More Like this

1. Rapid adaptation to a novel pathogen through disease tolerance in a wild songbird

   https://doi.org/10.1371/journal.ppat.1011408  

   Henschen, Amberleigh E. ; Vinkler, Michal ; Langager, Marissa M. ; Rowley, Allison A. ; Dalloul, Rami A. ; Hawley, Dana M. ; Adelman, James S. ( June 2023 , PLOS Pathogens)

   McGraw, Elizabeth A. (Ed.)

   Animal hosts can adapt to emerging infectious disease through both disease resistance, which decreases pathogen numbers, and disease tolerance, which limits damage during infection without limiting pathogen replication. Both resistance and tolerance mechanisms can drive pathogen transmission dynamics. However, it is not well understood how quickly host tolerance evolves in response to novel pathogens or what physiological mechanisms underlie this defense. Using natural populations of house finches ( Haemorhous mexicanus ) across the temporal invasion gradient of a recently emerged bacterial pathogen ( Mycoplasma gallisepticum ), we find rapid evolution of tolerance (<25 years). In particular, populations with a longer history of MG endemism have less pathology but similar pathogen loads compared with populations with a shorter history of MG endemism. Further, gene expression data reveal that more-targeted immune responses early in infection are associated with tolerance. These results suggest an important role for tolerance in host adaptation to emerging infectious diseases, a phenomenon with broad implications for pathogen spread and evolution. 

   more » « less
2. Disease tolerance alters host competence in a wild songbird

   https://doi.org/10.1098/rsbl.2021.0362  

   Ruden, Rachel M. ; Adelman, James S. ( October 2021 , Biology Letters)

   Individuals can express a range of disease phenotypes during infection, with important implications for epidemics. Tolerance, in particular, is a host response that minimizes the per-pathogen fitness costs of infection. Because tolerant hosts show milder clinical signs and higher survival, despite similar pathogen burdens, their potential for prolonged pathogen shedding may facilitate the spread of pathogens. To test this, we simulated outbreaks of mycoplasmal conjunctivitis in house finches, asking how the speed of transmission varied with tissue-specific and behavioural components of tolerance, milder conjunctivitis and anorexia for a given pathogen load, respectively. Because tissue-specific tolerance hinders pathogen deposition onto bird feeders, important transmission hubs, we predicted it would slow transmission. Because behavioural tolerance should increase interactions with bird feeders, we predicted it would speed transmission. Our findings supported these predictions, suggesting that variation in tolerance could help identify individuals most likely to transmit pathogens. 

   more » « less
3. Habitat quality influences pollinator pathogen prevalence through both habitat–disease and biodiversity–disease pathways

   https://doi.org/10.1002/ecy.3933  

   Fearon, Michelle L. ; Wood, Chelsea L. ; Tibbetts, Elizabeth A. ( January 2023 , Ecology)

   The dilution effect hypothesis posits that increasing biodiversity reduces infectious disease transmission. Here, we propose that habitat quality might modulate this negative biodiversity–disease relationship. Habitat may influence pathogen prevalence directly by affecting host traits like nutrition and immune response (we coined the term “habitat–disease relationship” to describe this phenomenon) or indirectly by changing host biodiversity (biodiversity–disease relationship). We used a path model to test the relative strength of links between habitat, biodiversity, and pathogen prevalence in a pollinator–virus system. High‐quality habitat metrics were directly associated with viral prevalence, providing evidence for a habitat–disease relationship. However, the strength and direction of specific habitat effects on viral prevalence varied based on the characteristics of the habitat, host, and pathogen. In general, more natural area and richness of land‐cover types were directly associated with increased viral prevalence, whereas greater floral density was associated with reduced viral prevalence. More natural habitat was also indirectly associated with reduced prevalence of two key viruses (black queen cell virus and deformed wing virus) via increased pollinator species richness, providing evidence for a habitat‐mediated dilution effect on viral prevalence. Biodiversity–disease relationships varied across viruses, with the prevalence of sacbrood virus not being associated with any habitat quality or pollinator community metrics. Across all viruses and hosts, habitat–disease and biodiversity–disease paths had effects of similar magnitude on viral prevalence. Therefore, habitat quality is a key driver of variation in pathogen prevalence among communities via both direct habitat–disease and indirect biodiversity–disease pathways, though the specific patterns varied among different viruses and host species. Critically, habitat–disease relationships could either contribute to or obscure dilution effects in natural systems depending on the relative strength and direction of the habitat–disease and biodiversity–disease pathways in that host–pathogen system. Therefore, habitat may be an important driver in the complex interactions between hosts and pathogens.

    

   more » « less
4. Variability in environmental persistence but not per capita transmission rates of the amphibian chytrid fungus leads to differences in host infection prevalence

   https://doi.org/10.1111/1365-2656.13612  

   Rumschlag, Samantha L. ; Roth, Sadie A. ; McMahon, Taegan A. ; Rohr, Jason R. ; Civitello, David J. ( November 2021 , Journal of Animal Ecology)

   Heterogeneities in infections among host populations may arise through differences in environmental conditions through two mechanisms. First, environmental conditions may alter host exposure to pathogens via effects on survival. Second, environmental conditions may alter host susceptibility, making infection more or less likely if contact between a host and pathogen occurs. Further, host susceptibility might be altered through acquired resistance, which hosts can develop, in some systems, through exposure to dead or decaying pathogens and their metabolites. Environmental conditions may alter the rates of pathogen decomposition, influencing the likelihood of hosts developing acquired resistance.

   The present study primarily tests how environmental context influences the relative contributions of pathogen survival and per capita transmission on host infection prevalence using the amphibian chytrid fungus (Batrachochytrium dendrobatidis; Bd) as a model system. Secondarily, we evaluate how environmental context influences the decomposition of Bd because previous studies have shown that dead Bd and its metabolites can illicit acquired resistance in hosts. We conducted Bd survival and infection experiments and then fit models to discern how Bd mortality, decomposition and per capita transmission rates vary among water sources [e.g. artificial spring water (ASW) or water from three ponds].

   We found that infection prevalence differed among water sources, which was driven by differences in mortality rates of Bd, rather than differences in per capita transmission rates. Bd mortality rates varied among pond water treatments and were lower in ASW compared to pond water.

   These results suggest that variation in Bd infection dynamics could be a function of environmental factors in waterbodies that result in differences in exposure of hosts to live Bd. In contrast to the persistence of live Bd, we found that the rates of decomposition of dead Bd did not vary among water sources, which may suggest that exposure of hosts to dead Bd or its metabolites might not commonly vary among nearby sites. Ultimately, a mechanistic understanding of the environmental dependence of free‐living pathogens could lead to a deeper understanding of the patterns of outbreak heterogeneity, which could inform surveillance and management strategies.

    

   more » « less
5. Cellular and immunological mechanisms influence host-adapted phenotypes in a vector-borne microparasite

   https://doi.org/10.1098/rspb.2021.2087  

   Lin, Yi-Pin ; Tufts, Danielle M. ; Combs, Matthew ; Dupuis, Alan P. ; Marcinkiewicz, Ashley L. ; Hirsbrunner, Andrew D. ; Diaz, Alexander J. ; Stout, Jessica L. ; Blom, Anna M. ; Strle, Klemen ; et al ( February 2022 , Proceedings of the Royal Society B: Biological Sciences)

   Predicting pathogen emergence and spillover risk requires understanding the determinants of a pathogens' host range and the traits involved in host competence. While host competence is often considered a fixed species-specific trait, it may be variable if pathogens diversify across hosts. Balancing selection can lead to maintenance of pathogen polymorphisms (multiple-niche-polymorphism; MNP). The causative agent of Lyme disease, Borrelia burgdorferi ( Bb ), provides a model to study the evolution of host adaptation, as some Bb strains defined by their outer surface protein C ( ospC ) genotype, are widespread in white-footed mice and others are associated with non-rodent vertebrates (e.g. birds). To identify the mechanisms underlying potential strain × host adaptation, we infected American robins and white-footed mice, with three Bb strains of different ospC genotypes. Bb burdens varied by strain in a host-dependent fashion, and strain persistence in hosts largely corresponded to Bb survival at early infection stages and with transmission to larvae (i.e. fitness). Early survival phenotypes are associated with cell adhesion, complement evasion and/or inflammatory and antibody-mediated removal of Bb, suggesting directional selective pressure for host adaptation and the potential role of MNP in maintaining OspC diversity. Our findings will guide future investigations to inform eco-evolutionary models of host adaptation for microparasites. 

   more » « less