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Over the past two decades, research on bat-associated microbes such as viruses, bacteria and fungi has dramatically increased. Here, we synthesize themes from a conference symposium focused on advances in the research of bats and their microbes, including physiological, immunological, ecological and epidemiological research that has improved our understanding of bat infection dynamics at multiple biological scales. We first present metrics for measuring individual bat responses to infection and challenges associated with using these metrics. We next discuss infection dynamics within bat populations of the same species, before introducing complexities that arise in multi-species communities of bats, humans and/or livestock. Finally, we outline critical gaps and opportunities for future interdisciplinary work on topics involving bats and their microbes. 

Anticoagulant rodenticides (ARs) deployed to control rodent pest populations can increase the risk of pathogen infection for some wildlife. However, it is unknown whether ARs also increase infection risk for target rodents, which are common hosts for zoonotic (animal-to-human transmitted) pathogens. In this study, we tested whether rats exposed to ARs were more likely to be infected with zoonotic pathogens, specifically Leptospira spp. or Escherichia coli , after controlling for known predictors of infection (i.e. sex, age, body condition). We collected biological samples from 99 rats trapped in Chicago alleys and tested these for Leptospira infection, E. coli shedding and AR exposure. We found that rats that had been exposed to ARs and survived until the time of trapping, as well as older rats, were significantly more likely to be infected with Leptospira spp. than other rats. We found no significant association between E. coli shedding and any predictors. Our results show that human actions to manage rats can affect rat disease ecology and public health risks in unintended ways, and more broadly, contribute to a growing awareness of bidirectional relationships between humans and natural systems in cities. 

Abstract Urban rats are widely distributed pests that have negative effects on public health and property. It is crucial to understand their distribution to inform control efforts and address drivers of rat presence. Analysing public rat complaints can help assess urban rat distribution and identify factors supporting rat populations. Both social and environmental factors could promote rat complaints and must be integrated to understand rat distributions. We analysed rat complaints made between 2011 and 2017 in Chicago, a city with growing rat problems and stark wealth inequality. We examined whether rat complaints at the census tract level are associated with factors that could influence rat abundance, rats’ visibility to humans, and the likelihood of people making a complaint. Complaints were significantly positively correlated with anthropogenic factors hypothesized to promote rat abundance (restaurants, older buildings, garbage complaints, and dog waste complaints) or rat visibility (building construction/demolition activity), and factors hypothesized to increase the likelihood of complaining (human population density, more owner-occupied homes); we also found that complaints were highest in the summer. Our results suggest that conflicts between residents and rats are mainly driven by seasonal variation in rat abundance and human activity and could be mitigated with strategies such as securing food waste from residential and commercial sources. Accounting for social factors such as population density, construction and demolition activity, and home ownership versus rental can also help cities more accurately predict blocks at higher risk of rat conflicts. 

Anthropogenic landscape modification such as urbanization can expose wildlife to toxicants, with profound behavioural and health effects. Toxicant exposure can alter the local transmission of wildlife diseases by reducing survival or altering immune defence. However, predicting the impacts of pathogens on wildlife across their ranges is complicated by heterogeneity in toxicant exposure across the landscape, especially if toxicants alter wildlife movement from toxicant-contaminated to uncontaminated habitats. We developed a mechanistic model to explore how toxicant effects on host health and movement propensity influence range-wide pathogen transmission, and zoonotic exposure risk, as an increasing fraction of the landscape is toxicant-contaminated. When toxicant-contaminated habitat is scarce on the landscape, costs to movement and survival from toxicant exposure can trap infected animals in contaminated habitat and reduce landscape-level transmission. Increasing the proportion of contaminated habitat causes host population declines from combined effects of toxicants and infection. The onset of host declines precedes an increase in the density of infected hosts in contaminated habitat and thus may serve as an early warning of increasing potential for zoonotic spillover in urbanizing landscapes. These results highlight how sublethal effects of toxicants can determine pathogen impacts on wildlife populations that may not manifest until landscape contamination is widespread.