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IntroductionThe long-distance, seasonal migrations of birds make them an effective ecological bridge for the movement of ticks. The introduction of exotic tick species to new geographical regions can cause the emergence of novel tick-borne pathogens. This study examined the prevalence of exotic tick species parasitizing migratory songbirds at stopover sites along the northern Gulf of Mexico using the mitochondrial 12S rRNA gene. MethodsOverall, 421 individual ticks in the generaAmblyomma,Haemaphysalis, andIxodeswere recorded from 28 songbird species, of whichAmblyommaandAmblyomma longirostrewere the most abundant tick genera and species, respectively. A high throughput 16S ribosomal RNA sequencing approach characterized the microbial communities and identified pathogenic microbes in all tick samples. Results and discussionMicrobial profiles showed that Proteobacteria was the most abundant phylum. The most abundant pathogens wereRickettsiaand endosymbiontFrancisella,Candidatus Midichloria, andSpiroplasma. Permutation multivariate analysis of variance revealed that the relative abundance ofFrancisellaandRickettsiadrives microbial patterns across the tick genera. We also noted a higher percentage of positive correlations in microbe-microbe interactions among members of the microbial communities. Network analysis suggested a negative correlation between a)FrancisellaandRickettsiaand, b)FrancisellaandCutibacterium. Lastly, mapping the distributions of bird species parasitized during spring migrations highlighted geographic hotspots where migratory songbirds could disperse ticks and their pathogens at stopover sites or upon arrival to their breeding grounds, the latter showing mean dispersal distances from 421–5003 kilometers. These findings spotlight the potential role of migratory birds in the epidemiology of tick-borne pathogens. 

Although the global conversion of wildlife habitat to built environments often has negative impacts on biodiversity, some wildlife species have the ability to cope by living in human-made structures. However, the determinants of this adaptation on a global scale are not well understood and may signify species with unique conservation needs at the human–wildlife interface. Here, we identify the trait profile associated with anthropogenic roosting in bats globally and characterize the evolution of this phenotype using an original dataset of roosting behavior developed across 1,279 extant species. Trait-based analyses showed that anthropogenic roosting is predictable across bats and is associated with larger geographic ranges, habitat generalism, temperate zone distributions, small litter and body size, and insectivory.Weidentified moderate phylogenetic signal in this complex trait profile, which has undergone both gains and losses across bat evolution and for which speciation rates are lower compared to natural roosting bats. 

Emerging infectious diseases, biodiversity loss, and anthropogenic environmental change are interconnected crises with massive social and ecological costs. In this Review, we discuss how pathogens and parasites are responding to global change, and the implications for pandemic prevention and biodiversity conservation. Ecological and evolutionary principles help to explain why both pandemics and wildlife die-offs are becoming more common; why land-use change and biodiversity loss are often followed by an increase in zoonotic and vector-borne diseases; and why some species, such as bats, host so many emerging pathogens. To prevent the next pandemic, scientists should focus on monitoring and limiting the spread of a handful of high-risk viruses, especially at key interfaces such as farms and live-animal markets. But to address the much broader set of infectious disease risks associated with the Anthropocene, decision-makers will need to develop comprehensive strategies that include pathogen surveillance across species and ecosystems; conservation-based interventions to reduce human–animal contact and protect wildlife health; health system strengthening; and global improvements in epidemic preparedness and response. Scientists can contribute to these efforts by filling global gaps in disease data, and by expanding the evidence base for disease–driver relationships and ecological interventions. 

ABSTRACT Accumulating data suggest that some bat species host emerging viruses that are highly pathogenic in humans and agricultural animals. Laboratory-based studies have highlighted important adaptations in bat immune systems that allow them to better tolerate viral infections compared to humans. Simultaneously, ecological studies have discovered critical extrinsic factors, such as nutritional stress, that correlate with virus shedding in wild-caught bats. Despite some progress in independently understanding the role of bats as reservoirs of emerging viruses, there remains a significant gap in the molecular understanding of factors that drive virus spillover from bats. Driven by a collective goal of bridging the gap between the fields of bat virology, immunology, and disease ecology, we hosted a satellite symposium at the 2024 American Society for Virology meeting. Bringing together virologists, immunologists, and disease ecologists, we discussed the intrinsic and extrinsic factors such as virus receptor engagement, adaptive immunity, and virus ecology that influence spillover from bat hosts. This article summarizes the topics discussed during the symposium and emphasizes the need for interdisciplinary collaborations and resource sharing. 

ABSTRACT Bacterial pathogens remain poorly characterized in bats, especially in North America. We describe novel (and in some cases panmictic) hemoplasmas (10.1% positivity) and bartonellae (25.6% positivity) across three colonies of Mexican free-tailed bats (Tadarida brasiliensis), a partially migratory species that can seasonally travel hundreds of kilometers. Molecular analyses identified three novelCandidatushemoplasma species most similar to another novelCandidatusspecies in Neotropical molossid bats. We also detected novel hemoplasmas in sympatric cave myotis (Myotis velifer) and pallid bats (Antrozous pallidus), with sequences in the latter 96.5% related toCandidatusMycoplasma haematohominis. We identified nineBartonellagenogroups, including those in cave myotis with 96.1% similarity toCandidatusBartonella mayotimonensis. We also detectedBartonella rochalimaein migratory Mexican free-tailed bats, representing the first report of this human pathogen in the Chiroptera. Monthly sampling of migratory Mexican free-tailed bats during their North American occupancy period also revealed significant seasonality in infection for both bacterial pathogens, with prevalence increasing following spring migration, peaking in the maternity season, and declining into fall migration. The substantial diversity and seasonality of hemoplasmas and bartonellae observed here suggest that additional longitudinal, genomic, and immunological studies in bats are warranted to inform One Health approaches. IMPORTANCEBats have been intensively sampled for viruses but remain mostly understudied for bacterial pathogens. However, bacterial pathogens can have significant impacts on both human health and bat morbidity and even mortality. Hemoplasmas and bartonellae are facultative intracellular bacteria of special interest in bats, given their high prevalence and substantial genetic diversity. Surveys have also supported plausible zoonotic transmission of these bacteria from bats to humans, includingCandidatusMycoplasma haematohominis andCandidatusBartonella mayotimonensis. Greater characterization of these bacteria across global bat diversity (over 1,480 species) is therefore warranted to inform infection risks for both bats and humans, although little surveillance has thus far been conducted in North American bats. We here describe novel (and in some cases panmictic) hemoplasmas and bartonellae across three colonies of Mexican free-tailed bats and sympatric bat species. We find high genetic diversity and seasonality of these pathogens, including lineages closely related to human pathogens, such asBartonella rochalimae. 

Habitat degradation can increase zoonotic disease risks by altering infection dynamics in wildlife and increasing wildlife–human interactions. Bats are an important taxonomic group to consider these effects, because they harbour many relevant zoonotic viruses and have species‐ and context‐dependent responses to degradation that could affect zoonotic virus dynamics. Yet our understanding of the associations between habitat degradation and bat virus prevalence and seroprevalence are limited to a small number of studies, which often differ in the bats or viruses sampled, the study region, and methodology. To develop a broad understanding of the associations between bat viruses and habitat degradation, we conducted an initial phylogenetic meta‐analysis that combines published prevalence and seroprevalence (‘(sero)prevalence') with remote‐sensing habitat degradation data. Our dataset includes 588 unique records of (sero)prevalence across 16 studies, 64 bat species, and five virus families. We quantified the overall strength and direction of the relationship between habitat degradation and bat virus outcomes and tested how this relationship is moderated by the time between habitat degradation and bat sampling and by ecological traits of bat hosts while controlling for phylogenetic non‐independence among bat species. We found no effect of degradation on prevalence overall, although a weak effect may exist when forest loss occurs the year prior to bat sampling. In contrast, we detected a negative but weak association between degradation and seroprevalence overall that was strengthened when forest loss occurred the year prior to bat sampling. No bat traits that we investigated interacted with habitat degradation to impact virus outcomes, suggesting observed trends are independent of these traits. Biases in our initial dataset highlight opportunities for future work; prevalence was highly zero‐inflated, and seroprevalence was dominated byDesmodus rotundusand rabies virus. These findings and subsequent analyses will improve our understanding of how global change affects host–pathogen dynamics. 

Abstract Pathogen evolution is one of the least predictable components of disease emergence, particularly in nature. Here, building on principles established by the geographic mosaic theory of coevolution, we develop a quantitative, spatially explicit framework for mapping the evolutionary risk of viral emergence. Driven by interest in diseases like Severe Acute Respiratory Syndrome (SARS), Middle East Respiratory Syndrome (MERS), and Coronavirus disease 2019 (COVID-19), we examine the global biogeography of bat-origin betacoronaviruses, and find that coevolutionary principles suggest geographies of risk that are distinct from the hotspots and coldspots of host richness. Further, our framework helps explain patterns like a unique pool of merbecoviruses in the Neotropics, a recently discovered lineage of divergent nobecoviruses in Madagascar, and—most importantly—hotspots of diversification in southeast Asia, sub-Saharan Africa, and the Middle East that correspond to the site of previous zoonotic emergence events. Our framework may help identify hotspots of future risk that have also been previously overlooked, like West Africa and the Indian subcontinent, and may more broadly help researchers understand how host ecology shapes the evolution and diversity of pandemic threats.