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Host populations often vary in the magnitude of coinfection they experience across environmental gradients. Furthermore, coinfection often occurs sequentially, with a second parasite infecting the host after the first has established a primary infection. Because the local environment and interactions between coinfecting parasites can both drive patterns of coinfection, it is important to disentangle the relative contributions of environmental factors and within‐host interactions to patterns of coinfection.Here, we develop a conceptual framework and present an empirical case study to disentangle these facets of coinfection. Across multiple lakes, we surveyed populations of five damselfly (host) species and quantified primary parasitism by aquatic, ectoparasitic water mites and secondary parasitism by terrestrial, endoparasitic gregarines. We first asked if coinfection is predicted by abiotic and biotic factors within the local environment, finding that the probability of coinfection decreased for all host species as pH increased. We then asked if primary infection by aquatic water mites mediated the relationship between pH and secondary infection by terrestrial gregarines.Contrary to our expectations, we found no evidence for a water mite‐mediated relationship between pH and gregarines. Instead, the intensity of gregarine infection correlated solely with the local environment, with the magnitude and direction of these relationships varying among environmental predictors.Our findings emphasize the role of the local environment in shaping infection dynamics that set the stage for coinfection. Although we did not detect within‐host interactions, the approach herein can be applied to other systems to elucidate the nature of interactions between hosts and coinfecting parasites within complex ecological communities. [ABSTRACT FROM AUTHOR]

Parasites, including pathogens, can adapt to better exploit their hosts on many scales, ranging from within an infection of a single individual to series of infections spanning multiple host species. However, little is known about how the genomes of parasites in natural communities evolve when they face diverse hosts. We investigated how Bartonella bacteria that circulate in rodent communities in the dunes of the Negev Desert in Israel adapt to different species of rodent hosts. We propagated 15 Bartonella populations through infections of either a single host species (Gerbillus andersoni or Gerbillus pyramidum) or alternating between the two. After 20 rodent passages, strains with de novo mutations replaced the ancestor in most populations. Mutations in two mononucleotide simple sequence repeats (SSRs) that caused frameshifts in the same adhesin gene dominated the evolutionary dynamics. They appeared exclusively in populations that encountered G. andersoni and altered the dynamics of infections of this host. Similar SSRs in other genes are conserved and exhibit ON/OFF variation in Bartonella isolates from the Negev Desert dunes. Our results suggest that SSR-based contingency loci could be important not only for rapidly and reversibly generating antigenic variation to escape immune responses but that they may also mediate the evolution of host specificity. Author summary: In nature, pathogens encounter a diverse range of host individuals and species. Understanding how pathogens respond to this high host diversity is essential for predicting and controlling infectious diseases in humans and wildlife. Does host diversity slow down and limit pathogen evolution or accelerate a pathogen's ability to access and adapt to novel hosts? Despite its importance, there are few experimental studies of how pathogens evolve in response to host diversity. To address this gap, we conducted a year-long laboratory evolution experiment to study how Bartonella bacteria from the Negev Desert dunes in Israel adapted to different native rodent species under low and high host diversity scenarios. Pathogen evolution did not proceed more slowly or quickly with the differences in host diversity. Instead, the pathogen rapidly adapted to the more challenging host species through mutations in mononucleotide repeats within an adhesion gene that is a virulence factor. Analysis of the genomes of Bartonella isolates from wild gerbils suggests that hypermutable repeats in this gene and others may have been selected and preserved by evolution, potentially enabling rapid and reversible adaptation to changing host environments. Our findings highlight a possible role for these "contingency loci" in the evolution of host specificity. [ABSTRACT FROM AUTHOR]

As animals age, they exhibit a suite of phenotypic changes, often including reductions in movement and social behaviour ('behavioural ageing'). By altering an individual's exposure to parasites, behavioural ageing may influence infection status trajectories over the lifespan. However, these processes could be confounded by age-related changes in other phenotypic traits, or by selective disappearance of certain individuals owing to parasite-induced mortality. Here, we uncover contrasting age-related patterns of infection across three helminth parasites in wild adult female red deer (Cervus elaphus). Counts of strongyle nematodes (order: Strongylida) increased with age, while counts of liver fluke (Fasciola hepatica) and tissue worm (Elaphostrongylus cervi) decreased, and lungworm (Dictyocaulus) counts did not change. These relationships could not be explained by socio-spatial behaviours, spatial structuring, or selective disappearance, suggesting behavioural ageing is unlikely to be responsible for driving age trends. Instead, social connectedness and strongyle infection were positively correlated, such that direct age–infection trends were directly contrasted with the effects implied by previously documented behavioural ageing. This suggests that behavioural ageing may reduce parasite exposure, potentially countering other age-related changes. These findings demonstrate that different parasites can show contrasting age trajectories depending on diverse intrinsic and extrinsic factors, and that behaviour's role in these processes is likely to be complex and multidirectional. This article is part of the discussion meeting issue 'Understanding age and society using natural populations'. [ABSTRACT FROM AUTHOR]

Despite the ubiquitous nature of parasitism, how parasitism alters the outcome of host–species interactions such as competition, mutualism and predation remains unknown. Using a phylogenetically informed meta‐analysis of 154 studies, we examined how the mean and variance in the outcomes of species interactions differed between parasitized and non‐parasitized hosts. Overall, parasitism did not significantly affect the mean or variance of host–species interaction outcomes, nor did the shared evolutionary histories of hosts and parasites have an effect. Instead, there was considerable variation in outcomes, ranging from strongly detrimental to strongly beneficial for infected hosts. Trophically‐transmitted parasites increased the negative effects of predation, parasites increased and decreased the negative effects of interspecific competition for parasitized and non‐parasitized heterospecifics, respectively, and parasites had particularly strong negative effects on host species interactions in freshwater and marine habitats, yet were beneficial in terrestrial environments. Our results illuminate the diverse ways in which parasites modify critical linkages in ecological networks, implying that whether the cumulative effects of parasitism are considered detrimental depends not only on the interactions between hosts and their parasites but also on the many other interactions that hosts experience. [ABSTRACT FROM AUTHOR]