence with increasing structural complexity in ticks, wood mice and bank vole; the effect was different for the different pathogens and between the different dominant tree species. No clear co-occurrence patterns of pathogens were found. The density of infected nymphs and thus the disease risk is higher in more complex forests. A potential solution is to focus on decreasing the human-tick interactions in forests instead of trying to decrease the number of questing ticks.

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