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Trichomonas vaginalis, a common sexually transmitted parasite that colonizes the human urogenital tract, secretes extracellular vesicles (TvEVs) that are taken up by human cells and are speculated to be taken up by parasites as well. While the crosstalk between TvEVs and human cells has led to insight into host:parasite interactions, roles for TvEVs in infection have largely been one-sided, with little known about the effect of TvEV uptake by T. vaginalis. Approximately 11% of infections are found to be coinfections of multiple T. vaginalis strains. Clinical isolates often differ in their adherence to and cytolysis of host cells, underscoring the importance of understanding the effects of TvEV uptake within the parasite population. To address this question, our lab tested the ability of a less adherent strain of T. vaginalis, G3, to take up fluorescently labeled TvEVs derived from both itself (G3-EVs) and TvEVs from a more adherent strain of the parasite (B7RC2-EVs). Here, we showed that TvEVs generated from the more adherent strain are internalized more efficiently compared to the less adherent strain. Additionally, preincubation of G3 parasites with B7RC2-EVs increases parasite aggregation and adherence to host cells. Transcriptomics revealed that TvEVs up-regulate expression of predicted parasite membrane proteins and identified an adherence factor, heteropolysaccharide binding protein (HPB2). Finally, using comparative proteomics and superresolution microscopy, we demonstrated direct transfer of an adherence factor, cadherin-like protein, from TvEVs to the recipient parasites surface. This work identifies TvEVs as a mediator of parasite:parasite communication that may impact pathogenesis during mixed infections.

Predators negatively affect prey outside of direct attack, and these nonconsumptive effects (NCEs) may cause over half the impacts of predators on prey populations. This “ecology of fear” framework has been extended to host–parasite interactions. The NCEs of parasites are thought to be small relative to those of predators. However, recent research shows ectoparasites exert NCEs on multiple life stages of Drosophila. In this study, we apply recent data to a matrix-based model of fly populations experiencing infection/consumption and NCEs from an ectoparasitic mite. We found the NCEs of parasites on larvae, which are not actively parasitized, decreased the size of simulated host populations. By contrast, the NCEs on adult flies increased population size through compensatory egg production. The negative NCEs on larvae outweighed the positive effects on adults to reduce population size. This study suggests that parasitic NCEs can suppress host populations independent of infection.

Nectonema nematomorphs utilize marine crustacean hosts in their life cycle; 16 decapod and 1 isopod genera have been reported to date as host genera. This study reports the first case of Nectonema parasitic in the Tanner crab Chionoecetes bairdi, adding another known host genus. A single nematomorph juvenile was recovered from the body cavity of each of 2 ovigerous female crabs. A nucleotide sequence for the 18S rRNA gene (1854 bp) was determined from 1 Nectonema individual. The 18S sequence showed Kimura 2-parameter (K2P) distances of 10.0, 2.0, and 1.7% from 18S sequences from Nectonema sp. from an isopod host, N. agile, and N. munidae, respectively. In an 18S-based tree, the unknown species was the sister taxon to a clade comprising N. agile and N. munidae, both of which also utilize decapod hosts. The phylogenetic relationships among the 3 Nectonema species parasitic in decapods were not congruent with the phylogeny of the hosts, not supporting a hypothesis of nematomorph-host co-evolution.

Personality traits, the consistent individual behavioral differences, are currently gaining much attention in studies of natural bird populations. However, associations between personality traits and parasite infections are not often investigated. Even less attention has been given to studies of birds in the high-elevation region such as the Tibetan plateau. This research aims to examine the relationship between avian malaria parasites and two personality traits in a population of the Chestnut Thrush (Turdus rubrocanus) breed in the Tibetan plateau. Our results revealed no evidence of sex bias in malaria parasite prevalence. Furthermore, we found no effect of infection status on two personality scores: activity and boldness. Additionally, no effects on the activity level or boldness were observed for different parasite lineages of Haemoproteus, Leucocytozoon, the sex of the birds, or their interactions. Similarly, we did not find any relationship between activity level and boldness with nestling numbers, sex, or their interactions. Notably, individuals with a larger number of offspring tended to display greater boldness. Our findings indicate that blood parasite infections are common in this population but do not significantly impact the personality of the birds.

Driven by co-evolution with pathogens, host immunity continuously adapts to optimize defence against pathogens within a given environment. Recent advances in genetics, genomics and transcriptomics have enabled a more detailed investigation into how immunogenetic variation shapes the diversity of immune responses seen across domestic and wild animal species. However, a deeper understanding of the diverse molecular mechanisms that shape immunity within and among species is still needed to gain insight into-and generate evolutionary hypotheses on-the ultimate drivers of immunological differences. Here, we discuss current advances in our understanding of molecular evolution underpinning jawed vertebrate immunity. First, we introduce the immunome concept, a framework for characterizing genes involved in immune defence from a comparative perspective, then we outline how immune genes of interest can be identified. Second, we focus on how different selection modes are observed acting across groups of immune genes and propose hypotheses to explain these differences. We then provide an overview of the approaches used so far to study the evolutionary heterogeneity of immune genes on macro and microevolutionary scales. Finally, we discuss some of the current evidence as to how specific pathogens affect the evolution of different groups of immune genes. This review results from the collective discussion on the current key challenges in evolutionary immunology conducted at the ESEB 2021 Online Satellite Symposium: Molecular evolution of the vertebrate immune system, from the lab to natural populations.

Personality traits, the consistent individual behavioral differences, are currently gaining much attention in studies of natural bird populations. However, associations between personality traits and parasite infections are not often investigated. Even less attention has been given to studies of birds in the high-elevation region such as the Tibetan plateau. This research aims to examine the relationship between avian malaria parasites and two personality traits in a population of the Chestnut Thrush (Turdus rubrocanus) breed in the Tibetan plateau. Our results revealed no evidence of sex bias in malaria parasite prevalence. Furthermore, we found no effect of infection status on two personality scores: activity and boldness. Additionally, no effects on the activity level or boldness were observed for different parasite lineages of Haemoproteus, Leucocytozoon, the sex of the birds, or their interactions. Similarly, we did not find any relationship between activity level and boldness with nestling numbers, sex, or their interactions. Notably, individuals with a larger number of offspring tended to display greater boldness. Our findings indicate that blood parasite infections are common in this population but do not significantly impact the personality of the birds.

Driven by co-evolution with pathogens, host immunity continuously adapts to optimize defence against pathogens within a given environment. Recent advances in genetics, genomics and transcriptomics have enabled a more detailed investigation into how immunogenetic variation shapes the diversity of immune responses seen across domestic and wild animal species. However, a deeper understanding of the diverse molecular mechanisms that shape immunity within and among species is still needed to gain insight into-and generate evolutionary hypotheses on-the ultimate drivers of immunological differences. Here, we discuss current advances in our understanding of molecular evolution underpinning jawed vertebrate immunity. First, we introduce the immunome concept, a framework for characterizing genes involved in immune defence from a comparative perspective, then we outline how immune genes of interest can be identified. Second, we focus on how different selection modes are observed acting across groups of immune genes and propose hypotheses to explain these differences. We then provide an overview of the approaches used so far to study the evolutionary heterogeneity of immune genes on macro and microevolutionary scales. Finally, we discuss some of the current evidence as to how specific pathogens affect the evolution of different groups of immune genes. This review results from the collective discussion on the current key challenges in evolutionary immunology conducted at the ESEB 2021 Online Satellite Symposium: Molecular evolution of the vertebrate immune system, from the lab to natural populations.

Personality traits, the consistent individual behavioral differences, are currently gaining much attention in studies of natural bird populations. However, associations between personality traits and parasite infections are not often investigated. Even less attention has been given to studies of birds in the high-elevation region such as the Tibetan plateau. This research aims to examine the relationship between avian malaria parasites and two personality traits in a population of the Chestnut Thrush (Turdus rubrocanus) breed in the Tibetan plateau. Our results revealed no evidence of sex bias in malaria parasite prevalence. Furthermore, we found no effect of infection status on two personality scores: activity and boldness. Additionally, no effects on the activity level or boldness were observed for different parasite lineages of Haemoproteus, Leucocytozoon, the sex of the birds, or their interactions. Similarly, we did not find any relationship between activity level and boldness with nestling numbers, sex, or their interactions. Notably, individuals with a larger number of offspring tended to display greater boldness. Our findings indicate that blood parasite infections are common in this population but do not significantly impact the personality of the birds.

Some parasites manipulate their hosts phenotype to enhance predation rates by the next host in the parasites life cycle. Our understanding of this parasite-increased trophic transmission is often stymied by study-design challenges. A recurring difficulty has been obtaining uninfected hosts with a coevolutionary history with the parasites, and conducting experimental infections that mimic natural processes. In 1996, Lafferty and Morris provided what has become a classic example of parasite-increased trophic transmission; they reported a positive association between the intensity of a brain-infecting trematode (Euhaplorchis californiensis) in naturally infected California killifish (Fundulus parvipinnis) and the frequency of conspicuous behaviors, which was thought to explain the documented 10-30× increase in predation by the final host birds. Here, we address the primary gap in that study by using experimental infections to assess the causality of E. californiensis infection for increased conspicuous behaviors in F. parvipinnis. We hatched and reared uninfected F. parvipinnis from a population co-occurring with E. californiensis, and infected them 1-2 times/week over half their life span with E. californiensis and a small cyathocotylid trematode (SMCY) that targets the hosts muscle tissue. At 3 time points throughout the hosts lives, we quantified several conspicuous behaviors: contorting, darting, scratching, surfacing, and vertical positioning relative to the waters surface. Euhaplorchis californiensis and SMCY infection caused 1.8- and 2.5-fold overall increases in conspicuous behaviors, respectively. Each parasite was also associated with increases in specific conspicuous behaviors, particularly 1.9- and 1.4-fold more darting. These experimental findings help solidify E. californiensis-F. parvipinnis as a classic example of behavioral manipulation. Yet our findings for E. californiensis infection-induced behavioral change were less consistent and strong than thos

Unicellular parasites of the apicomplexan phylum have a considerable effect on global health and agriculture. Two prominent examples of this phylum include malaria causing parasites of the Plasmodium genus and the widely prevalent parasite Toxoplasma gondii. While sharing a common ancestor, these parasites occupy unique biological niches, follow distinct life cycles, and result in different courses and outcomes of disease. In response to the parasite, the mammalian host has developed efficient and effective defense strategies. However, both Plasmodium and Toxoplasma have evolved strategies to evade the host’s defense response. Plasmodium parasites infect distinct tissues and cell types whereas T. gondii parasites are highly promiscuous and infect all nucleated cells. The identification of key factors involved in the interaction between the host and parasite is crucial for disease intervention, prevention, and eventually eradication efforts. Next-generation sequencing technologies have proven effective tools to investigate the response in a tissue or cell population of an infected organism. Novel genomics methods such as single-cell RNA-seq and spatial transcriptomics have enabled the investigation of heterogeneous transcriptional responses of individual cells in a population as well as heterogeneous expression profiles at spatially distinct tissue positions across entire tissue sections. This thesis pioneers the exploration of these methods in discerning the enormous complexity underlying host-parasite interplay. In Paper I, we determine spatial components of naive mouse liver in its true tissue context. We define gene expression gradients of pericentral and periportal zones in the liver and predict vein types with ambiguous annotations, based on in situ transcriptional profiles. We further identify novel spatial structures with distinct transcriptional profiles, associated with tissue integrity and integrate cell type proportions across the tissue. In Paper II we i

Croziers paradox suggests that genetic kin recognition will not be evolutionarily stable. The problem is that more common tags (markers) are more likely to be recognized and helped. This causes common tags to increase in frequency, eliminating the genetic variability that is required for genetic kin recognition. Two potential solutions to this problem have been suggested: host-parasite coevolution and multiple social encounters. We show that the host-parasite coevolution hypothesis does not work as commonly assumed. Host-parasite coevolution only stabilizes kin recognition at a parasite resistance locus if parasites adapt rapidly to hosts and cause intermediate or high levels of damage (virulence). Additionally, when kin recognition is stabilized at a parasite resistance locus, this can have an additional cost of making hosts more susceptible to parasites. However, we show that if the genetic architecture is allowed to evolve, meaning natural selection can choose the recognition locus, genetic kin recognition is more likely to be stable. The reason for this is that host-parasite coevolution can maintain tag diversity at another (neutral) locus by genetic hitchhiking, allowing that other locus to be used for genetic kin recognition. These results suggest a way that host-parasite coevolution can resolve Croziers paradox, without making hosts more susceptible to parasites. However, the opportunity for multiple social encounters may provide a more robust resolution of Croziers paradox.

A key aspect of parasitic nematode infection is the nematodes' ability to evade and/or suppress host immunity. This immunomodulatory ability is likely driven by the release of hundreds of excretory/secretory proteins (ESPs) during infection. While ESPs have been shown to display immunosuppressive effects on various hosts, our understanding of the molecular interactions between individual proteins released and host immunity requires further study. We have recently identified a secreted phospholipase A2 (sPLA2) released from the entomopathogenic nematode (EPN) Steinernema carpocapsae we have named Sc-sPLA2. We report that Sc-sPLA2 increased mortality of Drosophila melanogaster infected with Streptococcus pneumoniae and promoted increased bacterial growth. Furthermore, our data showed that Sc-sPLA2 was able to downregulate both Toll and Imd pathway-associated antimicrobial peptides (AMPs) including drosomycin and defensin, in addition to suppressing phagocytosis in the hemolymph. Sc-sPLA2 was also found to be toxic to D. melanogaster with the severity being both dose- and time-dependent. Collectively, our data highlighted that Sc-sPLA2 possessed both toxic and immunosuppressive capabilities.

Personality traits, the consistent individual behavioral differences, are currently gaining much attention in studies of natural bird populations. However, associations between personality traits and parasite infections are not often investigated. Even less attention has been given to studies of birds in the high-elevation region such as the Tibetan plateau. This research aims to examine the relationship between avian malaria parasites and two personality traits in a population of the Chestnut Thrush (Turdus rubrocanus) breed in the Tibetan plateau. Our results revealed no evidence of sex bias in malaria parasite prevalence. Furthermore, we found no effect of infection status on two personality scores: activity and boldness. Additionally, no effects on the activity level or boldness were observed for different parasite lineages of Haemoproteus, Leucocytozoon, the sex of the birds, or their interactions. Similarly, we did not find any relationship between activity level and boldness with nestling numbers, sex, or their interactions. Notably, individuals with a larger number of offspring tended to display greater boldness. Our findings indicate that blood parasite infections are common in this population but do not significantly impact the personality of the birds.

Driven by co-evolution with pathogens, host immunity continuously adapts to optimize defence against pathogens within a given environment. Recent advances in genetics, genomics and transcriptomics have enabled a more detailed investigation into how immunogenetic variation shapes the diversity of immune responses seen across domestic and wild animal species. However, a deeper understanding of the diverse molecular mechanisms that shape immunity within and among species is still needed to gain insight into-and generate evolutionary hypotheses on-the ultimate drivers of immunological differences. Here, we discuss current advances in our understanding of molecular evolution underpinning jawed vertebrate immunity. First, we introduce the immunome concept, a framework for characterizing genes involved in immune defence from a comparative perspective, then we outline how immune genes of interest can be identified. Second, we focus on how different selection modes are observed acting across groups of immune genes and propose hypotheses to explain these differences. We then provide an overview of the approaches used so far to study the evolutionary heterogeneity of immune genes on macro and microevolutionary scales. Finally, we discuss some of the current evidence as to how specific pathogens affect the evolution of different groups of immune genes. This review results from the collective discussion on the current key challenges in evolutionary immunology conducted at the ESEB 2021 Online Satellite Symposium: Molecular evolution of the vertebrate immune system, from the lab to natural populations.

Multiple parasites can infect a single host, creating a dynamic environment where each parasite must compete over host resources. Such interactions can cause greater harm to the host than single infections and can also have negative consequences for the parasites themselves. In their first intermediate hosts, trematodes multiply asexually and can eventually reach up to 20% of the host’s biomass. In most species, it is unclear whether this biomass results from a single infection or co-infection by 2 or more infective stages (miracidia), the latter being more likely a priori in areas where prevalence of infection is high. Using as model system the trematode Bucephalus minimus and its first intermediate host cockles, we examined the genetic diversity of the cytochrome c oxidase subunit I region in B. minimus from 3 distinct geographical areas and performed a phylogeographic study of B. minimus populations along the Northeast Atlantic coast. Within localities, the high genetic variability found across trematodes infecting different individual cockles, compared to the absence of variability within the same host, suggests that infections could be generally originating from a single miracidium. On a large spatial scale, we uncovered significant population structure of B. minimus, specifically between the north and south of Bay of Biscay. Although other explanations are possible, we suggest this pattern may be driven by the population structure of the final host.

Personality traits, the consistent individual behavioral differences, are currently gaining much attention in studies of natural bird populations. However, associations between personality traits and parasite infections are not often investigated. Even less attention has been given to studies of birds in the high-elevation region such as the Tibetan plateau. This research aims to examine the relationship between avian malaria parasites and two personality traits in a population of the Chestnut Thrush (Turdus rubrocanus) breed in the Tibetan plateau. Our results revealed no evidence of sex bias in malaria parasite prevalence. Furthermore, we found no effect of infection status on two personality scores: activity and boldness. Additionally, no effects on the activity level or boldness were observed for different parasite lineages of Haemoproteus, Leucocytozoon, the sex of the birds, or their interactions. Similarly, we did not find any relationship between activity level and boldness with nestling numbers, sex, or their interactions. Notably, individuals with a larger number of offspring tended to display greater boldness. Our findings indicate that blood parasite infections are common in this population but do not significantly impact the personality of the birds.

Multiple parasites can infect a single host, creating a dynamic environment where each parasite must compete over host resources. Such interactions can cause greater harm to the host than single infections and can also have negative consequences for the parasites themselves. In their first intermediate hosts, trematodes multiply asexually and can eventually reach up to 20% of the host’s biomass. In most species, it is unclear whether this biomass results from a single infection or co-infection by two or more infective stages (miracidia), the latter being more likely a priori in areas where prevalence of infection is high. Using as model system the trematode Bucephalus minimus and its first intermediate host cockles, we examined the genetic diversity of the cytochrome c oxidase subunit I (COI) region in B. minimus from three distinct geographical areas and performed a phylogeographic study of B. minimus populations along the Northeast Atlantic coast. Within localities, the high genetic variability found across trematodes infecting different individual cockles, compared to the absence of variability within the same host, suggests that infections could be generally originating from a single miracidium. On a large spatial scale, we uncovered significant population structure of B. minimus, specifically between the north and south of Bay of Biscay. Although other explanations are possible, we suggest this pattern may be driven by the population structure of the final host.

Complex life cycles are common across parasite taxa and frequently require trophic transfer of parasites from prey to predator; however, studies on parasite-host interactions often neglect variation in parasite life histories. Here I use two focal freshwater digenetic trematode species, Halipegus occidualis tongueworms and Haematoloechus complexus lungworms, as an empirical system to investigate how parasite life history traits drive host-parasite interactions across the life cycle. To examine how parasite life history and host ecology influence parasite genetic patterns, I characterized the genetic diversity of within-host infrapopulations, as well as overall population genetic structure, of sympatric tongueworm and lungworm populations. Infection load and genetic diversity of host-level parasite infrapopulations increased with host trophic level, highlighting the benefits of trophic transfer and multihost life cycles. Concurrently, first intermediate host population dynamics and dispersal ability played a role in predicting population-level parasite genetic diversity and structure., 2023, Includes bibliography., Degree granted: Dissertation (PhD)--Florida Atlantic University, 2023., Collection: FAU Electronic Theses and Dissertations Collection

Driven by co-evolution with pathogens, host immunity continuously adapts to optimize defence against pathogens within a given environment. Recent advances in genetics, genomics and transcriptomics have enabled a more detailed investigation into how immunogenetic variation shapes the diversity of immune responses seen across domestic and wild animal species. However, a deeper understanding of the diverse molecular mechanisms that shape immunity within and among species is still needed to gain insight into-and generate evolutionary hypotheses on-the ultimate drivers of immunological differences. Here, we discuss current advances in our understanding of molecular evolution underpinning jawed vertebrate immunity. First, we introduce the immunome concept, a framework for characterizing genes involved in immune defence from a comparative perspective, then we outline how immune genes of interest can be identified. Second, we focus on how different selection modes are observed acting across groups of immune genes and propose hypotheses to explain these differences. We then provide an overview of the approaches used so far to study the evolutionary heterogeneity of immune genes on macro and microevolutionary scales. Finally, we discuss some of the current evidence as to how specific pathogens affect the evolution of different groups of immune genes. This review results from the collective discussion on the current key challenges in evolutionary immunology conducted at the ESEB 2021 Online Satellite Symposium: Molecular evolution of the vertebrate immune system, from the lab to natural populations.

Unicellular parasites of the apicomplexan phylum have a considerable effect on global health and agriculture. Two prominent examples of this phylum include malaria causing parasites of the Plasmodium genus and the widely prevalent parasite Toxoplasma gondii. While sharing a common ancestor, these parasites occupy unique biological niches, follow distinct life cycles, and result in different courses and outcomes of disease. In response to the parasite, the mammalian host has developed efficient and effective defense strategies. However, both Plasmodium and Toxoplasma have evolved strategies to evade the host’s defense response. Plasmodium parasites infect distinct tissues and cell types whereas T. gondii parasites are highly promiscuous and infect all nucleated cells. The identification of key factors involved in the interaction between the host and parasite is crucial for disease intervention, prevention, and eventually eradication efforts. Next-generation sequencing technologies have proven effective tools to investigate the response in a tissue or cell population of an infected organism. Novel genomics methods such as single-cell RNA-seq and spatial transcriptomics have enabled the investigation of heterogeneous transcriptional responses of individual cells in a population as well as heterogeneous expression profiles at spatially distinct tissue positions across entire tissue sections. This thesis pioneers the exploration of these methods in discerning the enormous complexity underlying host-parasite interplay. In Paper I, we determine spatial components of naive mouse liver in its true tissue context. We define gene expression gradients of pericentral and periportal zones in the liver and predict vein types with ambiguous annotations, based on in situ transcriptional profiles. We further identify novel spatial structures with distinct transcriptional profiles, associated with tissue integrity and integrate cell type proportions across the tissue. In Paper II we i

Unicellular parasites of the apicomplexan phylum have a considerable effect on global health and agriculture. Two prominent examples of this phylum include malaria causing parasites of the Plasmodium genus and the widely prevalent parasite Toxoplasma gondii. While sharing a common ancestor, these parasites occupy unique biological niches, follow distinct life cycles, and result in different courses and outcomes of disease. In response to the parasite, the mammalian host has developed efficient and effective defense strategies. However, both Plasmodium and Toxoplasma have evolved strategies to evade the host’s defense response. Plasmodium parasites infect distinct tissues and cell types whereas T. gondii parasites are highly promiscuous and infect all nucleated cells. The identification of key factors involved in the interaction between the host and parasite is crucial for disease intervention, prevention, and eventually eradication efforts. Next-generation sequencing technologies have proven effective tools to investigate the response in a tissue or cell population of an infected organism. Novel genomics methods such as single-cell RNA-seq and spatial transcriptomics have enabled the investigation of heterogeneous transcriptional responses of individual cells in a population as well as heterogeneous expression profiles at spatially distinct tissue positions across entire tissue sections. This thesis pioneers the exploration of these methods in discerning the enormous complexity underlying host-parasite interplay. In Paper I, we determine spatial components of naive mouse liver in its true tissue context. We define gene expression gradients of pericentral and periportal zones in the liver and predict vein types with ambiguous annotations, based on in situ transcriptional profiles. We further identify novel spatial structures with distinct transcriptional profiles, associated with tissue integrity and integrate cell type proportions across the tissue. In Paper II we i

Driven by co-evolution with pathogens, host immunity continuously adapts to optimize defence against pathogens within a given environment. Recent advances in genetics, genomics and transcriptomics have enabled a more detailed investigation into how immunogenetic variation shapes the diversity of immune responses seen across domestic and wild animal species. However, a deeper understanding of the diverse molecular mechanisms that shape immunity within and among species is still needed to gain insight into-and generate evolutionary hypotheses on-the ultimate drivers of immunological differences. Here, we discuss current advances in our understanding of molecular evolution underpinning jawed vertebrate immunity. First, we introduce the immunome concept, a framework for characterizing genes involved in immune defence from a comparative perspective, then we outline how immune genes of interest can be identified. Second, we focus on how different selection modes are observed acting across groups of immune genes and propose hypotheses to explain these differences. We then provide an overview of the approaches used so far to study the evolutionary heterogeneity of immune genes on macro and microevolutionary scales. Finally, we discuss some of the current evidence as to how specific pathogens affect the evolution of different groups of immune genes. This review results from the collective discussion on the current key challenges in evolutionary immunology conducted at the ESEB 2021 Online Satellite Symposium: Molecular evolution of the vertebrate immune system, from the lab to natural populations.

Unicellular parasites of the apicomplexan phylum have a considerable effect on global health and agriculture. Two prominent examples of this phylum include malaria causing parasites of the Plasmodium genus and the widely prevalent parasite Toxoplasma gondii. While sharing a common ancestor, these parasites occupy unique biological niches, follow distinct life cycles, and result in different courses and outcomes of disease. In response to the parasite, the mammalian host has developed efficient and effective defense strategies. However, both Plasmodium and Toxoplasma have evolved strategies to evade the host’s defense response. Plasmodium parasites infect distinct tissues and cell types whereas T. gondii parasites are highly promiscuous and infect all nucleated cells. The identification of key factors involved in the interaction between the host and parasite is crucial for disease intervention, prevention, and eventually eradication efforts. Next-generation sequencing technologies have proven effective tools to investigate the response in a tissue or cell population of an infected organism. Novel genomics methods such as single-cell RNA-seq and spatial transcriptomics have enabled the investigation of heterogeneous transcriptional responses of individual cells in a population as well as heterogeneous expression profiles at spatially distinct tissue positions across entire tissue sections. This thesis pioneers the exploration of these methods in discerning the enormous complexity underlying host-parasite interplay. In Paper I, we determine spatial components of naive mouse liver in its true tissue context. We define gene expression gradients of pericentral and periportal zones in the liver and predict vein types with ambiguous annotations, based on in situ transcriptional profiles. We further identify novel spatial structures with distinct transcriptional profiles, associated with tissue integrity and integrate cell type proportions across the tissue. In Paper II we i

The trematode Fasciola hepatica is the most widespread causative agent of fasciolosis, a parasitic disease that mainly affects humans and ruminants worldwide. During F. hepatica infection, newly excysted juveniles (FhNEJ) emerge in the duodenum of the mammalian host and migrate towards their definitive location, the intra-hepatic biliary ducts. Understanding how F. hepatica traverses the intestinal wall and migrates towards the liver is pivotal for the development of more successful strategies against fasciolosis. The central enzyme of the mammalian fibrinolytic system is plasmin, a serine protease whose functions are exploited by a number of parasite species owing to its broad spectrum of substrates, including components of tissue extracellular matrices. The aim of the present work is to understand whether FhNEJ co-opt the functions of their host fibrinolytic system as a mechanism to facilitate trans-intestinal migration.

Whereas the latitudinal diversity gradient has been shown for a diverse set of taxa, a related macroecological pattern, the latitudinal specialization gradient (LSG), remains controversial. A classical expectation is that species should present more specialized interactions towards the equator, however, recent studies have provided conflicting evidence for this hypothesis. Here, we tested the LSG in a set of bird–malarial parasite networks across South America. Our analyses comprise 9763 individual birds surveyed in 52 communities, within eight biomes and spanning a gradient of 4700 km. We measured network-level specialization through indices that account for increasingly comprehensive information. Binary specialization considers the occurrence/absence of interactions between each host–parasite pair; quantitative specialization is also affected by the frequency of interactions between each host–parasite pair; and phylogenetic specialization takes into account the phylogeny and abundances of host species. We found that, while binary specialization increases towards the equator, quantitative specialization decreases. Thus, despite each parasite lineage infecting a more restricted set from the available host species in low latitudes, infections were more evenly distributed among host species, than in higher latitudes. Additionally, using a structural equation model, we show that both direct and indirect effects contribute to this unexpected relationship. Direct effects are weak, and network-specialization was mostly explained by host species and parasite lineage richness, evidencing that changes in network specialization along latitude are in a large part explained by the latitudinal diversity gradient for birds and malarial-parasites. In the light of the accumulated evidence over the past years, reinforced by our findings, we suggest that the classical latitudinal specialization hypothesis should be reevaluated, making room for a theoretical framework able to encompas

Parasite-mediated sexual selection has been the topic of extensive research and enthusiastic debate for more than three decades. Here, we suggest that secondary sexual characters may not only signal parasite resistance but also defensive tolerance. We exemplify this possibility by analysing information on two sexually selected traits, annual reproductive success, and ectoparasitism in a barn swallow Hirundo rustica population followed for more than 30 years. For each individual, we estimated the slope of the association between reproductive success and parasitism as an index of tolerance and subsequently explored the association with the expression of the sexually selected traits. In accordance with expectations of parasites playing a role in sexual selection, tail length was negatively related to load of chewing lice and nest size was positively related to tolerance to chewing lice. We discuss the importance of considering defensive tolerance for understanding the role of parasite-mediated sexual selection.

Milkweed butterflies in the genus Danaus are studied in a diverse range of research fields including the neurobiology of migration, biochemistry of plant detoxification, host-parasite interactions, evolution of sex chromosomes, and speciation. We have assembled a nearly chromosomal genome for Danaus chrysippus (known as the African Monarch, African Queen, and Plain Tiger) using long-read sequencing data. This species is of particular interest for the study of genome structural change and its consequences for evolution. Comparison with the genome of the North American Monarch Danaus plexippus reveals generally strong synteny but highlights 3 inversion differences. The 3 chromosomes involved were previously found to carry peaks of intraspecific differentiation in D. chrysippus in Africa, suggesting that these inversions may be polymorphic and associated with local adaptation. The D. chrysippus genome is over 40% larger than that of D. plexippus, and nearly all of the additional ∼100 Megabases of DNA comprises repeats. Future comparative genomic studies within this genus will shed light on the evolution of genome architecture.

Neuropeptides comprise a diverse and broad group of neurotransmitters in vertebrates and invertebrates, with critical roles in neuronal signal transduction. While their role in controlling learning and memory in the brains of mammals is known, their extra-synaptic function in infection and inflammation with effects on distinct tissues and immune cells is increasingly recognized. Helminth infections especially of the central nervous system (CNS), such as neurocysticercosis, induce neuropeptide production by both host and helminth, but their role in host-parasite interplay or host inflammatory response is unclear. Here, we review the neurobiology of helminths, and discuss recent studies on neuropeptide synthesis and function in the helminth as well as the host CNS and immune system. Neuropeptides are summarized according to structure and function, and we discuss the complex enzyme processing for mature neuropeptides, focusing on helminth enzymes as potential targets for novel anthelminthics. We next describe known immunomodulatory effects of mammalian neuropeptides discovered from mouse infection models and draw functional parallels with helminth neuropeptides. Last, we discuss the anti-microbial properties of neuropeptides, and how they may be involved in host-microbiota changes in helminth infection. Overall, a better understanding of the biology of helminth neuropeptides, and whether they affect infection outcomes could provide diagnostic and therapeutic opportunities for helminth infections.

The blood–brain barrier (BBB) efficiently protects the central nervous system (CNS) from infectious insults. Yet, the apicomplexan parasite Toxoplasma gondii has a remarkable capability to establish latent cerebral infection in humans and other vertebrates. In addition to the proposed mechanisms for access to the brain parenchyma, recent findings highlight a paramount role played by the BBB in restricting parasite passage and minimizing parasite loads in the brain. Consistent with clinically asymptomatic primary infections in humans, mounting evidence indicates that the original colonization of the brain by T. gondii encompasses previously unappreciated, nondisruptive translocation processes that precede the onset of parasite-limiting immune responses.

Neuropeptides comprise a diverse and broad group of neurotransmitters in vertebrates and invertebrates, with critical roles in neuronal signal transduction. While their role in controlling learning and memory in the brains of mammals is known, their extra-synaptic function in infection and inflammation with effects on distinct tissues and immune cells is increasingly recognized. Helminth infections especially of the central nervous system (CNS), such as neurocysticercosis, induce neuropeptide production by both host and helminth, but their role in host-parasite interplay or host inflammatory response is unclear. Here, we review the neurobiology of helminths, and discuss recent studies on neuropeptide synthesis and function in the helminth as well as the host CNS and immune system. Neuropeptides are summarized according to structure and function, and we discuss the complex enzyme processing for mature neuropeptides, focusing on helminth enzymes as potential targets for novel anthelminthics. We next describe known immunomodulatory effects of mammalian neuropeptides discovered from mouse infection models and draw functional parallels with helminth neuropeptides. Last, we discuss the anti-microbial properties of neuropeptides, and how they may be involved in host-microbiota changes in helminth infection. Overall, a better understanding of the biology of helminth neuropeptides, and whether they affect infection outcomes could provide diagnostic and therapeutic opportunities for helminth infections.

One question that has endlessly fascinated ecologists and evolutionary biologists is why there is so much biotic diversity on earth. At the advent of the field, Darwin grappled with these questions to propose that trade-offs between fitness traits constrained the evolution of hypothetical all-fit organisms termed ‘Darwinian demons’. Trade-offs in the co-evolution of antagonistic biotic partners are thought to be particularly important for diversification processes. Despite the centrality of trade-off theory to evolutionary biology, the genetic underpinnings of and selection dynamics on trade-offs remain poorly understood.My dissertation therefore focuses on trade-offs: what forms them, what influences them, and how they interact. To do this, I use experimental evolution methods in the Plodia interpunctella, or Indian meal moth, and granulosis virus model system. I focus on two trade-offs—one for each partner in a host-parasite interaction. On the host side, I focus on the trade-off to resistance to viral in infection. Understanding this trade-off is important for predicting when we expect to see resistance evolve and how it would alter ecological dynamics or persist in the absence of the pathogen. In chapter 1 of the dissertation, I ask whether the trade-off to resistance is symmetric such that selection for the longer development time phenotype constituting a cost to resistance produces symmetric gains in resistance. In chapter 2 of the dissertation, I ask why resistance inconsistently evolves in the system and how time scales and resource levels affect such resistance evolution and its costs. With these two chapters, I find that the shape of the trade-off between resistance to infection and development time can change depending on the population’s specific selection conditions when trade-offs are influenced by many genes. This is important because such differences in trade-off shape would alter the outcome of evolution.On the virus side, I examine how trade-offs b

Disease results from interactions among the host, pathogen, and environment. Inoculation trials can quantify interactions among these players and explain aspects of disease ecology to inform management in variable and dynamic natural environments. White-nose Syndrome, a disease caused by the fungal pathogen, Pseudogymnoascus destructans (Pd), has caused severe population declines of several bat species in North America. We conducted the first experimental infection trial on the tri-colored bat, Perimyotis subflavus, to test the effect of temperature and humidity on disease severity. We also tested the effects of temperature and humidity on fungal growth and persistence on substrates. Unexpectedly, only 37% (35/95) of bats experimentally inoculated with Pd at the start of the experiment showed any infection response or disease symptoms after 83 days of captive hibernation. There was no evidence that temperature or humidity influenced infection response. Temperature had a strong effect on fungal growth on media plates, but the influence of humidity was more variable and uncertain. Designing laboratory studies to maximize research outcomes would be beneficial given the high costs of such efforts and potential for unexpected outcomes. Understanding the influence of microclimates on host-pathogen interactions remains an important consideration for managing wildlife diseases, particularly in variable environments.

Innate immune systems are key defenses of animals and particularly important in species that lack the sophisticated adaptive immune systems as found in vertebrates. Here, we were interested to quantify variation in innate immune responses of insects in hosts that differ in their parasite susceptibility. To do this, we studied immune responses in honey bees, which can host a remarkable number of different parasites, which are major contributors of declining bee health and colony losses. The most significant parasite of honey bees is the mite Varroa destructor, which has infested the majority of global honey bee populations, and its control remains a major challenge for beekeepers. However, a number of nonmanaged honey bees seem able to control Varroa infections, for example, the Eastern honey bee Apis ceranacerana or the African honey bee Apis mellifera scutellata. These bees therefore make interesting study subjects to identify underlaying resistance traits, for example, by comparing them to more susceptible bee genotypes such as Western honey bees (A. melliferaligustica). We conducted a series of interlinked experiments and started with behavioral assays to compare the attractiveness of bee larvae to mites using different honey bee genotypes and castes. We found that 6-day-old larvae are always most attractive to mites, independently of genotype or castes. In a next step, we compared volatile profiles of the most attractive larvae to test whether they could be used by mites for host selection. We found that the abundance of volatile compounds differed between larval ages, but we also found significant differences between genotypes and castes. To further study the expected underlaying physiological differences between potentially resistant and susceptible host larvae, we compared the larval hemolymph proteomes of the three honey bee genotypes and two castes in response to mite exposure. We identified consistent upregulation of immune and stress-related genes in

For parasites, finding their hosts in vast and heterogeneous environments is a task that can be complex. Some parasite species rely on elaborate strategies to increase encounter rate with their hosts (e.g., behavioral modification of host), but others do not. For these parasites, a key issue is to reveal the processes that enable them to successfully find their hosts and complete their life cycles. Here, we tested the hypothesis that infective larvae of the freshwater ectoparasite Tracheliastes polycolpus are not homogeneously distributed along the river and preferentially occur in very specific microhabitats that maximize encounter rate, and hence infection rate, with their host fish. To do this, we combined an in-situ experiment (caging) with an empirical survey carried out on the same sites to identify potential “hotspots” of infection at the microgeographic scale and their environmental characteristics. Experimental and empirical results demonstrated that infections were not evenly distributed among microhabitats, and that infections were spatially aggregated in hotspots at a very fine spatial grain. We further found that certain combinations of environmental variables were consistently and non-linearly associated with higher infection rate for both caged and wild-caught fish. Microhabitats characterized by very low or high stream velocities, associated with medium and very small substrate respectively and a deep water column were strongly and repeatedly associated with higher infection rates. These microhabitats could concentrate parasites and/or promote physical contact with the hosts. We conclude that the characteristics of some microhabitats could facilitate contact between hosts and parasites and explain how some parasites manage to find their hosts in complex environments.

Crozier's paradox suggests that genetic kin recognition will not be evolutionarily stable. The problem is that more common tags (markers) are more likely to be recognised and helped. This causes common tags to increase in frequency, and hence eliminates the genetic variability that is required for genetic kin recognition. It has therefore been assumed that genetic kin recognition can only be stable if there is some other factor maintaining tag diversity, such as the advantage of rare alleles in host-parasite interactions. We show that allowing for multiple social encounters before each social interaction can eliminate Crozier's paradox, because it allows individuals with rare tags to find others with the same tag. We also show that rare tags are better indicators of relatedness, and hence better at helping individuals avoid interactions with non-cooperative cheats. Consequently, genetic kin recognition provides an advantage to rare tags that maintains tag diversity, and stabilises itself.

Forward genetic approaches have been widely used in parasitology and have proven their power to reveal the complexities of host-parasite interactions in an unbiased fashion. Many aspects of the parasites biology, including the identification of virulence factors, replication determinants, antibiotic resistance genes, and other factors required for parasitic life, have been discovered using such strategies. Forward genetic approaches have also been employed to understand host resistance mechanisms to parasitic infection. Here, we will introduce and review all forward genetic approaches that have been used to identify host factors involved with Apicomplexa infections, which include classical genetic screens and QTL mapping, GWAS, ENU mutagenesis, overexpression, RNAi and CRISPR-Cas9 library screens. Collectively, these screens have improved our understanding of host resistance mechanisms, immune regulation, vaccine and drug designs for Apicomplexa parasites. We will also discuss how recent advances in molecular genetics give present opportunities to further explore host-parasite relationships.

For parasites, finding their hosts in vast and heterogeneous environments is a task that can be complex. Some parasite species rely on elaborate strategies to increase encounter rate with their hosts (e.g., behavioral modification of host), but others do not. For these parasites, a key issue is to reveal the processes that enable them to successfully find their hosts and complete their life cycles. Here, we tested the hypothesis that infective larvae of the freshwater ectoparasite Tracheliastes polycolpus are not homogeneously distributed along the river and preferentially occur in very specific microhabitats that maximize encounter rate, and hence infection rate, with their host fish. To do this, we combined an in-situ experiment (caging) with an empirical survey carried out on the same sites to identify potential “hotspots” of infection at the microgeographic scale and their environmental characteristics. Experimental and empirical results demonstrated that infections were not evenly distributed among microhabitats, and that infections were spatially aggregated in hotspots at a very fine spatial grain. We further found that certain combinations of environmental variables were consistently and non-linearly associated with higher infection rate for both caged and wild-caught fish. Microhabitats characterized by very low or high stream velocities, associated with medium and very small substrate respectively and a deep water column were strongly and repeatedly associated with higher infection rates. These microhabitats could concentrate parasites and/or promote physical contact with the hosts. We conclude that the characteristics of some microhabitats could facilitate contact between hosts and parasites and explain how some parasites manage to find their hosts in complex environments.

[Background]: Sparicotylosis is an enzootic parasitic disease that is well established across the Mediterranean Sea. It is caused by the polyopisthocotylean monogenean Sparicotyle chrysophrii and affects the gills of gilthead sea bream (GSB; Sparus aurata). Current disease management, mitigation and treatment strategies are limited against sparicotylosis. To successfully develop more efficient therapeutic strategies against this disease, understanding which molecular mechanisms and metabolic pathways are altered in the host is critical. This study aims to elucidate how S. chrysophrii infection modulates the plasma proteome of GSB and to identify the main altered biological processes involved. [Methods]: Experimental infections were conducted in a recirculating aquaculture system (RAS) in which naïve recipient GSB ([R]; 70 g; n = 50) were exposed to effluent water from S. chrysophrii-infected GSB (98 g; n = 50). An additional tank containing unexposed naïve fish (control [C]; 70 g; n = 50) was maintained in parallel, but with the open water flow disconnected from the RAS. Haematological and infection parameters from sampled C and R fish were recorded for 10 weeks. Plasma samples from R fish were categorised into three different groups according to their infection intensity, which was based on the number of worms fish−1: low (L: 1–50), medium (51–100) and high (H: > 100). Five plasma samples from each category and five C samples were selected and subjected to a SWATH-MS proteome analysis. Additional assays on haemoglobin, cholesterol and the lytic activity of the alternative complement pathway were performed to validate the proteome analysis findings. [Results]: The discriminant analysis of plasma protein abundance revealed a clear separation into three groups (H, M/L and C). A pathway analysis was performed with the differentially quantified proteins, indicating that the parasitic infection mainly affected pathways related to haemostasis, the immune system and lipid

Parasites are generally considered the most commonly occurring type of consumers, yet their biomass and population dynamics are rarely quantified at community level. Here, we used 12 years of weekly or fortnightly monitoring data (518 time points) to determine the occurrence of chytrids, fungal parasites of phytoplankton, to assess their seasonality and long-term (seasonally-detrended) dynamics in the pelagic plankton community of a temperate, eutrophic, and polymictic lake. Chytrid infections were observed in c. 75% of all samples with recurrent infections in multiple host taxa. Infection prevalence was highest in spring, but infections occurred throughout the entire year with an average of 2.3 host taxa infected per time point (ranging from 0 to 10 host taxa) and an average infection prevalence of 2.78% (ranging from 0% to 47.35%). Infected host biomass equalled that of the carnivorous zooplankton and decreased over time, while infection prevalence remained unchanged. Seasonal infection prevalence increased with phytoplankton biomass, but decreased with increasing temperature and phosphorus concentrations, reflecting that peak prevalence occurred in spring when temperature and phosphorus concentrations were relatively low. In contrast, seasonally-detrended prevalence increased with temperature, but decreased with increasing phosphorus concentrations. Chytrids are a common component of the pelagic plankton community with sizeable biomass and removing an—at times—substantial proportion of the primary production, challenging the long-standing underrepresentation of parasites in ecological studies. Chytrids responded differentially to seasonal variation and long-term trends in host density, water temperature and nutrient availability, highlighting the need to disentangle seasonal signals from long-term changes.

Hyperparasitoids are some of the most diverse members of insect food webs. True hyperparasitoids parasitize the larvae of other parasitoids, reaching these larvae with their ovipositor through the herbivore that hosts the parasitoid larva. During pupation, primary parasitoids also may be attacked by pseudohyperparasitoids that lay their eggs on the parasitoid (pre)pupae. By attacking primary parasitoids, hyperparasitoids may affect herbivore population dynamics, and they have been identified as a major challenge in biological control. Over the past decades, research, especially on aphid- and caterpillar-associated hyperparasitoids, has revealed that hyperparasitoids challenge rules on nutrient use efficiency in trophic chains, account for herbivore outbreaks, or stabilize competitive interactions in lower trophic levels, and they may use cues derived from complex interaction networks to locate their hosts. This review focuses on the fascinating ecology of hyperparasitoids related to how they exploit and locate their often inconspicuous hosts and the insect community processes in which hyperparasitoids are prominent players.

Pathogens are thought to use host molecular cues to control when to initiate life-cycle transitions, but these signals are mostly unknown, particularly for the parasitic disease malaria caused by Plasmodium falciparum. The chemokine CXCL10 is present at high levels in fatal cases of cerebral malaria patients, but is reduced in patients who survive and do not have complications. Here we show a Pf 'decision-sensing-system' controlled by CXCL10 concentration. High CXCL10 expression prompts P. falciparum to initiate a survival strategy via growth acceleration. Remarkably, P. falciparum inhibits CXCL10 synthesis in monocytes by disrupting the association of host ribosomes with CXCL10 transcripts. The underlying inhibition cascade involves RNA cargo delivery into monocytes that triggers RIG-I, which leads to HUR1 binding to an AU-rich domain of the CXCL10 3'UTR. These data indicate that when the parasite can no longer keep CXCL10 at low levels, it can exploit the chemokine as a cue to shift tactics and escape.

Soil-transmitted helminths (STH) affect hundreds of millions worldwide and are some of the most important neglected tropical diseases in terms of morbidity. Due to the difficulty in studying STH human infections, rodent models have become increasingly used, mainly because of their similarities in life cycle. Ascaris suum and Trichuris muris have been proven appropriate and low maintenance models for the study of ascariasis and trichuriasis. In the case of hookworms, despite most of the murine models do not fully reproduce the life cycle of Necator americanus, their proteomic similarity makes them highly suitable for the development of novel vaccine candidates and for the study of hookworm biological features. Furthermore, these models have been helpful in elucidating some basic aspects of our immune system, and are currently being used by numerous researchers to develop novel molecules with immunomodulatory proteins. Herein we review the similarities in the proteomic composition between Nippostrongylus brasiliensis, Heligmosomoides polygyrus bakeri and Trichuris muris and their respective human counterpart with a focus on the vaccine candidates and immunomodulatory proteins being currently studied., Miguel Servet Fellow, Instituto de Salud Carlos III, Depto. de Microbiología y Parasitología, Fac. de Farmacia, TRUE, pub

Parasites are important components of ecosystems, influencing trophic networks, competitive interactions and biodiversity patterns. Nonetheless, we are not nearly close to disentangling their complex roles in natural systems. Southeast Asia falls within global areas targeted as most likely to source parasites with zoonotic potential, where high rates of land conversion and fragmentation have altered the circulation of wildlife species and their parasites, potentially resulting in altered host-parasite systems. Although the overall biodiversity in the region predicts equally high, or even higher, parasite diversity, we know surprisingly little about wild primate parasites, even though this constitutes the first step towards a more comprehensive understanding of parasite transmission processes. Here, we characterise the gastrointestinal helminth parasite assemblages of a community of Bornean primates living along the Kinabatangan floodplain in Sabah (Malaysian Borneo), including two species endemic to the island. Through parasitological analyses, and by using several measures of parasite infection as proxies for parasite diversity and distribution, we show that (i) most parasite taxonomic groups are not limited to a single host, suggesting a greater flexibility for habitat disturbance, (ii) parasite infracommunities of nocturnal primates differ from their diurnal counterparts, reflecting both phylogenetic and ecological constraints, and (iii) soil-transmitted helminths such as whipworm, threadworm and nodule worm are widespread across the primate community. This study also provides new parasite records for southern pig-tailed macaques (Macaca nemestrina), silvered langurs (Trachypithecus cristatus) and Western tarsiers (Cephalopachus bancanus) in the wild, while adding to the limited records for the other primate species in the community. Given the information gap regarding primate-parasite associations in the region, the information presented here should prove releva

The biogeography of host-parasite dynamics is an area that has received little attention in studies of island ecology. While a few studies have shed insight on patterns of parasitism in insular host populations, more empirical evidence is needed to ascertain how isolation impacts parasites. Biogeography generally theorizes that the physical size of islands and the duration of each island’s isolation can be driving geographic factors controlling species interactions and populations dynamics. To test this, we assessed the effect of island structure and population isolation on the endemic insular lizard Podarcis erhardii and its native hemogregarine parasite (Apicomplexa: Adeleorina) in the Cyclades (Aegean Sea). We analyzed the relationships of prevalence and parasitemia of hemogregarine infection with several factors concerning the island (size, time of isolation, spatial isolation, population density) and host (body size) levels using regression and structural equation models, respectively. Regressions indicate that islands with greater host density and islands which have been isolated for shorter timespans tend to have higher hemogregarine prevalences; structural equation models suggest a similar pattern for parasitemia. We hypothesize this may be driven by insular density compensation. Hosts on islands that are more temporally and spatially isolated also tend to have higher prevalence and parasitemia of hemogregarines. Our results indicate that island area, island isolation, and host population density are likely to be significant drivers of changes in host-parasite interactions in fragmented populations.

Trichomonas vaginalis is a highly prevalent, sexually transmitted parasite which adheres to mucosal epithelial cells to colonize the human urogenital tract. Despite adherence being crucial for this extracellular parasite to thrive within the host, relatively little is known about the mechanisms or key molecules involved in this process. Here, we have identified and characterized a T. vaginalis hypothetical protein, TVAG_157210 (TvAD1), as a surface protein that plays an integral role in parasite adherence to the host. Quantitative proteomics revealed TvAD1 to be ∼4-fold more abundant in parasites selected for increased adherence (MA parasites) than the isogenic parental (P) parasite line. De novo modeling suggested that TvAD1 binds N-acetylglucosamine (GlcNAc), a sugar comprising host glycosaminoglycans (GAGs). Adherence assays utilizing GAG-deficient cell lines determined that host GAGs, primarily heparan sulfate (HS), mediate adherence of MA parasites to host cells. TvAD1 knockout (KO) parasites, generated using CRISPR-Cas9, were found to be significantly reduced in host cell adherence, a phenotype that is rescued by overexpression of TvAD1 in KO parasites. In contrast, there was no significant difference in parasite adherence to GAG-deficient lines by KO parasites compared with wild-type, which is contrary to that observed for KO parasites overexpressing TvAD1. Isothermal titration calorimetric (ITC) analysis showed that TvAD1 binds to HS, indicating that TvAD1 mediates host cell adherence via HS interaction. In addition to characterizing the role of TvAD1 in parasite adherence, these studies reveal a role for host GAG molecules in T. vaginalis adherence.IMPORTANCE The ability of the sexually transmitted parasite Trichomonas vaginalis to adhere to its human host is critical for establishing and maintaining an infection. Yet how parasites adhere to host cells is poorly understood. In this study, we employed a novel adherence selection method to identify proteins i

Parasitic nematodes cause significant morbidity and mortality globally. Excretory/secretory products (ESPs) such as fatty acid- and retinol- binding proteins (FARs) are hypothesized to suppress host immunity during nematode infection, yet little is known about their interactions with host tissues. Leveraging the insect parasitic nematode, Steinernema carpocapsae, we describe here the first in vivo study demonstrating that FARs modulate animal immunity, causing an increase in susceptibility to bacterial co-infection. Moreover, we show that FARs dampen key components of the fly immune response including the phenoloxidase cascade and antimicrobial peptide (AMP) production. Our data also reveal that FARs deplete lipid signaling precursors in vivo as well as bind to these fatty acids in vitro, suggesting that FARs elicit their immunomodulatory effects by altering the availability of lipid signaling molecules necessary for an efficient immune response. Collectively, these data support a complex role for FARs in immunosuppression in animals and provide detailed mechanistic insight into parasitism in phylum Nematoda.

Individual hosts are often infected with multiple parasite species or strains simultaneously. Co-occurring parasites can profoundly impact each other and their hosts via interspecific interactions. To further our understanding of co-infection in wildlife, I censused the parasite communities of fathead minnows (Pimephales promelas) from southern Alberta over three years. Nearly all minnows were co-infected, and the larval trematodes Ornithodiplostomum ptychocheilus and Ornithodiplostomum sp. co-occurred more frequently than expected by chance. I exposed minnows to cercariae of these species to evaluate the effects of intensity dependence and co-infection on parasite development. While negative intensity-dependent growth occurred only for O. ptychocheilus, both species were significantly smaller post-encystment in co-infections than in mono-infections. Thus, Ornithodiplostomum spp. development is influenced by conspecifics and heterospecifics. Taken together, my results suggest that naturally co-occurring parasites in spatially segregated infection sites can influence one another’s growth within their shared intermediate host, with possible ecological and evolutionary consequences.

Individual hosts are often infected with multiple parasite species or strains simultaneously. Co-occurring parasites can profoundly impact each other and their hosts via interspecific interactions. To further our understanding of co-infection in wildlife, I censused the parasite communities of fathead minnows (Pimephales promelas) from southern Alberta over three years. Nearly all minnows were co-infected, and the larval trematodes Ornithodiplostomum ptychocheilus and Ornithodiplostomum sp. co-occurred more frequently than expected by chance. I exposed minnows to cercariae of these species to evaluate the effects of intensity dependence and co-infection on parasite development. While negative intensity-dependent growth occurred only for O. ptychocheilus, both species were significantly smaller post-encystment in co-infections than in mono-infections. Thus, Ornithodiplostomum spp. development is influenced by conspecifics and heterospecifics. Taken together, my results suggest that naturally co-occurring parasites in spatially segregated infection sites can influence one another’s growth within their shared intermediate host, with possible ecological and evolutionary consequences.

Individual hosts are often infected with multiple parasite species or strains simultaneously. Co-occurring parasites can profoundly impact each other and their hosts via interspecific interactions. To further our understanding of co-infection in wildlife, I censused the parasite communities of fathead minnows (Pimephales promelas) from southern Alberta over three years. Nearly all minnows were co-infected, and the larval trematodes Ornithodiplostomum ptychocheilus and Ornithodiplostomum sp. co-occurred more frequently than expected by chance. I exposed minnows to cercariae of these species to evaluate the effects of intensity dependence and co-infection on parasite development. While negative intensity-dependent growth occurred only for O. ptychocheilus, both species were significantly smaller post-encystment in co-infections than in mono-infections. Thus, Ornithodiplostomum spp. development is influenced by conspecifics and heterospecifics. Taken together, my results suggest that naturally co-occurring parasites in spatially segregated infection sites can influence one another’s growth within their shared intermediate host, with possible ecological and evolutionary consequences.