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In order to fully understand pathogen induced natural variation in fitness in wild animal populations it is important to identify and study the degree of non‐synonymous alleles in genes that code for components of the immune system. This study investigates the degree of natural genetic variation at 6 innate immune genes belonging to the β‐defensin family within a single population of birds, the great tits Parus major. In 40 adult individuals, all belonging to the same local population in Wytham Woods, Oxford, UK, screened across 6 different β‐defensin genes, all but one individual showed non‐synonymous heterozygosity within the exon coding for the mature defensin peptide. The non‐synonomous variation was thus associated with the part of the defensin gene that directly interacts with potential pathogens. Within the sample, 31 different genotypes were identified across the 6 different loci. Much of the found allelic variation affected the amino acid composition, which in turn alter the net charge and hydrophilicity of the produced peptide; properties associated with the efficiency of binding to and rupture pathogens. This study demonstrates that non‐synonymous genetic variation exists at β‐defensins genes, a part of the immune system that forms an important first line of defence against various pathogens. Understanding the degree of underlying genetic variation at different parts of the immune system will help achieve a holistic view of the reasons behind individual variation in pathogen susceptibility, as well as why individuals are affected differently once they become infected.

Background: The globally transmitted avian malaria parasite Plasmodium relictum (lineage SGS1) has been found to infect hundreds of different bird species with differences in infection outcomes ranging from more or less latent to potentially mortal. However, to date basic knowledge about the links between genetic differentiation and variation in infection outcome within this single malaria parasite species is lacking. Methods: In this study, two different isolates of SGS1, obtained in the wild from two different host species, were used to investigate differences in their development in the blood and virulence in the experimentally infected canaries. Simultaneously, 258 kb of the parasite genome was screened for genetic differences using parasite mRNA and compared between experimental groups. Results: The two isolates showed differences in development and caused mortality as well as effects on the blood parameters of their hosts. Although previous studies using single genes have shown very limited within lineage genetic diversity in the European population of SGS1, 226 SNPs were found across 322 genes, which separated the two experimental groups with a total of 23 SNPs that were fixed in either of the experimental groups. Moreover, genetic variation was found within each experimental group, hinting that each avian malaria infection harbours standing genetic variation that might be selected during each individual infection episode. Conclusion: These results highlight extensive genetic variation within the SGS1 population that is transferred into individual infections, thus adding to the complexity of the infection dynamics seen in these host–parasite interactions. Simultaneously, the results open up the possibility of understanding how genetic variation within the parasite populations is linked to the commonly observed differences in infection outcomes, both in experimental settings and in the wild. Graphical : (Figure presented.).

Generalist parasites experience selective pressures from the various host species they infect. However, it is unclear if parasite transmission among host species precludes the establishment of host-specific adaptations and population genetic structure. We assessed the population genetic structure of the vector-transmitted avian haemosporidian parasite Haemoproteus majoris (lineage WW2; n  = 34 infections) in a single site in southern Sweden among 10 of its host species. The 2 best-sampled host genera were Phylloscopus (2 species, n  = 15 infections) and Sylvia (4 species, n  = 15). We designed a sequence capture protocol to isolate 1.13 Mbp ( ca. 5%) of the parasite genome and identified 1399 variable sites among the sequenced infections. In a principal components analysis, infections of Phylloscopus and Sylvia species mostly separated along the first 2 principal components. Sites with the highest F ST values between the genera were found in genes that have mostly not been implicated in infection pathways, but several sites code for amino acid changes. An analysis of molecular variance confirmed significant variation among host genera, but not among host species within genera. The distribution of Tajima’s D among sequenced loci was negatively skewed, plausibly reflecting a history of bottleneck followed by population expansion. Tajima’s D was lower in infections of Phylloscopus than Sylvia , plausibly because WW2 began infecting Phylloscopus hosts after it was already a parasite of Sylvia hosts. Our results provide evidence of vector-transmitted parasite population differentiation among host species in a single location. Future work should focus on identifying the mechanisms underlying this genetic population structure.

A parasite's ability to be a specialist vs. a generalist may have consequences for its prevalence within one or more if its host species. In this study we investigated the relationship between host specialization and prevalence in the highly species diverse avian blood parasites of the genera Plasmodium and Haemoproteus. Contrary to trade-off hypotheses that may explain host specialization, within both genera the parasites with the ability to complete their life cycles and be transmitted across a wide host range (broad compatibility) were also the most common parasites within their compatible host species. These patterns remained unchanged when the host species with the highest prevalence were excluded, which reduces the possibility that the observed pattern was caused by parasites reaching high prevalence in a single main host, and being \"spilled over\" to other host species. We hypothesize that a positive relationship between parasite host range and prevalence might be explained by an overall higher encounter rate for the parasites with broad host range, which compensates for possibly reduced performance of parasites in each host species. Overall, these results show that parasites with the ability to successfully infect a wide variety of host species of broad ancestry also can have the ability to be the most prevalent in single host species.

Background Migratory birds play an important part in the spread of parasites, with more or less impact on resident birds. Previous studies focus on the prevalence of parasites, but changes in infection intensity over time have rarely been studied. As infection intensity can be quantified by qPCR, we measured infection intensity during different seasons, which is important for our understanding of parasite transmission mechanisms. Methods Wild birds were captured at the Thousand Island Lake with mist nets and tested for avian hemosporidiosis infections using nested PCR. Parasites were identified using the MalAvi database. Then, we used qPCR to quantify the infection intensity. We analyzed the monthly trends of intensity for all species and for different migratory status, parasite genera and sexes. Results Of 1101 individuals, 407 were infected (37.0%) of which 95 were newly identified and mainly from the genus Leucocytozoon . The total intensity trend shows peaks at the start of summer, during the breeding season of hosts and during the over-winter season. Different parasite genera show different monthly trends. Plasmodium causes high prevalence and infection intensity of winter visitors. Female hosts show significant seasonal trends of infection intensity. Conclusions The seasonal changes of infection intensity is consistent with the prevalence. Peaks occur early and during the breeding season and then there is a downward trend. Spring relapses and avian immunity are possible reasons that could explain this phenomenon. In our study, winter visitors have a higher prevalence and infection intensity, but they rarely share parasites with resident birds. This shows that they were infected with Plasmodium during their departure or migration and rarely transmit the disease to resident birds. The different infection patterns of different parasite species may be due to vectors or other ecological properties. Graphical abstract

Invertebrate host–parasite associations are one of the keystones in order to understand vector-borne diseases. The study of these specific interactions provides information not only about how the vector is affected by the parasite at the gene-expression level, but might also reveal mosquito strategies for blocking the transmission of the parasites. A very well-known vector for human malaria is Anopheles gambiae. This mosquito species has been the main focus for genomics studies determining essential key genes and pathways over the course of a malaria infection. However, to-date there is an important knowledge gap concerning other non-mammophilic mosquito species, for example some species from the Culex genera which may transmit avian malaria but also zoonotic pathogens such as West Nile virus. From an evolutionary perspective, these 2 mosquito genera diverged 170 million years ago, hence allowing studies in both species determining evolutionary conserved genes essential during malaria infections, which in turn might help to find key genes for blocking malaria cycle inside the mosquito. Here, we extensively review the current knowledge on key genes and pathways expressed in Anopheles over the course of malaria infections and highlight the importance of conducting genomic investigations for detecting pathways in Culex mosquitoes linked to infection of avian malaria. By pooling this information, we underline the need to increase genomic studies in mosquito–parasite associations, such as the one in Culex–Plasmodium, that can provide a better understanding of the infection dynamics in wildlife and reduce the negative impact on ecosystems.

Background Generating parasite genomes is challenging when little of the DNA in infected host tissue is from the parasite. We used selective whole genome amplification (SWGA) to generate genomic data from wildlife samples of the avian haemosporidian Haemoproteus majoris (lineage PARUS1) and its host, the blue tit ( Cyanistes caeruleus ). Methods We used SWGA to amplify the parasite DNA in nine avian blood samples collected between 1996 and 2021, and subsequently performed short-read sequencing and bioinformatically separated the host and parasite reads in each sample. Results SWGA increased the percentage of parasite reads significantly. Sequencing to a depth of about 56 million reads (forward and reverse) per sample resulted on average (± standard error [SE]) in 11.3X ± 1.85 for the host genome and 1.17X ± 0.446 mean depth of coverage for the host and parasite, respectively, after SWGA. Furthermore, about 74% of the host genome (genome size approx. 1.2 Gb) and 33% of the parasite genome (approx. 23.9 Mb) had at least 1X coverage on average; two samples had 1X coverage of approximately 60% of the parasite genome. Parasite sequencing success was positively correlated with parasitemia. When comparing the parasite sequences in the four best samples, we identified 9895 sites (minimum 5X coverage) that varied among the infections. When filtering the full dataset to at least six samples per variant, we identified 14,512,339 and 7068 sites that varied among samples in the host and parasite populations, respectively, revealing variation among samples and years. Conclusions SWGA facilitates dual host-parasite population genomics in this system and will greatly expand our understanding of host-parasite interactions over space and time. Graphical Abstract

Aim Migrating birds transport their parasites, often over long distances, but little is known about the transfer of these parasites to resident hosts in either the wintering or breeding ranges of the migratory host populations. We investigated the haemosporidian parasite faunas of migratory and resident birds to determine connections among distant parasite faunas, plausibly brought about by migratory host populations. Location Samples were obtained, primarily during or shortly after the local breeding season, throughout the Americas, from the United States through the Caribbean Basin and into northern South America. Methods Infections were identified by PCR and sequencing of parasite DNA in avian blood samples. The analyses were based on c. 4700 infections representing 79 parasite lineages of Plasmodium and Haemoproteus spp. Geographical connections of lineages between regions in the Americas were compared to those in the Euro-African migration system, where migration distances are longer for many host species and the migrant and resident avifaunas in the wintering areas are phylogenetically more divergent. Results Haemosporidian lineages exhibited considerable variation in distribution in the Americas, and patterns of distribution differ markedly between the Americas and the Euro-African migration system. In particular, few lineages were recovered from resident species in both temperate and tropical latitudes, particularly in the Euro-African system, in which a large proportion of lineages were restricted to migrants. Parasite lineages in the Euro-African system exhibited considerable phylogenetic conservatism in their distributions, that is, a tendency of related lineages to exhibit similar geographical distributions. In contrast, clades of parasites in the Americas displayed more geographical diversity, with four of 12 clades exhibiting all four of the distribution types representing the combinations of resident and migrant host species in both temperate and tropical latitudes. Main conclusions Long-distance migrants connect communities of avian haemosporidian parasites in breeding and wintering areas with disparate avifaunas and different vector communities. The degree of parasite lineage sharing between migrants and residents in breeding and wintering areas appears to reflect, to a large degree, the taxonomic similarity of migrants to the resident species in both areas.

Background Imbalances in the gut microbial community (dysbiosis) of vertebrates have been associated with several gastrointestinal and autoimmune diseases. However, it is unclear which taxa are associated with gut dysbiosis, and if particular gut regions or specific time periods during ontogeny are more susceptible. We also know very little of this process in non-model organisms, despite an increasing realization of the general importance of gut microbiota for health. Methods Here, we examine the changes that occur in the microbiome during dysbiosis in different parts of the gastrointestinal tract in a long-lived bird with high juvenile mortality, the ostrich ( Struthio camelus ). We evaluated the 16S rRNA gene composition of the ileum, cecum, and colon of 68 individuals that died of suspected enterocolitis during the first 3 months of life (diseased individuals), and of 50 healthy individuals that were euthanized as age-matched controls. We combined these data with longitudinal environmental and fecal sampling to identify potential sources of pathogenic bacteria and to unravel at which stage of development dysbiosis-associated bacteria emerge. Results Diseased individuals had drastically lower microbial alpha diversity and differed substantially in their microbial beta diversity from control individuals in all three regions of the gastrointestinal tract. The clear relationship between low diversity and disease was consistent across all ages in the ileum, but decreased with age in the cecum and colon. Several taxa were associated with mortality ( Enterobacteriaceae , Peptostreptococcaceae , Porphyromonadaceae , Clostridium ), while others were associated with health ( Lachnospiraceae , Ruminococcaceae , Erysipelotrichaceae , Turicibacter , Roseburia ). Environmental samples showed no evidence of dysbiosis-associated bacteria being present in either the food, water, or soil substrate. Instead, the repeated fecal sampling showed that pathobionts were already present shortly after hatching and proliferated in individuals with low microbial diversity, resulting in high mortality several weeks later. Conclusions Identifying the origins of pathobionts in neonates and the factors that subsequently influence the establishment of diverse gut microbiota may be key to understanding dysbiosis and host development. 2dRYXYkxWvrfQp8YyiPnfy Video Abstract

Flight speed is expected to increase with mass and wing loading among flying animals and aircraft for fundamental aerodynamic reasons. Assuming geometrical and dynamical similarity, cruising flight speed is predicted to vary as (body mass)(1/6) and (wing loading)(1/2) among bird species. To test these scaling rules and the general importance of mass and wing loading for bird flight speeds, we used tracking radar to measure flapping flight speeds of individuals or flocks of migrating birds visually identified to species as well as their altitude and winds at the altitudes where the birds were flying. Equivalent airspeeds (airspeeds corrected to sea level air density, Ue) of 138 species, ranging 0.01-10 kg in mass, were analysed in relation to biometry and phylogeny. Scaling exponents in relation to mass and wing loading were significantly smaller than predicted (about 0.12 and 0.32, respectively, with similar results for analyses based on species and independent phylogenetic contrasts). These low scaling exponents may be the result of evolutionary restrictions on bird flight-speed range, counteracting too slow flight speeds among species with low wing loading and too fast speeds among species with high wing loading. This compression of speed range is partly attained through geometric differences, with aspect ratio showing a positive relationship with body mass and wing loading, but additional factors are required to fully explain the small scaling exponent of Ue in relation to wing loading. Furthermore, mass and wing loading accounted for only a limited proportion of the variation in Ue. Phylogeny was a powerful factor, in combination with wing loading, to account for the variation in Ue. These results demonstrate that functional flight adaptations and constraints associated with different evolutionary lineages have an important influence on cruising flapping flight speed that goes beyond the general aerodynamic scaling effects of mass and wing loading.