Biology subjects

Dubin, S.

Publications and source records attributed to Dubin, S..

4 recordsLinked to original sources

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

Linking land-use change, water quality, and host-parasite dynamics with droplet digital PCR and Bayesian path analyses

Global changes in land use and nutrient cycling are transforming ecosystems at unprecedented rates, with significant consequences for infectious disease dynamics. Aquatic environments are particularly vulnerable because the interplay of habitat modification, nutrient enrichment, and biodiversity loss can drive pronounced changes in the community composition of food webs, including hosts and parasites. Yet, despite well-documented effects of habitat modification on aquatic communities and food webs, the mechanisms through which these changes influence infectious disease dynamics remain poorly resolved. This gap arises, in part, because it remains challenging to disentangle how multiple stressors interact to shape disease outcomes and quantify parasite levels and host densities from field-collected samples. Here, we illustrate two tools that might help address these challenges. First, highly sensitive droplet digital PCR can quantify infection loads even when the signal:noise ratio is low. Second, stepwise Bayesian path analyses can identify the direct and indirect pathways connecting land-use changes to infectious disease dynamics. As a case study, we examined cyclopoid copepods and their helminth parasite, Schistocephalus solidus, across 47 freshwater lakes on Vancouver Island, a region strongly shaped by commercial logging, including widespread clear-cutting of old-growth forests. Our results reveal a positive correlation between copepod density and deforestation, potentially mediated by associated changes in water quality and calanoid copepods, key competitors of the focal host. ddPCR enabled sensitive detection of extremely low parasite signals in field-collected copepods. We detected positive infections in only 19.5% of the lakes surveyed, highlighting the difficulty of assessing disease dynamics in natural populations. Nonetheless, this study highlights the challenges of linking land-use change to disease outcomes, while also demonstrating that sensitive molecular and statistical tools offer new ways to reveal these hidden connections.

ecology↗

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

Constitutive and inducible fibrosis explain immune variation among threespine stickleback populations

Understanding how immune variation arises in natural populations requires disentangling the relative contributions of host genetic differences, environmental variation, and parasite effects, which is rarely possible in wild systems. Threespine stickleback populations vary in their use of intraperitoneal fibrosis as a defense against the helminth parasite Schistocephalus solidus, providing a natural system to study the genetic and ecological drivers of immune variation. We combined a 46-lake field survey with common garden experiments on 20 representative populations exposed to multiple parasite genotypes to test whether population differences in fibrosis persist under controlled conditions and whether they depend on parasite genotype or lake ecology. Fibrosis variation was strongly heritable, with both constitutive and inducible components persisting under common garden conditions. In contrast, parasite genotype had only a weak effect on fibrosis responses. Moreover, inducible fibrosis covaried with lake environmental conditions, with populations from more eutrophic-like lakes exhibiting stronger responses than those from more oligotrophic-like lakes. Together, these results reveal ecologically structured divergence in heritable immune responses among natural populations.

evolutionary biology↗