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Wolinska, J.

Publications and source records attributed to Wolinska, J..

9 recordsLinked to original sources

Warmer world gets sicker: meta-analysis reveals strong increase in parasitism at elevated temperatures across diverse host-parasite systems

Climate change is expected to alter infectious disease dynamics worldwide, yet evidence that rising temperatures increase infection (warmer, sicker world hypothesis; WSWH) remains equivocal. We conducted a meta-analysis of 775 effect sizes from 124 experimental studies spanning terrestrial, freshwater, and marine host-parasite systems to test whether warming increases parasitism. Elevated temperatures increased infection, producing moderate positive effects on prevalence and infection intensity in non-phylogenetic models. Temperature effects were significant in terrestrial systems and varied markedly among taxa. Strong responses were observed in nematodes and fungal parasites as well as in plant, invertebrate, and bacterial hosts, whereas vertebrates showed little evidence of consistent increases. Phylogenetically-controlled analyses yielded similar but less precise estimates, indicating that responses are unevenly distributed across the Tree of Life. Our synthesis provides the most comprehensive experimental test of the WSWH to date and shows that warming can elevate infection risk while generating heterogeneous outcomes among host-parasite systems.

ecology↗

Host outnumbered: microbiomes and a fungal parasite interact to shape host genotype-dependent survival

Microbiomes are key determinants of host health, yet empirical evidence demonstrating their influence on host-parasite interactions is limited. We conducted a proof-of-principle experiment using the water flea Daphnia magna and its virulent yeast para-site Australozyma monospora (formerly Metschnikowia bicuspidata) to test if micro-biome composition alters infection outcomes. Axenic hosts were inoculated with a control microbiome (homogenates of laboratory-cultured Daphnia reared in natural freshwater) or a single bacterial strain (Rhizobium sp.), and exposed to the parasite. Host survival differed markedly between microbiome treatments and depended on parasite exposure. Prior to parasite exposure, hosts of one genotype exhibited high juvenile mortality when inoculated with the control microbiome (79%), compared to Rhizobium (19%) (the other genotype: 48% vs. 50%). Parasite exposure reduced survival, but the extent varied with microbiome composition: survival of hosts with a control microbiome (averaged across genotypes) declined from 66% to 0%; survival of those inoculated with Rhizobium sp. declined from 35% to 10%. In contrast, micro-biome composition did not influence parasite infectivity or net reproduction. Our results indicate that microbiome effects on host survival are genotype- and life-stage-dependent, differ between parasite-free and parasite-exposed conditions and may impact host-parasite dynamics primarily by influencing host viability rather than para-site performance.

ecology↗

Herbicide metolachlor alters gene expression and influences the interaction between a bloom-forming cyanobacterium and its chytrid parasite

Metolachlor (MET) is among the most widely used herbicides worldwide and a common freshwater contaminant. Beyond direct toxicity, MET can reshape ecological interactions, including those between bloom-forming cyanobacteria and their chytrid parasites. Although MET is known to reduce chytrid fitness and alter cyanobacterium-chytrid interaction, the molecular basis of these effects remains unknown. Using dual RNA-sequencing, we analysed the gene expression of the toxigenic cyanobacterium Planktothrix agardhii and its obligate chytrid parasite Rhizophydium megarrhizum under exposure to an environmentally relevant concentration of MET. MET reprogrammed the parasite R. megarrhizum by altering the expression of genes governing developmental transitions, xenobiotic stress responses and intracellular signalling in both free-living and infecting cells. The transcriptional signature that typically distinguishes zoospores from infecting chytrids disappeared under MET exposure. This was not due to an arrest of the infection process, but rather to an increase in the baseline expression of infection-associated genes in zoospores, thus blurring the dispersal-to-infection transition. In contrast, P. agardhii showed no transcriptional response to MET in the absence of infection, whereas co-exposure to both the parasite and MET was associated with transcriptional changes related to energy acquisition and carbohydrate metabolism. Overall, our results suggest that MET weakens chytrid top-down control and favours cyanobacterial persistence, with consequences for bloom formation and energy transfer through aquatic trophic webs. Our study provides the first replicated molecular view, using a dual-RNA transcriptomic approach, of how herbicide exposure reshapes the interaction between a bloom-forming cyanobacterium and its chytrid parasite.

microbiology↗

Synergistic and antagonistic effects of chemical pollutants and parasitic fungi on cyanobacterial metabolism

Freshwater communities are increasingly impacted by anthropogenic pollutants, such as the widely used herbicide metolachlor (MET) and chemicals leached from cigarette butts (CBs), one of the most common types of litter worldwide. Cyanobacteria often interact with their parasitic chytrid fungi, which play a role in controlling their growth. Parasites represent an additional biotic stressor that can alter the effects of pollutants on their hosts. However, the metabolic responses of cyanobacteria to simultaneous exposure to pollutants and parasites remain poorly understood. In this study, we investigated the combined effects of abiotic (MET and CB leachate) and biotic (chytrid parasite Rhizophydium megarrhizum) stressors on the metabolic response of the toxigenic cyanobacterium Planktothrix agardhii. Co-exposure to MET and chytrids led to a synergistic effect, inducing oxidative stress, countered primarily by non-enzymatic mechanisms, whereas MET alone had no measurable effect. In contrast, CB leachate alone induced oxidative stress, but this effect was mitigated when cyanobacteria were also infected by chytrids, indicating an antagonistic interaction. This study demonstrates the complexity of cyanobacterial responses to interacting biotic and abiotic stressors and highlights the importance of considering host-parasite interactions in ecotoxicological assessments of cyanobacteria. A deeper understanding of how pollutants such as MET and CB leachate affect cyanobacteria-chytrid interactions at the metabolic level is crucial for evaluating their broader ecological impacts.

microbiology↗

Warming increases richness and shapes assemblages of eukaryotic parasitic plankton

BackgroundAnthropogenic activities have led to a global rise in water temperatures, prompting increased interest in how warming affects infectious disease ecology. While most studies have focused on individual host-parasite systems, there is a gap in understanding the impact of warming on multi-host, multi-parasite assemblages in natural ecosystems. To address this gap, we investigated freshwater eukaryotic parasite communities in ten natural lakes near Konin, Poland: five artificially heated and five non-heated "control" lakes. Since 1958, the heated lakes have experienced a mean annual temperature increase of 2 {degrees}C due to hot water discharge from two adjacent power plants. We collected seasonal environmental DNA (eDNA) samples from surface waters over a two-year period and applied targeted metabarcoding to compare the richness and distribution of eukaryotic parasites across lake types, with a focus on protists and fungi. ResultsUsing literature searches and sequence metadata from GenBank, we identified putative parasites which included Alveolates, Stramenopiles, basal Fungi and Ichthyosporeans, as well as their associated hosts. Heated lakes harboured distinct parasite assemblages, with higher richness of chytrids and aphelids, suggesting thermal preferences among certain freshwater microeukaryotic parasites. Other groups exhibited clear seasonal trends, with richness of oomycetes peaking in spring and summer, and that of Cryptomycota in winter and autumn. A general linear model revealed a marginally positive correlation between chytrid parasite richness and richness of their green algal, diatom, and dinoflagellate hosts. Post-hoc analyses indicated that heated lakes exhibited greater seasonal variation in chytrid parasite richness and a stronger correlation between host and parasite richness than control lakes. ConclusionThese findings demonstrate that warming can induce strong shifts in the richness and assemblages of freshwater microeukaryotic parasites. Using chytrids as a focal group, we additionally demonstrate that warming may amplify seasonal variation in parasite richness and strengthen host-parasite richness relationships.

ecology↗

Zooplankton bacterial communities are influenced by infection status, environmental conditions and diet quantity across natural epidemics

Zooplankton-associated microbiomes play an important role for host health and contribute to ecosystem processes such as nutrient cycling. Yet, few studies have assessed how environmental gradients and biotic interactions, including parasitism and diet, may shape the microbiome composition of wild zooplankton. Here, we analysed the microbiomes of water fleas from the Daphnia longispina species complex using 16S rRNA gene sequencing and a long-term field dataset spanning six sampling events over 13 years. Sampling coincided with outbreaks of the virulent eukaryotic gut parasite Caullerya mesnili. Additionally, we explored how microbiome structure varied in relation to water parameters, phytoplankton density (i.e. Daphnia diet), and zooplankton density and community structure. Daphnia microbiomes displayed strong temporal variation, and comparatively small differences based on host infection status. Microbiome beta diversity correlated with phytoplankton density but not with its community composition, including green algae, protists and cyanobacteria. Environmental conditions, including temperature, dissolved oxygen and cyanobacterial abundance - previously found to drive Caullerya epidemics - were also associated with distinct microbiome structures. Importantly, microbiome beta diversity co-varied with infection prevalence, suggesting a link between microbiome shifts, epidemic size, and environmental conditions driving large epidemics. Dominant bacterial taxa correlated with Daphnia density, whereas the phylogenetic composition of rare taxa was associated with total zooplankton density. These findings demonstrate the dynamic nature of Daphnia microbiomes and suggest potential mechanisms by which they may mediate disease dynamics, particularly through associations with diet quantity, temperature, and host population density.

ecology↗

Warming-induced excess deaths of infected animals depend on pathogen kingdom and evolutionary history

Climate change is causing extreme heating events. Simultaneously, climate change and human activities are leading to more prolonged and intense infectious disease outbreaks. The extent to which warming and infection may together impact host species persistence is, however, unclear. Using a meta-analysis of >190 effect sizes representing 101 ectothermic animal host-pathogen systems, we provide broad evidence that experimentally increased temperatures drove higher pathogen virulence, specifically pathogen-induced host mortality. Such pattern was mainly driven by excess host death caused by bacterial infections combined with warming, particularly if the pathogenic bacteria were naturally established within the host species, though novel infections without known host-pathogen evolutionary history were more lethal at lower temperatures. Importantly, larger temperature increases were associated with more host deaths hinting at the escalating threat for animal species as the world continues to warm. We found that the virulence of fungal pathogens increased only when temperatures were shifted upwards towards their thermal optimum. The magnitude of these effects was not impacted by host life-stage, immune complexity, or variable experimental protocols. Overall, our findings reveal distinct patterns of pathogen virulence change under warmer temperatures, suggesting that the impact of global warming on infectious disease outcomes would depend on pathogen traits (taxonomic kingdom, thermal tolerance) and host-pathogen evolutionary history. Author SummaryHuman-induced climate warming is one of the biggest challenges in our times. Simultaneously, climate change is associated with more intense infectious disease outbreaks, suggesting that temperature rises also influence disease dynamics. Growing numbers of studies have investigated the effect of warming on disease severity (or pathogen virulence) in different animal host-pathogen systems. However, individual studies did not always agree with each other, and how increased temperature and pathogen infection together impact animal survival remains unclear. Here, we resolved this uncertainty by conducting a meta-analysis of >190 effect sizes representing 101 animal host-pathogen systems. We provided broad evidence that, higher temperatures caused more deaths of infected animals, particularly for animals with bacterial infections under warmer conditions. We found that larger temperature rises were associated with more animal deaths, suggesting the increased threat for host species as the world continues to warm. We also found that pathogenic fungi were more sensitive to heat than bacterial pathogens, and temperature changes the virulence of fungal pathogens in relation to their thermal optimum.

ecology↗

Phylogenomics including new sequence data of phytoplankton-infecting chytrids reveals multiple independent lifestyle transitions across the phylum

Parasitism is the most common lifestyle on Earth and has emerged many times independently across the eukaryotic tree of life. It is frequently found among chytrids (Chytridiomycota), which are early-branching unicellular fungi that feed osmotrophically via rhizoids as saprotrophs or parasites. Chytrids are abundant in most aquatic and terrestrial environments and fulfil important ecosystem functions. As parasites, they can have significant impacts on host populations. They cause global amphibian declines and influence the Earths carbon cycle by terminating algal blooms. To date, the evolution of parasitism within the chytrid phylum remains unclear due to the low phylogenetic resolution of rRNA genes for the early diversification of fungi, and because few parasitic lineages have been cultured and genomic data for parasites is scarce. Here, we combine transcriptomics, culture-independent single-cell genomics and a phylogenomic approach to overcome these limitations. We newly sequenced 29 parasitic taxa and combined these with existing data to provide a robust backbone topology for the diversification of Chytridiomycota. Our analyses reveal multiple independent lifestyle transitions between parasitism and saprotrophy among chytrids, multiple host shifts by parasites, and suggest that the chytrid last common ancestor was a parasite of phytoplankton.

evolutionary biology↗

Infection by a eukaryotic gut parasite in wild Daphnia sp. associates with a distinct bacterial community

Host-associated bacterial communities can play an important role in host fitness and resistance to diseases. Yet, few studies have investigated tripartite interaction between a host, parasite and host-associated bacterial communities in natural settings. Here, we use 16S amplicon sequencing to compare gut- and body-bacterial communities of wild water fleas belonging to the Daphnia longispina complex, between uninfected hosts and those infected with the common and virulent eukaryotic gut parasite Caullerya mesnili (Family: Ichthyosporea). We report community-level changes in host-associated bacteria with the presence of the parasite infection; namely decreased alpha diversity and increased beta diversity at the site of infection, i.e. host gut (but not host body). We also report decreased abundance of bacterial taxa proposed elsewhere to be beneficial for the host, and an appearance of taxa specifically associated with infected hosts. Our study highlights the host-microbiota-infection link in a natural system and raises questions about the role of host-associated microbiota in natural disease epidemics as well as the functional roles of bacteria specifically associated with infected hosts.

ecology↗