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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]

Aim: To advance our understanding of the mechanisms that mediate the relationships between global climatic and anthropogenic processes and pathogen occurrence, it is crucial to evaluate the exact pathways connecting the ecological mediators and the pathogen responses across spatial and temporal heterogeneities at various scales. We investigated the pathways connecting these two types of heterogeneities in sand stabilization that were created by contrasting forces of various human activities and long‐term droughts, and pathogen occurrence in host populations. The considered candidate ecological mediators were various components of host community structure, arthropod vector traits, and the pathogen occurrence in these vectors. Location: North‐western Negev Desert's sands in Israel. Time period: 1982–2018. Major taxa studied: Gerbillus andersoni, Gerbillus floweri, Gerbillus gerbillus, Mycoplasma, Bartonella, Synosternus cleopatrae. Methods: We combined information from satellite images, 36 years of rodent censuses, a natural experiment, and causal modelling. Results: We found evidence that the spatial heterogeneity in sand biocrusts is largely correlated with structural differences between host communities, especially at medium spatial scales. Pathogen sampling, followed by causal modelling, suggested that the cascading effect of sand stabilization on pathogen occurrence is mainly mediated through changes in host community structure and vector burdens. Importantly, we found that structural changes in the same host community can simultaneously amplify and dilute different pathogens. Main conclusions: These findings suggest that global processes can translate into local processes, where the importance of the mediation effects depend on the magnitude of environmental heterogeneity. These mediation effects can benefit some organisms while adversely affecting others. [ABSTRACT FROM AUTHOR]

Structural equation modelling (SEM) can illuminate complex interaction networks of the sort found in ecology. However, selecting optimally complex, data‐supported SEM models and quantifying their uncertainty are difficult processes. To this end, we recommend a formal model selection approach (MSA) that uses information criteria.Using a suite of numerical simulations, we compare MSA‐SEM against two traditional methods.We find that MSA‐SEM exhibits superior, unbiased results under the suboptimal realistic conditions characteristic of ecological studies. We then provide a road map for MSA‐SEM and demonstrate its use via a case study.We illustrate the unique abilities of SEM to confirm a network structure within the realm of known causal pathways and delineate the boundaries within which MSA‐SEM should be applied. [ABSTRACT FROM AUTHOR]

Based on molecular data, previous studies have suggested a high overall diversity and co‐infection rates of Bartonella bacteria in wild rodents and their fleas. However, partial genetic characterization of uncultured co‐infecting bacteria limited sound conclusions concerning intra‐ and inter‐specific diversity of the circulating Bartonella. To overcome this limitation, Bartonella infections of wild populations of two sympatric gerbil species and their fleas were explored by multiple isolations of Bartonella organisms. Accordingly, 448 pure Bartonella isolates, obtained from 20 rodent blood and 39 flea samples, were genetically characterized to the genotype and species levels. Results revealed a remarkable diversity and co‐infection rates of Bartonella among these sympatric rodents and their associated fleas. Specifically, 38 genotypes, classified into four main Bartonella species, were identified. Co‐infection was confirmed in 56% of the samples, which contained two to four Bartonella genotypes per sample, belonging to up to three different species. Recombination within and between these species was demonstrated, serving as a direct evidence of the frequent bacteria–bacteria interactions. Moreover, despite the noticeable interchange of common Bartonella genotypes between rodents and fleas, the co‐occurrence of genotypes was not random and differences in the overall diversity, and the ecological and phylogenetic similarities of the infection compositions were significantly associated with the carrier type (rodent vs. flea) and the rodent species. Thus, comprehensive identification of the co‐infecting organisms enabled the elucidation of ecological factors affecting the Bartonella distribution among reservoirs and vectors. This study may serve as a model for the investigation of other vector‐borne organisms and their relationships with Bartonella. [ABSTRACT FROM AUTHOR]