Biology subjects

Hite, J. L.

Publications and source records attributed to Hite, J. L..

9 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

Immune variation and host ontogeny constrain pathogen virulence and transmission in a helminth parasite

Host immune strategies vary widely, yet how this variation shapes parasite virulence and transmission in natural systems remains unresolved. We tested whether host immune strategy governs macroparasite transmission timing and magnitude in Schistocephalus solidus, a cestode with a three-host life cycle. Over 13 months, we surveyed infection and immune activation (fibrosis) in second-intermediate host populations (threespine stickleback) from eight lakes. Host immune strategy (ranging from resistance to tolerance) strongly influenced whether and when parasites reached transmissible sizes, and shifted the synchrony between transmissible-stage peaks and definitive host availability. Across populations, transmission potential peaked at intermediate parasite burdens, consistent with virulence-transmission trade-off theory. These findings demonstrate that host immune phenotype alters epidemiological outcomes in complex life cycle parasites, by shifting both the magnitude and phenology of parasite growth to structure the effective transmission window.

ecology↗

bioRxiv2026

Antimicrobial use contributes to resistance gene enrichment across cattle groups on commercial dairy farms

Antimicrobial use (AMU) in agricultural systems is frequently linked to antimicrobial resistance (AMR). Yet, the scale at which AMU reshapes host-associated resistomes remains unclear. This gap arises, in part, from the scarcity of farm-level AMU data from commercial production systems. Here, we combine detailed AMU records from commercial dairy farms with metagenomic analyses of bovine fecal resistomes from calves, lactating cows, sick cows, and cull cows. At a broad level, resistome profiles were similar regardless of farm AMU. Resistance associated with historically common antibiotics, such as tetracyclines, was frequent on low- and high-AMU farms, indicating that some resistance classes are ubiquitous in dairy systems regardless of current AMU. In contrast, resistance to other drug classes varied systematically with AMU. Higher AMU was associated with increased resistance to aminoglycosides, {beta}-lactams, and macrolides, drug classes that are critical for treating mastitis and bovine respiratory disease. Resistance gene richness and diversity were highest in calves, underscoring the importance of accounting for host traits alongside AMU when evaluating resistance patterns. Together, these findings underscore the need for detailed, farm-level AMU data to understand how management practices shape AMR and to inform strategies for sustaining the effectiveness of existing antimicrobials in agricultural and public-health contexts.

genomics↗

bioRxiv2026

A Multi-Scale Ecological Approach to Assessing Antimicrobial Resistance in a Freshwater Fish

Antimicrobial resistance (AMR) genes are increasingly recognized as an emerging environmental contaminant. Yet, the ecological mechanisms shaping their distribution across natural landscapes remain poorly understood. Here, we quantified AMR gene abundances in microbial communities sampled from wild fish from eight freshwater lakes on Vancouver Island and paired these gene-level measurements with fine-scale limnological and land-use data. Using droplet digital PCR, field surveys, and an iterative spatial forecasting framework that integrates Random Forest models with regression kriging, we explored how watershed-scale processes relate to variation in AMR genes across lakes. Our analyses reveal potential associations between elevated AMR gene levels, changes in water quality, deforestation, and geographic proximity to salmon aquaculture. By integrating data across biological and spatial scales, from genes within microbial communities to lake-level conditions and landscape patterns, this study illustrates the value of combining quantitative molecular measurements with geospatial modeling to identify environmental factors that may promote antimicrobial resistance in natural systems. Our approach provides a proof-of-concept and a general predictive framework for generating hypotheses and informing future monitoring efforts aimed at understanding, managing, and forecasting environmental reservoirs of resistance. SignificanceAntimicrobial resistance (AMR) genes are ancient components of environmental microbiomes. Yet, the mechanisms that generate modern hotspots of resistance across natural landscapes remain unclear. Here, we reveal how watershed-scale environmental change, including water quality metrics linked with deforestation and proximity to salmon aquaculture, predicts elevated AMR gene levels in the microbiomes of wild fish populations. By combining quantitative droplet digital PCR with ecological data and geospatial modeling, we move beyond isolated surveillance data to identify ecological mechanisms that promote antimicrobial resistance in freshwater ecosystems. This integrative approach provides mechanistic insight into why certain habitats, and the organisms within them, become reservoirs of resistance while others do not. Our findings highlight the importance of ecological context in understanding resistance evolution and offer a predictive tool for informing proactive monitoring and management strategies.

ecology↗

bioRxiv2026

From exposure to infection: divergent fitness consequences of parasite encounters in a trophically-transmitted system

Parasites can alter host populations in fundamentally different ways depending on whether exposure results in infection. Yet, most epidemiological and evolutionary inference focuses on established infections, leaving the fitness consequences of parasite exposure comparatively understudied. This gap is consequential because hosts are frequently exposed to diverse parasite genotypes, and these encounters can impose substantial fitness costs even when infection does not occur. Theory predicts that hosts may mitigate these costs when interacting with commonly encountered parasite genotypes, such that exposure to sympatric parasites incurs lower fitness consequences than exposure to novel, allopatric parasites. Here, we examine the fitness consequences of exposure and infection in the first intermediate host of the trophically transmitted tapeworm Schistocephalus solidus, a cyclopoid copepod that serves as the first host in a three-host life cycle. Using sympatric (Vancouver Island, Canada) and allopatric (Norway) host-parasite combinations, we found a striking reciprocal asymmetry. Sympatric parasites were significantly more infective, yet exposure to sympatric parasites imposed weaker fitness costs when infection did not establish. In contrast, allopatric parasites were less infective, but exposed females produced fewer eggs and had lower hatching success than both controls and females exposed to sympatric parasites, indicating substantial genotype-dependent costs of exposure. Moreover, we found that infection was highly virulent across all genotypes: a single parasite caused near-complete reproductive suppression and reduced host survival across all host-parasite pairings, confirming S. solidus as a castrating parasite in copepods. Together, these results demonstrate that exposure, not just infection, acts as a critical ecological filter with potentially large and underappreciated consequences for host population dynamics and parasite transmission.

evolutionary biology↗

bioRxiv2025

The nutritional content of anthropogenic resources affects wildlife disease dynamics

Wildlife have become increasingly reliant on human-supplemented food, affecting interactions between individuals and subsequently disease transmission. Much of the research investigating the impact of human-supplemented food has focused on host behavioral changes and food availability. However, the nutritional quality of food can significantly impact disease transmission depending on whether it boosts or hinders immunity. Few studies have investigated links between nutrition, immunity, and pathogen transmission, which weakens efforts to guide and manage infectious disease at the wildlife-human interface. We investigate these interactions using a data-driven transmission model that explicitly incorporates feedback between nutrition, immunity, and pathogen transmission in the bacterial pathogen, Mycoplasma gallisepticum and its avian hosts which are heavily dependent on supplemental food sources. We also examine the nutritional content and sales frequency of one of, if not the, most common source of anthropogenic food supplementation, bird feeder food. We find that food with lower nutritional quality is purchased for wild bird supplementation far more frequently than food with high nutritional quality. Further, our transmission model demonstrates that these lower quality food sources result in large epidemics that cause destabilizing population declines. Our results suggest that nutritional quality plays an important role in disease transmission and provide insight into the ecological and immunological consequences of human behavior on infectious disease in wildlife.

ecology↗

bioRxiv2025

Needle in a haystack: A droplet digital polymerase chain reaction assay to detect rare helminth parasites infecting natural host populations

Helminths infect humans, livestock, and wildlife, yet remain understudied despite their significant impact on public health and agriculture. Because many of the most prevalent helminth-borne diseases are zoonotic, the health of diverse host species are closely interconnected. Therefore, understanding helminth transmission among wildlife could improve predictions and management of infection risks across species. A key challenge to understanding helminth transmission dynamics in wildlife is accurately and quantitatively tracking infection levels across hosts and environments. Traditional methods, such as visual parasite identification from environmental samples or infected hosts, are time-consuming, while standard molecular techniques (e.g., PCR and qPCR) often lack the sensitivity to reliably detect lower parasit burdens. These limitations often underestimate the prevalence and severity of infection, hindering efforts to manage infectious diseases. Here, we developed a multiplexed droplet digital PCR (ddPCR) assay to quantify helminth levels in aquatic habitats using 18S rRNA target genes. Using Schistocephalus solidus and their copepod hosts as a case study, we demonstrate ddPCRs sensitivity and precision. By establishing a 1:1 infection standard in the lab, we contextualize ddPCR gene concentration data to quantify both host and parasite numbers in field samples. The assay is highly reproducible, reliably detecting target genes at concentrations as low as 1 picogram of DNA in lab standards and field samples (multi-species and eDNA). Thus, we provide a toolkit for quantifying infection loads in intermediate hosts and monitoring infection dynamics across spatio-temporal scales in multiple helminth systems of concern for public health, agriculture, and conservation biology. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=139 SRC="FIGDIR/small/634533v1_ufig1.gif" ALT="Figure 1"> View larger version (66K): org.highwire.dtl.DTLVardef@1bc2e40org.highwire.dtl.DTLVardef@180822eorg.highwire.dtl.DTLVardef@1e2c2c8org.highwire.dtl.DTLVardef@621909_HPS_FORMAT_FIGEXP M_FIG Applications of ddPCR probe-primer design to parallel systems. Cyclopoid copepods serve as initial hosts for diverse helminthic diseases distributed globally. The primers designed in this assay are suitable for other systems, with minimal work required for probe design specific to each helminth species. C_FIG

molecular biology↗

bioRxiv2022

Natural variation in host defense strategies impacts both host and pathogen fitness

O_LIAnimals ranging from mosquitoes to humans often vary their feeding behavior when infected or merely exposed to pathogens. For example, some individuals drastically reduce their food intake ( illness-mediated anorexia) while others increase food intake ( hyperphagia). While these so-called sickness behaviors are well documented, their functional consequences remain poorly resolved. C_LIO_LIHere, we examine links between natural genetic variation in susceptibility to infection, feeding behaviors, multiple traits of the host, and within-host pathogen production. Using a zooplankton host (Daphnia dentifera) and a fungal pathogen (Metschnikowia bicuspidata) as a case study, we show that genotypic and dose-dependent variation in feeding behaviors are associated with both resistance and tolerance mechanisms. C_LIO_LIIn one genotype, immune-mediated anorexia was associated with increased tolerance to infection; unlike other genotypes, these individuals did not upregulate phenoloxidase activity, but lived longer, had the highest overall fecundity, and produced higher pathogen loads, despite their reduced growth rates and resultant smaller body sizes. In these hosts, peak parasite load remained unchanged, suggesting a tolerance mechanism that offset fecundity costs. C_LIO_LIIn other genotypes, feeding behaviors followed either a flat or hump-shaped pattern with pathogen dose, exhibiting hyperphagia at intermediate doses and anorexia at higher doses. In these cases, anorexia functioned primarily in resistance. C_LIO_LIOur results suggest that infection-mediated changes in host feeding behavior -- which are traditionally interpreted as immunopathology -- may in fact serve as crucial components of host defense strategies. Moreover, these phenomena vary across host genotypes, and were associated with apparent trade-offs with another melanization component of immune defense. Together, these results underscore that while resistance and tolerance are typically viewed as alternative and fixed defense strategies, the immense genetic diversity for immune defense may result in more of a plastic spectrum spanning a gradient from resistance to tolerance. C_LI

ecology↗

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↗