Geology topics

Malina Mariko Loeher

Publications and source records attributed to Malina Mariko Loeher.

3 recordsLinked to original sources

USGS2026

Stochastic within-host dynamics and climate-sensitive traits generate predictable patterns of variation in disease outcomes

Understanding how climatic variables impact host-pathogen relationships in temperature-sensitive ectothermic host organisms is crucial under global change. Few studies have explored how temperature gradients generate inter-individual variation in epidemiological traits like host susceptibility or pathogen replication. Here, we develop a mathematical model to explore a novel hypothesis: stochastic within-host dynamics and simulated thermal mismatches between host and pathogen traits generate predictable variation in infection outcomes among hosts and across thermal gradients. Our model demonstrates that varying trait thermal optima in host immunity and pathogen replication, and stochastic within-host processes produced variation in infection outcomes. Variability was low when temperatures strongly favored host or pathogen traits, but high and diverse when their performance was similar across a broad thermal range. In contrast, when trait performance was equal across all temperatures (no mismatch) variability remained low at all temperatures. Further, the magnitude of variation, quantified by entropy, exhibited predictable patterns depending on host-pathogen thermal mismatches. We conclude that interactions between trait thermal mismatches and within-host stochasticity provide a theoretical framework to improve ectotherm disease models under climate change, providing a valuable tool for exploring the impacts of environmental change on epizootic or epidemic dynamics, particularly in vulnerable marine ecosystems.

Philosophical Transactions of the Royal Society, S↗

USGS2026

The impacts of co-circulating pathogens in Pacific herring depend on interactions between viral life-cycle traits and transmission parameters, highlighting interdependencies between pathogen epizootics

The average host susceptibility decreases as the epizootic progresses because easily infected hosts are first removed from the population. While host susceptibility is pathogen-specific, it is likely that host susceptibility is correlated between different pathogens, so that co-circulating pathogens may have reciprocal impacts on their epidemics. However, despite well-documented examples of concomitant infections in marine hosts, reciprocal epizootic effects have not been documented in wild marine organisms. We quantify reciprocal impacts between viral haemorrhagic septicaemia and viral erythrocytic necrosis in Pacific herring ( Clupea pallasii ) using field and laboratory work. We show that the causative viruses for both diseases circulate through herring populations and that infection with one pathogen has negative impacts on the epizootic and infection characteristics of the other pathogen, suggesting positive correlations in the susceptibility to infection between pathogens. We then use simulations of a two-strain pathogen model to show that the impact of the correlation is modulated by transmission parameters, such as the incubation period and the initial transmission rate. Our work shows that co-occurring epizootics pose a management challenge because single-pathogen management actions may amplify the epizootics of the non-targeted pathogen. This study provides a framework to evaluate the consequences of reciprocal epizootic impacts through field, experimental and modelling work.

Washington↗

USGS2025

Virulence evolution of a salmonid virus following a host jump

Emergent viral diseases remain a critical obstacle to welfare across landscapes and species, encompassing humans, wildlife, and agriculture. Following a jump to a novel host, the severity of disease resulting from infection is a critical determinant of the overall emergent pathogen threat. Conventional wisdom posits that virulence, defined here as host mortality, attenuates to intermediate levels as a pathogen adapts to a novel host, but this is largely based on data from just one system, myxoma virus, which was intentionally introduced as a biocontrol agent in rabbits ( Oryctolagus cuniculus ) in mid-1900s Australia. In this study, we demonstrate that infectious hematopoietic necrosis virus (IHNV), which made a host jump from sockeye salmon ( Oncorhynchus nerka , ancestral host) to rainbow trout ( O. mykiss , novel host), has not conformed to classical theory. We quantified virulence in the ancestral and novel hosts using common garden in vivo experiments with 16 archival IHNV isolates collected from 1972-2017, which span the period from shortly after the host jump and the subsequent 45 years of host adaptation. These virus isolates also represent two distinct phylogenetic genogroups, each associated with either the ancestral or novel host. The experiments were replicated across two research facilities, two challenges dosages, and two temperatures. While isolates from the ancestral genogroup showed no temporal change in virulence in either host, isolates from the novel viral genogroup displayed a significant increase in virulence over time in the novel host. Some possible indication of a virus temperature adaption after the host jump was also present. Potential drivers of virulence evolution are discussed. This represents one of only a handful of systems in which the evolution of increased virulence has been empirically characterized after a host jump and subsequent adaptation. It contributes to a growing body of evidence that contradicts the classical case study of myxoma virus attenuation after adaptation.

PLoS Pathogens↗