Biology subjects

Hector, T. E.

Publications and source records attributed to Hector, T. E..

5 recordsLinked to original sources

bioRxiv2025

Coinfections dampen the effects of temperature on host-parasite interactions

Coinfections by multiple parasite species are widespread and modify disease outcomes. To what degree other forms of ecological complexity, such as environmental change, influence the impacts of coinfecting parasites on disease remains unclear. We exposed nematodes (Caenorhabditis elegans) to naturally coinfecting parasites (Leucobacter celer and musarum) at temperatures across the hosts thermal range. While we found that host mortality varied widely with temperature during single infections, coinfections buffered hosts against temperature-mediated variation via ongoing parasite competition. We extended our experiments with mathematical models indicating that changing virulence, rather than transmission, most plausibly underpins temperature-dependent host mortality. At moderate, but not extreme temperatures, we found coinfection continued to dampen mortality outcomes due to another source of host variation, genotypic susceptibility. Coinfection may provide a stabilizing effect on disease in a warming world - but this effect can falter when hosts are faced with multiple stressors.

ecology↗

bioRxiv2025

Competition constrains parasite adaptation to thermal heterogeneity

Temporal thermal heterogeneity is expected to favour intermediate, generalist phenotypes that can maintain growth across a broad thermal range but have sub-optimal growth at any single temperature. Yet, thermal variation typically occurs in the presence of additional selection pressures which may interact to constrain adaptation to temperature. We propagated competing lytic viral parasites (bacteriophages {phi}14-1 and {phi}LUZ19) of Pseudomonas aeruginosa under fluctuating temperatures (37-42{degrees}C) in monoculture and in co-culture. Without competition, fluctuating temperatures favoured intermediate thermal phenotypes in the phage {phi}14-1 and resulted in more variable evolutionary outcomes compared to static conditions. However, co-selection from fluctuating temperatures and competition led to restricted thermal adaptation, slower evolutionary rates, and fewer putative adaptive mutations in the {phi}LUZ19 competitor. Our study highlights the potential for reduced adaptive capacity in interacting communities amidst global climate change.

evolutionary biology↗

bioRxiv2025

Rising temperatures favour parasite virulence and parallel molecular evolution following a host jump

Climate change is facilitating the poleward emergence of parasites, increasing the risk of jumping into new animal species, including humans. Whether more virulent or transmissible variants will spread during these climate-driven outbreaks is unclear. We experimentally evolved a wild parasitic bacterium, across the thermal range (20-30{degrees}C) and extremes (35{degrees}C) of Cape Verde - the site of field collection - in a novel, temperate animal host. At the parasites typical warm environmental temperature, we found that virulence escalated across evolutionary time. Parasites evolved at hot temperatures, towards the limit of host-parasite survival, displayed a cryptic virulence boost, deadlier once infecting animals at cooler temperatures. Patterns of molecular evolution were constrained to parallel changes in fewer loci at extreme temperatures. Our findings suggest that rising temperatures will leave predictable phenotypic and genomic signatures on evolving parasites as they emerge with climate change.

evolutionary biology↗

bioRxiv2024

Within-host competition sparks pathogen molecular evolution and perpetual microbiota dysbiosis.

Pathogens newly invading a host must compete with resident microbiota. This within-host microbial warfare could lead to more severe disease outcomes or constrain the evolution of virulence. Using experimental evolution of a widespread pathogen (Staphylococcus aureus) and a native microbiota community in C. elegans nematode hosts, we show that a competitively superior pathogen displaced microbiota and reduced species richness, whilst maintaining virulence across generations. Conversely, pathogen populations and microbiota passaged separately caused more host harm relative to their respective ancestral controls. We find the evolved increase in virulence exhibited by pathogen populations passaged independently (compared to ancestral controls) was partly mediated by enhanced expression of the global virulence regulator agr and increased biofilm formation. Whole genome sequencing revealed shifts in the mode of selection from directional (on pathogens evolving alone) to fluctuating (on pathogens evolving with a host microbiota), with competitive interactions driving early diversification among pathogen populations. Metagenome sequencing of the evolved microbiota shows that evolution in infected hosts caused a significant reduction in community stability, along with restrictions on the co- existence of some species based on nutrient competition. Our study reveals how microbial competition during emerging infection determines the patterns and processes of evolution with major consequences for host health.

evolutionary biology↗

bioRxiv2022

Thermal acclimation to warmer temperatures can protect host populations from both further heat stress and the potential invasion of pathogens

Phenotypic plasticity in response to shifts in temperature, known as thermal acclimation, is an essential component of the ability of a species to cope with environmental change. Not only does this process potentially improve an individuals thermal tolerance, it will also act simultaneously on various fitness related traits that determine whether a population increases or decreases in size. In light of global change, thermal acclimation therefore has consequences for population persistence that extend beyond simply coping with heat stress. This particularly important when we consider the additional threat of parasitism associated with global change, as the ability of a pathogen to invade a host population depends on both its capacity to proliferate within a host and spread between hosts, and thus the supply of new susceptible hosts in a population. Here, we use the host Daphnia magna and its bacterial pathogen Pasteuria ramosa to investigate how thermal acclimation may impact various aspects of host and pathogen performance at the scale of both an individual and the population. We independently test the effect of maternal thermal acclimation and direct thermal acclimation on host thermal tolerance, measured as knockdown times, as well as host fecundity and lifespan, and pathogen infection success and spore production. We find that direct thermal acclimation enhances host thermal tolerance and intrinsic rates of population growth, despite a decline observed for host fecundity and lifespan. Pathogens, on the other hand, faired consistently worse at warmer temperatures at the within-host scale, and also in their potential to invade a host population. Our results suggest that hosts could benefit more from warming than their pathogens, but highlight that considering both within- and between-host thermal performance, including thermal tolerance and fitness traits, is needed to fully appreciate how increasing thermal variability will impact host and pathogen populations.

ecology↗