Biology subjects

Stevens, E. J.

Publications and source records attributed to Stevens, E. J..

3 recordsLinked to original sources

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

The evolution of colistin resistance increases bacterial resistance to host antimicrobial peptides and virulence

Antimicrobial peptides (AMPs) offer a promising solution to the antibiotic resistance crisis. However, an unresolved serious concern is that the evolution of resistance to therapeutic AMPs may generate cross-resistance to host AMPs, compromising a cornerstone of the innate immune response. We systematically tested this hypothesis using globally disseminated mobile colistin resistance (MCR) that has been selected by the use of colistin in agriculture and medicine. Here we show that MCR provides a selective advantage to E. coli in the presence of key AMPs from humans and agricultural animals by increasing AMP resistance. Moreover, MCR promotes bacterial growth in human serum and increases virulence in a Galleria mellonella infection model. Our study shows how the anthropogenic use of AMPs can drive the accidental evolution of resistance to the innate immune system of humans and animals. These findings have major implications for the design and use of therapeutic AMPs and they suggest that MCR will be difficult to eradicate, even if colistin use is withdrawn.

microbiology↗