The discovery of the key role of Toll-like receptors (TLRs) in initiating innate immune responses and modulating adaptive immunity has revolutionized our understanding of vertebrate defence against pathogens. Yet, despite their central role in pathogen recognition and defence initiation, there is little information on how variation in TLRs influences disease susceptibility in natural populations. Here, we assessed the extent of naturally occurring polymorphisms at TLR2 in wild bank voles (Myodes glareolus) and tested for associations between TLR2 variants and infection with Borrelia afzelii, a common tick-transmitted pathogen in rodents and one of the causative agents of human Lyme disease. Bank voles in our population had 15 different TLR2 haplotypes (10 different haplotypes at the amino acid level), which grouped in three well-separated clusters. In a large-scale capture-markrecapture study, we show that voles carrying TLR2 haplotypes of one particular cluster (TLR2 c2 ) were almost three times less likely to be Borrelia infected than animals carrying other haplotypes. Moreover, neutrality tests suggested that TLR2 has been under positive selection. This is, to our knowledge, the first demonstration of an association between TLR polymorphism and parasitism in wildlife, and a striking example that genetic variation at innate immune receptors can have a large impact on host resistance.

Genetically diverse infections are common but little is known about what effects coinfecting strains have on each other in natural host-parasite systems. To explore the nature and consequences of interactions in the wild, we studied the tick-transmitted bacterium Borrelia afzelii in one of its main reservoir hosts, the bank vole Myodes glareolus. We measured overall infection intensity with quantitative polymerase chain reaction (PCR) and resolved the composition of multiple infections using strain-specific PCR assays targeting the ospC gene (which encodes an immunodominant surface protein). We found seven different strains, as defined by ospC genotype. There was little evidence for interactions affecting infection intensities, but strains were highly aggregated (i.e., there were more multiple infections than expected from random co-occurrence). Moreover, there was a positive correlation between the difference at the amino acid level between two OspC types and their degree of association. Overall, the observed patterns suggest that facilitation is more important than competition in this system and that more diverse infections have an advantage in establishing and/or maintaining infection. We propose that this advantage is one of the factors that favors antigenic diversity.

The genetic structure of a pathogen is an important determinant of its potential rate of adaptation and can thereby influence the dynamics of host–parasite interactions. We investigated how the genetic structure of Borrelia afzelii varies with geographic and ecological sampling scale. Genetic structure was measured as the degree of linkage disequilibrium (LD) across three loci. To test for the effects of geographic and ecological scale, we calculated LD across or within populations 4–82 km apart and across or within different mammal host species. There was highly significant LD across populations and host species. However, there was also evidence for genome‐wide recombination, and the LD largely resulted from epidemic spread of certain haplotypes, rather than lack of recombination. Interestingly, the degree of LD was higher in each population than in the sample as a whole, i.e. LD increased with decreasing geographic scale. In contrast, there was no effect of ecological sampling scale on LD. Strong LD may impede the rate of adaptive evolution. Our results suggest this effect might be particularly strong at a small geographic scale.

We examined small mammals as hosts for Anaplasmataceae in southern Sweden. Of 771 rodents, 68 (8.8%) were infected by Candidatus Neoehrlichia mikurensis, but no other Anaplasmataceae were found. Candidatus N. mikurensis has recently been found in human patients in Germany, Switzerland, and Sweden, which suggests that this could be an emerging pathogen in Europe.

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