Effects of rodent abundance on ticks and Borrelia: results from an experimental and observational study in an island system.

BACKGROUND: Lyme borreliosis is the most common tick-borne disease in Europe and is often caused by Borrelia afzelii, which is transmitted by Ixodes ricinus ticks. The prevalence and abundance of infected ticks fluctuate in time and space, influencing human infection risk. Rodents are reservoir hosts for B. afzelii and important feeding hosts for larval ticks. In the study reported here, we examined how variation in rodent abundance is associated with B. afzelii infection prevalence in ticks, the density of nymphs (DON) and the density of infected nymphs (DIN) in the following year. We further analysed the relationships between the abundance of infected rodents and nymphal infection prevalence (NIP) and DIN. METHODS: We conducted a study that combined experimental and observational approaches on 15 islands (10 small islands and 5 large islands) in Finland. On all of the islands, ticks and rodents were monitored and sampled during the summer of 2019, with the monitoring of tick abundance and sampling continuing into the spring of 2020. On five of the 10 small islands, captured rodents were removed from the island ("removal" islands), and on the other five small islands, captured rodents were released back to the trapping site after marking and sampling ("control" islands). On the five large islands, captured rodents were released back to the trapping site after marking and sampling. The presence of B. afzelii from nymph and rodent samples was examined. RESULTS: The results of the experimental study showed that neither treatment (removal), rodent abundance index nor abundance index of infected rodents in 2019 was associated with DON, NIP or DIN in 2020. Based on data from the observational study, the NIP in 2020 decreased with increasing rodent abundance index and abundance index of infected rodents in 2019. However, the DIN in 2020 was not associated with the rodent abundance index or the abundance index of infected rodents in 2019. In addition, in the observational study, DON in 2020 increased with increasing rodent abundance index. CONCLUSIONS: Our results suggest that low rodent abundance during the tick activity period is not sufficient for reducing the disease hazard and, hence, rodent removal may not be a feasible control measure in natural ecosystems.

Idiosyncratic effects of coinfection on the association between systemic pathogens and the gut microbiota of a wild rodent, the bank vole Myodes glareolus.

The effects of systemic pathogens on gut microbiota of wild animals are poorly understood. Furthermore, coinfections are the norm in nature, yet most studies of pathogen-microbiota interactions focus on effects of single pathogen infections on gut microbiota. We examined the effects of four systemic pathogens (bacteria Anaplasma phagocytophilum and Borrelia burgdorferi sensu lato, apicomplexan protozoa Babesia microti and Puumala orthohantavirus) and coinfections among them on the (bacterial) gut microbiota of wild bank voles Myodes glareolus. We hypothesized that: (1) the effects of coinfection on gut microbiota generally differ from those of a single pathogen infection, (2) systemic pathogens have individual (i.e. distinct) associations with gut microbiota, which are modified by coinfection and (3) the effects of coinfection (compared with those of single infection) are idiosyncratic (i.e. pathogen-specific). The gut microbiota of coinfected bank voles differed from that of single pathogen infected individuals, although, as predicted, the effects of coinfections were unique for each pathogen. After accounting for coinfections, only Puumala orthohantavirus was associated with higher α-diversity; however, all pathogens affected gut microbiota ß-diversity in a pathogen-specific way, affecting both rare and abundant gut bacteria. Our results showed that the effects of systemic pathogens on host's gut microbiota vary depending on the pathogen species, resulting in idiosyncratic signatures of coinfection. Furthermore, our results emphasize that neglecting the impact of coinfections can mask patterns of pathogen-microbiota associations.

Urban forest soils harbour distinct and more diverse communities of bacteria and fungi compared to less disturbed forest soils.

Anthropogenic changes to land use drive concomitant changes in biodiversity, including that of the soil microbiota. However, it is not clear how increasing intensity of human disturbance is reflected in the soil microbial communities. To address this issue, we used amplicon sequencing to quantify the microbiota (bacteria and fungi) in the soil of forests (n = 312) experiencing four different land uses, national parks (set aside for nature conservation), managed (for forestry purposes), suburban (on the border of an urban area) and urban (fully within a town or city), which broadly represent a gradient of anthropogenic disturbance. Alpha diversity of bacteria and fungi increased with increasing levels of anthropogenic disturbance, and was thus highest in urban forest soils and lowest in the national parks. The forest soil microbial communities were structured according to the level of anthropogenic disturbance, with a clear urban signature evident in both bacteria and fungi. Despite notable differences in community composition, there was little change in the predicted functional traits of urban bacteria. By contrast, urban soils exhibited a marked loss of ectomycorrhizal fungi. Soil pH was positively correlated with the level of disturbance, and thus was the strongest predictor of variation in alpha and beta diversity of forest soil communities, indicating a role of soil alkalinity in structuring urban soil microbial communities. Hence, our study shows how the properties of urban forest soils promote an increase in microbial diversity and a change in forest soil microbiota composition.

Low-level environmental metal pollution is associated with altered gut microbiota of a wild rodent, the bank vole (Myodes glareolus).

Mining and related industries are a major source of metal pollution. In contrast to the well-studied effects of exposure to metals on animal physiology and health, the impacts of environmental metal pollution on the gut microbiota of wild animals are virtually unknown. As the gut microbiota is a key component of host health, it is important to understand whether metal pollution can alter wild animal gut microbiota composition. Using a combination of 16S rRNA amplicon sequencing and quantification of metal levels in kidneys, we assessed whether multi-metal exposure (the sum of normalized levels of fifteen metals) was associated with changes in gut microbiota of wild bank voles (Myodes glareolus) from two locations in Finland. Exposure to increased metal load was associated with higher gut microbiota species diversity (α-diversity) and altered community composition (ß-diversity), but not dispersion. Multi-metal exposure and increased levels of several metals (Cd, Hg, Pb and Se) were associated with differences in the abundance of microbial taxa, especially those within the families Clostridiales vadinBB60 group, Desulfovibrionaceae, Lachnospiraceae, Muribaculaceae and Ruminococcaceae. Our data indicate that even low-level metal pollution can affect the diversity of microbiota and be associated with deterministic differences in composition of host gut microbiota in wild animal populations. These findings highlight the need to study a broader range of metals and their cocktails that are more representative of the types of environmental exposure experienced by wild animals.