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1. What Does Tolerance Mean for Animal Disease Dynamics When Pathology Enhances Transmission?

   https://doi.org/10.1093/icb/icz065  

   Henschen, Amberleigh E.; Adelman, James S. (May 2019, Integrative and Comparative Biology)

   Abstract Host competence, or how well an individual transmits pathogens, varies substantially within and among animal populations. As this variation can alter the course of epidemics and epizootics, revealing its underlying causes will help predict and control the spread of disease. One host trait that could drive heterogeneity in competence is host tolerance, which minimizes fitness losses during infection without decreasing pathogen load. In many cases, tolerance should increase competence by extending infectious periods and enabling behaviors that facilitate contact among hosts. However, we argue that the links between tolerance and competence are more varied. Specifically, the different physiological and behavioral mechanisms by which hosts achieve tolerance should have a range of effects on competence, enhancing the ability to transmit pathogens in some circumstances and impeding it in others. Because tissue-based pathology (damage) that reduces host fitness is often critical for pathogen transmission, we focus on two mechanisms that can underlie tolerance at the tissue level: damage-avoidance and damage-repair. As damage-avoidance reduces transmission-enhancing pathology, this mechanism is likely to decrease host competence and pathogen transmission. In contrast, damage-repair does not prevent transmission-relevant pathology from occurring. Rather, damage-repair provides new, healthy tissues that pathogens can exploit, likely extending the infectious period and increasing host competence. We explore these concepts through graphical models and present three disease systems in which damage-avoidance and damage-repair alter host competence in the predicted directions. Finally, we suggest that by incorporating these links, future theoretical studies could provide new insights into infectious disease dynamics and host–pathogen coevolution. 

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2. A legacy of competitive exclusion: Host demography and amplified disease

   https://doi.org/10.1093/icb/icaf035  

   Suh, Daniel_C; Schroeder, Katie; Landolt, Emily_F; Tejada, Jenavier; Strauss, Alexander_T (May 2025, Integrative And Comparative Biology)

   Synopsis Dilution effects arise when increases in species diversity reduce disease risk, and amplification effects arise when the opposite occurs. Despite ample evidence for both phenomena, the mechanisms driving dilution and amplification effects and how they are mediated by environmental factors remain poorly understood. Mechanisms involving demographic rates or stage structure of hosts are particularly lacking in the diversity–disease literature. In Midwestern lakes, Metschnikowia bicuspidata parasites infect Daphnia dentifera focal hosts in autumn, with epidemics beginning when water is warm (∼25°C) and peaking when lakes have cooled (∼15°C). Epidemics are smaller in lakes with more Ceriodaphnia dubia alternative hosts, which serve as key diluters of disease. However, it is unclear whether seasonal changes in temperature affect their ability to alter host population dynamics and reduce disease. We conducted a mesocosm experiment to test how temperature (15, 20, or 25°C) mediated the effects of these key alternative hosts on density, stage structure, and disease dynamics in focal host populations. The experiment yielded several surprising results. First, focal hosts rapidly outcompeted alternative hosts at all temperatures. By the time parasites were added, alternative hosts had been almost completely excluded. Second, despite diluting disease in the field, initial presence of these alternative hosts amplified infection prevalence in the experiment. Third, this amplification arose as a legacy effect, lasting generations after alternative hosts were gone. Our explanation for this legacy amplification effect centers on focal host stage structure and demography. Competition with alternative hosts resulted in focal host populations that were more adult-biased when parasites were added, at all 3 temperatures. Additionally, host densities in these treatments increased more rapidly in the subsequent 10 days, consistent with reduced background death rates. Since adults consume more parasites than juveniles, and since exposed hosts must survive 10 days before producing infectious spores, these initial differences in stage structure and population growth seem to have set disease dynamics along amplified trajectories. These results highlight the need for a broader understanding of the mechanisms that can amplify or dilute disease, including altered host stage structure and mortality of exposed hosts in diverse communities. 

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3. Beyond single host, single parasite interactions: Quantifying competence for complete multi‐host, multi‐parasite communities

   https://doi.org/10.1111/1365-2435.14068  

   Stewart Merrill, Tara E.; Calhoun, Dana M.; Johnson, Pieter T. J. (May 2022, Functional Ecology)

   Abstract Understanding parasite transmission in communities requires knowledge of each species' capacity to support transmission. This property, ‘competence’, is a critical currency for modelling transmission under community change and for testing diversity–disease theory. Despite the central role of competence in disease ecology, we lack a clear understanding of the factors that generate competence and drive its variation.We developed novel conceptual and quantitative approaches to systematically quantify competence for a multi‐host, multi‐parasite community. We applied our framework to an extensive dataset: five amphibian host species exposed to four parasitic trematode species across five ecologically realistic exposure doses. Together, this experimental design captured 20 host–parasite interactions while integrating important information on variation in parasite exposure. Using experimental infection assays, we measured multiple components of the infection process and combined them to produce competence estimates for each interaction.With directly estimated competence values, we asked which components of the infection process best explained variation in competence: barrier resistance (the initial fraction of administered parasites blocked from infecting a host), internal clearance (the fraction of established parasites lost over time) or pre‐transmission mortality (the probability of host death prior to transmission). We found that variation in competence among the 20 interactions was best explained by differences in barrier resistance and pre‐transmission mortality, underscoring the importance of host resistance and parasite pathogenicity in shaping competence.We also produced dose‐integrated estimates of competence that incorporated natural variation in exposure to address questions on the basis and extent of variation in competence. We found strong signals that host species identity shaped competence variation (as opposed to parasite species identity). While variation in infection outcomes across hosts, parasites, individuals and doses was considerable, individual heterogeneity was limited compared to among‐species differences. This finding highlights the robustness of our competence estimates and suggests that species‐level values may be strong predictors for community‐level transmission in natural systems.Competence emerges from distinct underlying processes and can have strong species‐level characteristics; thus, this property has great potential for linking mechanisms of infection to epidemiological patterns. Read the freePlain Language Summaryfor this article on the Journal blog. 

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4. Host adaptation drives genetic diversity in a vector-borne disease system.

   Combs, MA (January 2022, bioRxiv)

   The range of hosts a pathogen can infect is a key trait influencing human disease risk and reservoir host infection dynamics. Borrelia burgdorferi sensu stricto (Bb), an emerging zoonotic pathogen, causes Lyme disease and is widely considered a host generalist, commonly infecting mammals and birds. Yet the extent of intraspecific variation in Bb host breadth, its role in determining host competence and potential implications to human infection remain unclear. We conducted a long-term study of Bb diversity, defined by the polymorphic ospC locus, across white-footed mice, passerine birds, and tick vectors leveraging long-read amplicon sequencing. Our results reveal strong variation in host breadth across Bb genotypes, exposing a spectrum of genotype-specific host-adapted phenotypes. We found support for multiple niche polymorphism maintaining Bb diversity in nature and little evidence of temporal shifts in genotype dominance, as would be expected under negative frequency-dependent selection. Passerine birds support the circulation of several human invasive strains in the local tick population and harbor greater Bb genotypic diversity compared to white-footed mice. Mouse-adapted Bb genotypes exhibited longer persistence in individual mice compared to non-adapted genotypes and infection communities infecting individual mice preferentially became dominated by mouse-adapted genotypes over time. We posit that intraspecific variation in Bb host breadth and specificity helps maintain overall species fitness in response to transmission by a generalist vector. Because pathogen genotypes vary in host breadth and result in diverse human disease manifestations, our findings indicate that a more nuanced definition of ‘host competence’ incorporating local genotype frequency is warranted. 

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5. Host adaptation drives genetic diversity in a vector-borne disease system

   https://doi.org/10.1101/2022.05.19.492734  

   Combs, MA; Tufts, DM; Adams, B; Lin, YP; Kolokotronis, SO; Diuk-Wasser, MA (May 2022, bioRxiv)

   The range of hosts a pathogen can infect is a key trait influencing human disease risk and reservoir host infection dynamics. Borrelia burgdorferi sensu stricto (Bb), an emerging zoonotic pathogen, causes Lyme disease and is widely considered a host generalist, commonly infecting mammals and birds. Yet the extent of intraspecific variation in Bb host breadth, its role in determining host competence and potential implications to human infection remain unclear. We conducted a long-term study of Bb diversity, defined by the polymorphic ospC locus, across white-footed mice, passerine birds, and tick vectors leveraging long-read amplicon sequencing. Our results reveal strong variation in host breadth across Bb genotypes, exposing a spectrum of genotype-specific host-adapted phenotypes. We found support for multiple niche polymorphism maintaining Bb diversity in nature and little evidence of temporal shifts in genotype dominance, as would be expected under negative frequency-dependent selection. Passerine birds support the circulation of several human invasive strains in the local tick population and harbor greater Bb genotypic diversity compared to white-footed mice. Mouse-adapted Bb genotypes exhibited longer persistence in individual mice compared to non-adapted genotypes and infection communities infecting individual mice preferentially became dominated by mouse-adapted genotypes over time. We posit that intraspecific variation in Bb host breadth and specificity helps maintain overall species fitness in response to transmission by a generalist vector. Because pathogen genotypes vary in host breadth and result in diverse human disease manifestations, our findings indicate that a more nuanced definition of ‘host competence’ incorporating local genotype frequency is warranted. 

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