Biology subjects

Cressler, C. E.

Publications and source records attributed to Cressler, C. E..

11 recordsLinked to original sources

bioRxiv2026

Environmental heterogeneity facilitates competitive suppression of drug resistance

Antimicrobial resistance (AMR) is a growing threat to human health, agriculture, and natural ecosystems. While antimicrobial use is a primary driver of resistance evolution, growing evidence suggests that anthropogenic environmental change may also contribute to the emergence and spread of resistant microbes. Yet the mechanisms linking environmental conditions to AMR remain poorly understood and are largely absent from current strategies to manage resistance. This gap arises, in part, because we still know surprisingly little about how ecological interactions shape the evolutionary dynamics of antimicrobial resistance. Here, we develop a general eco-evolutionary modeling framework to investigate how spatial structure, resource availability, and growth-efficiency trade-offs shape competition between drug-sensitive and drug-resistant strains. We show that spatial heterogeneity influences resistance evolution not simply by strengthening or weakening competition, but by altering the ecological mechanisms through which competition suppresses resistant strains. In homogeneous environments, resistance is suppressed primarily by faster-growing drug-sensitive competitors and only under a relatively narrow range of ecological conditions. In contrast, heterogeneous environments with limited resources favor more resource-efficient drug-sensitive strains, which outcompete resistant strains through a distinct colonization advantage that operates across a broader region of parameter space. These patterns emerge regardless of whether resistant mutants are initially present or arise de novo through mutation. Together, our results provide insight into mechanistic links between environmental change and AMR emergence, suggesting that environmental homogenization and resource enrichment may reduce opportunities for competitive suppression and thereby increase resistance risk. More broadly, this work demonstrates how ecological interactions and environmental structure shape the evolution of resistance and offers possible insight into resistance management. Author summaryAntimicrobial resistance (AMR) is often viewed as a direct consequence of antimicrobial use. However, mounting evidence suggests that ecological processes may often suppress resistant strains before they can emerge and spread. Despite growing recognition that ecological interactions influence AMR, we still know relatively little about the environmental conditions that strengthen or weaken those interactions. We developed a general eco-evolutionary modeling framework that integrates consumer-resource theory, spatial ecology, and stochastic trait evolution to investigate how spatial structure, resource availability, and growth-efficiency trade-offs shape competition between drug-sensitive and drug-resistant strains. Whereas previous theoretical and empirical work has largely focused on spatial variation in antimicrobial exposure, our framework examines how spatial variation in resource availability interacts with growth-efficiency trade-offs to influence the evolutionary dynamics of AMR. Our analyses reveal that environmental heterogeneity does not simply strengthen or weaken competition; it fundamentally alters the ecological mechanisms through which competition suppresses resistance. In homogeneous environments, resistance is constrained primarily by faster-growing sensitive strains but only under a relatively narrow range of ecological conditions. In contrast, heterogeneous environments favor more resource-efficient competitors that suppress resistant strains through a distinct colonization-based mechanism that operates across a larger region of parameter space. The key takeaway is not just that spatial structure or resource availability matter for AMR. Instead, the main lesson is that environmental homogenization may help promote AMR. Because many human activities homogenize environments (e.g., invasive plants, chemically intensive agriculture typical across much of the US Corn Belt), it is critical to determine whether they do so at the spatial scales relevant to microbial competition. Future studies integrating AMR surveillance data and environmental metadata with this eco-evolutionary model could help move environmental heterogeneity and microbial community structure from correlates of resistance into mechanistic predictors of AMR.

evolutionary biology↗

bioRxiv2026

Age-dependent effects of infection on survival of a wild rodent reservoir host

Due to long co-evolutionary histories, many zoonotic pathogens are thought to exert little or no negative effects on their wildlife reservoir hosts. However, there remains a lack of rigorous investigations in natural settings. We conducted a 3-year factorial field experiment to investigate how survival of the Puumala hantavirus (PUUV) reservoir, the bank vole, is impacted by PUUV infection, nematode infections, and food availability. We hypothesized that PUUV would not impact survival, but that coinfection with nematodes would negatively impact survival, and that increased food availability would mitigate the negative effects of coinfection. Surprisingly, we demonstrated that PUUV infected voles had substantially reduced survival when compared to uninfected voles, and this strong negative effect manifested in young voles. Nematode removal increased survival of young voles and food supplementation interacted with movement rather than survival. Our results provide empirical evidence in a natural system for infection reducing survival of its reservoir host.

ecology↗

bioRxiv2026

Food Supplementation Reduces Nematode Super-Shedding in a Wild Mammal

Anthropogenic changes to the environment, including altered food resource availability, influence host physiology, behaviour, and population dynamics, which can have strong downstream consequences on wildlife disease dynamics. Additionally, some individuals within a population contribute disproportionately to infection as super-shedders of infection, but the extent to which food availability alters the likelihood of super-shedding and overall parasite infection patterns is poorly understood. We conducted a three-year field experiment in southern Finland to investigate how food supplementation and parasite removal affect nematode infection measures and the relationship between nematode infection and fitness of wild bank voles (Clethrionomys glareolus). Using a factorial design across 12 populations, we manipulated food availability and administered anthelmintic treatments to assess effects on nematode infection status, intensity, and two measures of super-shedding (abundance super-shedding, intensity super-shedding). We also examined parasite impacts on host fitness, including apparent survival probability and reproductive status. Food supplementation did not affect likelihood of infection, intensity or intensity super-shedding, but did reduce the likelihood of abundance super-shedding, suggesting an effect of food availability on infection heterogeneity. We also identified an interaction between nematode infection status and host age on fitness. Notably, infected younger individuals had reduced survival and reproduction, but infected older individuals had greater survival and reproduction compared to their uninfected counterparts. Our study provides novel empirical evidence on how anthropogenic changes in food availability can influence parasite transmission dynamics and the fitness consequences of these sub-lethal parasites in a wildlife system.

ecology↗

bioRxiv2024

Ecological factors alter how spatial overlap predicts viral infection dynamics in wild rodent populations

Spatial overlap between animals in wildlife populations can have important implications for pathogen transmission. Ecological factors and animal demographic traits can influence animal space use and spatial overlap, but it is unclear how these interactions drive pathogen transmission. We experimentally manipulated wild bank vole populations via resource supplementation and anthelmintic treatment. Using network analysis, we investigated the relationship between spatial overlap and infection likelihood of an endemic zoonotic hantavirus, including how vole sex and reproductive status interact with spatial behaviour to affect infection likelihood. Spatial overlap in a previous month drove the likelihood of current hantavirus infection, and food supplementation and anthelmintic treatment altered the effects of spatial overlap on infection likelihood. Vole sex and reproductive status were important factors determining whether spatial overlap increased or decreased the likelihood of hantavirus infection and interacted with resource supplementation and anthelmintic treatment, generating different infection dynamics in each treatment. Our research provides rare empirical evidence linking previous spatial overlap to current infection status in wildlife populations, with implications for understanding disease dynamics and persistence as well as developing effective management efforts. We further highlight the importance of incorporating variation in ecological factors and host demography when studying pathogen transmission in wildlife systems.

ecology↗

bioRxiv2021

Social hosts evade predation but have deadlier parasites

Parasites exploit hosts to replicate and transmit, but overexploitation kills host and parasite (1): predators may shift this cost-benefit balance by consuming hosts (2-4) or changing host behavior, but the strength of these effects remains unclear. Modeling both, we find a primary, strong effect: hosts group to defend against predators (5), increasing parasite transmission, thus multiple infections, and therefore favoring more exploitative, virulent, parasites (6). Indeed, among 18 Trinidadian Gyrodactyus spp. parasite lines, those collected from high predation guppy populations were more virulent in common garden than those from low predation populations. Our model accurately predicted this result when parametrized with our experimentally demonstrated virulence-transmission trade-off, implicating the behavioral effects of predation. Broadly, our results indicate that reduced social contact selects against parasite virulence. One-Sentence SummaryOur theory and data show predators cause increased host social grouping; the resulting transmission favors parasite virulence.

ecology↗

bioRxiv2021

Metamorphosis imposes variable constraints on genome expansion

Genome size varies ~ 100,000-fold across eukaryotes and has long been hypothesized to be influenced by metamorphosis in animals. Transposable element accumulation has been identified as a major driver of increase, but the nature of constraints limiting the size of genomes has remained unclear, even as traits such as cell size and rate of development co-vary strongly with genome size. Salamanders, which possess diverse metamorphic and non-metamorphic life histories, have the largest vertebrate genomes -- 3 to 40 times that of humans -- as well as the largest range of variation in genome size. We tested 13 biologically-inspired hypotheses exploring how the form of metamorphosis imposes varying constraints on genome expansion in a broadly representative phylogeny containing 118 species of salamanders. We show that metamorphosis during which animals undergo the most extensive and synchronous remodeling imposes the most severe constraint against genome expansion, with the severity of constraint decreasing with reduced extent and synchronicity of remodeling. More generally, our work demonstrates the potential for broader interpretation of phylogenetic comparative analysis in exploring the balance of multiple evolutionary pressures shaping phenotypic evolution.

evolutionary biology↗

bioRxiv2021

Multiple generations of antibiotic exposure and isolation influence host fitness and the microbiome in a model zooplankton species

BackgroundChronic antibiotic exposure impacts host health through changes to the microbiome, increasing disease risk and reducing the functional repertoire of community members. The detrimental effects of antibiotic perturbation on microbiome structure and function after one host generation of exposure have been well-studied. However, much less is understood about the multigenerational effects of antibiotic exposure and how the microbiome may recover across host generations. ResultsIn this study, we examined microbiome composition and host fitness across five generations of exposure to a suite of three antibiotics in the model zooplankton host Daphnia magna. By utilizing a split-brood design where half of the offspring from antibiotic-exposed parents were allowed to recover and half were maintained in antibiotics, we aimed to examine recovery and resilience of the microbiome. Unexpectedly, we discovered that experimental isolation of single host individuals across generations also exerted a strong effect on microbiome composition, with composition becoming less diverse over generations regardless of treatment. Simultaneously, Daphnia magna body size and cumulative reproduction increased across generations while survival decreased. Though antibiotics did cause substantial changes to microbiome composition, the microbiome generally became similar to the no antibiotic control treatment within one generation of recovery no matter how many prior generations were spent in antibiotics. ConclusionsContrary to results found in vertebrate systems, Daphnia magna microbiome composition recovers quickly after antibiotic exposure. However, our results suggest that the isolation of individual hosts leads to the stochastic extinction of rare taxa in the microbiome, indicating that these taxa are likely maintained via transmission in host populations rather than intrinsic mechanisms. This may explain the intriguing result that microbiome diversity loss increased host fitness.

ecology↗

bioRxiv2020

Targeted manipulation of abundant and rare taxa in the Daphnia magna microbiota with antibiotics impacts host fitness differentially

Host-associated microbes contribute to host fitness, but it is unclear whether these contributions are from rare keystone taxa, numerically abundant taxa, or interactions among community members. Experimental perturbation of the microbiota can highlight functionally important taxa; however, this approach is primarily applied in systems with complex communities where the perturbation affects hundreds of taxa, making it difficult to pinpoint contributions of key community members. Here, we use the ecological model organism Daphnia magna to examine the importance of rare and abundant taxa by perturbing its relatively simple microbiota with targeted antibiotics. We used sublethal antibiotic doses to target either rare or abundant members across two temperatures, then measured key host life history metrics and shifts in microbial community composition. We find that removal of abundant taxa had greater impacts on host fitness than did removal of rare taxa and that the abundances of non-target taxa were impacted by antibiotic treatment, suggesting no rare keystone taxa exist in the Daphnia magna microbiota but microbe-microbe interactions may play a role in host fitness. We also find that microbial community composition was impacted by antibiotics differently across temperatures, indicating ecological context shapes within-host microbial responses and effects on host fitness. ImportanceUnderstanding the contributions of rare and abundant taxa to host fitness is an outstanding question in host microbial ecology. In this study, we use the model zooplankton Daphnia magna and its relatively simple cohort of bacterial taxa to disentangle the roles of distinct taxa on host life history metrics, using a suite of antibiotics to selectively reduce the abundance of functionally important taxa. We also examine how environmental context shapes the importance of these bacterial taxa on host fitness.

ecology↗

bioRxiv2019

Establishing the phenotypic basis of adherent-invasive Escherichia coli (AIEC) pathogenicity in intestinal inflammation

Background & AimsAdherent-invasive Escherichia coli (AIEC) are enriched in ileal Crohns disease patients and implicated in disease etiology. However, AIEC pathogenesis is poorly understood, and it is unclear if the expansion of these organisms contributes to inflammatory bowel disease (IBD). Questions also remain as to what extent the various in vitro phenotypes used to classify AIEC are pathologically relevant.\n\nMethodsWe utilized a combination of in vitro phenotyping and a murine model of intestinal inflammation to systematically relate AIEC phenotypes to pathogenicity for 30 mucosa-associated human-derived E. coli strains. In vitro assays used included survival/replication in and TNF- production by J774 macrophages as well as invasion/replication in Caco2 intestinal epithelial cells.\n\nResultsAIEC do not form a phenotypic group that is clearly separated from non-AIEC. However, E. coli strains displaying in vitro AIEC phenotypes caused, on average, more severe intestinal inflammation. Survival/replication of strains in J774 and Caco2 cells were positively correlated with disease in vivo, while adherence to Caco2 cells and TNF- production by J774 cells were not. Importantly, co-colonization with adherent non-AIEC strains ameliorated AIEC-mediated disease.\n\nConclusionOur findings do not support the existence of an AIEC pathovar that can be clearly separated from commensal E. coli. However, intracellular survival/replication phenotypes do contribute to murine intestinal inflammation, suggesting that the AIEC overgrowth observed in human IBD makes a causal contribution to disease. The ability to differentiate pathologically-relevant AIEC phenotypes from those that are not provides an important foundation for developing strategies to predict, diagnose and treat human IBD through characterizing and modulating patient E. coli populations.

microbiology↗

bioRxiv2019

Characterization of core bacterial species in the Daphnia magna microbiota using shotgun metagenomics

BackgroundThe keystone zooplankton Daphnia magna has recently been used as a model system for understanding host-microbiota interactions. However, the bacterial species present and functions associated with their genomes are not well understood. In order to understand potential functions of these species, we combined 16S rRNA sequencing and shotgun metagenomics to characterize the whole-organism microbiota of Daphnia magna.\n\nResultsFive metagenome-assembled genomes (MAGs) were assembled from the Daphnia magna microbiota. Phylogenetic placement of these MAGs indicated that two belong to the Limnohabitans genus, one to Polaromonas, one to Pedobacter, and one unclassifiable below the Burkholderiaceae family. Average nucleotide identity of these MAGs to their closest sequenced relative was <95%, suggesting these may be new species in known genera. 16S rRNA community profiling shows that the Daphnia magna microbiota is distinct from its culture environment. Genes involved in host colonization and immune system evasion were detected across the MAGs. Some metabolic pathways were specific to some MAGs, including sulfur oxidation, nitrate reduction, and flagellar assembly. Threonine and arginine exporters were encoded by the Limnohabitans and Burkholderiaceae MAGs, and pathways for key vitamin biosynthesis and export were identified across MAGs.\n\nConclusionsIn this study, we characterize five metagenome-assembled bacterial genomes within the Daphnia magna microbiota. Our examination of functions associated with these genomes shows a diversity of nutrient acquisition and metabolism pathways present that may benefit the host, as well as genomic signatures of host association and immune system evasion.

genomics↗

bioRxiv2018

Parasite-mediated anorexia increases or decreases virulence evolution, depending on dietary context

Parasite-mediated anorexia is a ubiquitous, but poorly understood component of host-parasite interactions. These temporary but substantial reductions in food intake (range: 4-100%) limit exposure to parasites and alter within-host physiological processes that regulate parasite development, production, and survival, such as energy allocation, immune function, host-microbiota interactions, and gastrointestinal conditions. By altering the duration, severity, and spread of infection, anorexia could substantially alter ecological, evolutionary, and epidemiological dynamics. However, these higher-order implications are typically overlooked and remain poorly understood -- even though medical (e.g., non-steroidal anti-inflammatory drugs, vaccines, targeted signaling pathways, calorie restriction) and husbandry practices (e.g., antibiotic and diet use for rapid growth, nutrient supplementation) often directly or indirectly alter host appetite and nutrient intake. Here, we develop theory that helps elucidate why reduced food intake (anorexia) can enhance or diminish disease severity and illustrates that the population-level outcomes often contrast with the individual-level outcomes: treatments that increase the intake of high quality nutrients (suppressing anorexia), can drive rapid individual-level recovery, but inadvertently increase infection prevalence and select for more virulent parasites. Such a theory-guided approach offers a tool to improve targeting host nutrition to manage disease in both human and livestock populations by revealing a means to predict how nutrient-driven feedbacks will affect both the host and parasite.

evolutionary biology↗