Biology subjects

Gibson, A. K.

Publications and source records attributed to Gibson, A. K..

7 recordsLinked to original sources

bioRxiv2026

Diet alters epidemic size and timing in a trophically-transmitted parasite

A hosts diet can alter the course of parasite infection. This is especially true of trophic parasites, which a host acquires through feeding. While a large body of work attests to the role of diet in the spread of disease within-hosts, diet can also impact host density and encounter rate with parasites, both of which are expected to modify disease dynamics. When parasites are acquired through feeding, epidemics may be larger and more severe on high-quality diets if these diets support a higher density of hosts that feed more and thus ingest more parasites. Alternately, epidemics may be more severe on low-quality diets if malnourishment decreases hosts ability to resist disease. To differentiate these hypothesized effects of diet on disease, we quantified individual infections and epidemic dynamics for the natural microsporidian parasite Nematocida ironsii infecting its nematode host Caenorhabditis elegans. We measured feeding rate, parasite transmission, and host fitness across three bacterial diets that vary in quality and elicit distinct feeding behaviors in C. elegans. We found that low-quality diets reduced feeding rate, which corresponded to reduced acquisition of parasite spores. However, these diet-mediated differences in parasite acquisition did not directly map onto fitness consequences: hosts eating the poor-quality diet had similar reductions in fitness to those on higher quality diets. During epidemics, a combination of increased parasite acquisition and higher population growth rates resulted in higher parasite abundance for hosts on high-quality diets. Our work underscores the importance of considering both individual- and population-level impacts acting in concert to determine how diet affects the spread of infectious disease.

ecology↗

bioRxiv2026

Temperature alters specificity in a host-parasite interaction

The Red Queen Hypothesis proposes that genetic variation is maintained in populations through antagonistic coevolution of hosts and parasites. A major assumption of the Red Queen Hypothesis is tight genetic specificity for infection. However, it has been argued that this genetic interaction of host and parasite (GHxGP) is sensitive to environmental context (GHxGPxE). Environmental change could accordingly disrupt coevolutionary oscillations on relevant time scales, calling into question antagonistic coevolution as a general and robust explanation for the maintenance of genetic diversity. To evaluate this critique, we used the plant-parasitic nematode Meloidogyne arenaria and its natural bacterial parasite Pasteuria penetrans to determine if specificity is altered by temperature. We exposed six isofemale host lines to five parasite sources at three ecologically relevant temperatures. We found that, at two of three temperatures, susceptibility to infection depended on the specific combination of host line and parasite source (GHxGP). This specificity varied across temperatures, consistent with a GHxGPxE effect. This three-way interaction was driven both by quantitative changes in the strength of specificity across temperatures and shifts in the susceptibility rankings of host-parasite combinations. Our study contributes a rare experimental test of a proposed challenge to the Red Queen Hypothesis and suggests the potential for environmental context to change host-parasite specificity.

evolutionary biology↗

bioRxiv2026

Parasite defense covaries with reproductive timing, not with resistance

Defense is the ability of a host to minimize fitness loss to parasites. It is among the most variable phenotypes in host populations, and this variation facilitates rapid adaptation under parasite-mediated selection. We do not, however, know the underlying host traits that explain this variation in defense against parasites. A common assumption is that the most defended hosts are the most resistant, meaning they limit the establishment and growth of infecting parasites. Under this assumption, resistance traits should evolve readily under parasite selection. Resistance is, however, just one of many strategies hosts use to defend against parasites, and it does not consistently covary with fitness in the presence of parasites. We accordingly asked: which host traits covary with defense against parasites? We use controlled exposures to characterize genetic variation in defense of the nematode Caenorhabditis elegans against its natural microsporidian parasites. We report extensive variation in defense among wild strains of C. elegans: some strains lost 60% of fecundity under parasite exposure, while others were unaffected. We then tested the covariance of defense with two prominent host traits, resistance and reproductive timing. Our results did not support the hypothesis that resistance covaries with defense: strains with lower parasite burden did not have higher relative fecundity under exposure. Our results instead supported the hypothesis that life history covaries with defense: host strains that reproduced quickly had higher relative fecundity under exposure, consistent with the idea that parasites diminish future reproductive opportunities. The observed variation in defense among host strains indicates significant potential for wild C. elegans populations to evolve in response to their natural parasites. Because reproductive timing underpins this variation in defense, parasite-mediated selection could operate directly on host life history traits and should also be highly sensitive to shifts in life history driven by other biotic and abiotic factors. AUTHOR SUMMARYSome hosts fare much better than others in the face of parasite infection. What traits differentiate defended hosts from undefended hosts? The answer to this question is critical for identifying the strategies that best protect hosts from their parasites. It also allows us to predict and interpret the evolution of host populations over the course of epidemics. To address this question, we surveyed wild strains of a tractable model host, the nematode Caenorhabditis elegans, for their response to two species of microsporidian parasites. We found that, on average, parasite exposure substantially impaired the ability of hosts to reproduce. Host strains, however, varied widely: some experienced major losses in fecundity with exposure, while others were highly defended, showing little to no change. We identified reproductive timing as a key trait that differentiated defended hosts from undefended hosts. Our results suggest that reproducing quickly may have been protective, by allowing hosts to make most of their offspring before parasites impaired reproduction. We did not find evidence that resistance was protective: host strains with lower parasite burdens did not reproduce better than those with high parasite burdens. These findings give added weight to life history as a major component of host defense against parasites.

evolutionary biology↗

bioRxiv2026

Juvenile hosts and natal dispersers are protected in the early stages of epidemics

Parasite prevalence varies in time and space. Thus, hosts may escape infection by dispersing out of habitats where parasites are present. However, it is not clear if the advantage of avoiding parasites outweighs the cost of dispersing. Juvenile hosts are expected to be relatively protected from environmentally-transmitted parasites, and we hypothesize that this age bias in transmission could magnify the benefits of juvenile (i.e., natal) dispersal. We tested these ideas in the model nematode Caenorhabditis elegans, a host with discrete life stages and natal dispersal, and its environmentally transmitted microsporidian parasite Nematocida parisii. We found that under standardized exposure conditions, larger C. elegans individuals (corresponding to older life stages) acquired many more parasites than smaller (younger) individuals. We found this same bias during multigeneration epidemics, especially during early stages of the epidemics. We also found that C. elegans dispersal larvae were less likely to be infected and harbored less severe infections than the population mean. We conclude that the early stages of an epidemic can provide young hosts with a window of opportunity to escape infection by dispersing.

ecology↗

bioRxiv2025

From manual counting to YOLO: Using computer vision to automate large-scale fecundity assays in C. elegans

Fecundity measurements play a crucial role in life history research, providing insights into reproductive fitness, population dynamics, and environmental responses. In the model nematode Caenorhabditis elegans, fecundity assays are widely used to study development, aging, and genetic or environmental influences on reproduction. C. elegans hermaphrodites have large numbers of offspring (>100), so manual counting of viable offspring is time-consuming and susceptible to human error. Automated counting methods have the potential to enhance throughput, accuracy, and precision in data collection. We applied computer vision to 9,972 images of broods from individual C. elegans hermaphrodites from several strains under multiple treatments to capture variation in fecundity. We trained models using YOLO versions v8 to v11 (large and extra-large variants) to detect and count viable offspring, then compared the model results to estimates from manual counting. The best model was trained by YOLO v11-L. After fine-tuning, this model correctly detected 92% of all offspring visible in the images (recall) and was correct about 94.6% of the offspring it marked (precision). Manual counts differed from verified ground-truth counts by an average of 2.65 offspring per image, compared to 0.95 for the trained computer vision model. In addition, we detected significant effects of counter identity, experimental block, and their interaction on manual counts. Computer vision counts were not affected by these biases and outperformed manual counting in both speed and consistency. We demonstrate that computer vision can be a powerful tool for fecundity assays in C. elegans and provide a pipeline for applying this approach to new image sets. More broadly, applying computer vision to digital collections can advance ecological and evolutionary research by accelerating the study of fitness and life history.

evolutionary biology↗

bioRxiv2025

Host avoidance and resistance vary independently and are specific to parasite genotype

Hosts can reduce the negative fitness effects of parasite infection by avoiding contact with parasites or by resisting infection after contact. Because of their shared outcome, avoidance and resistance have been hypothesized to trade off with one another. Assuming these defenses carry fitness costs, hosts are expected to have high levels of one defense or the other, but not both. Alternatively, avoidance and resistance may covary positively, if, for example, they complement one another or are genetically or mechanistically linked. Testing these hypotheses requires measuring avoidance and resistance independently, which is challenging because they are functionally linked. In this study, we separated avoidance and resistance of the host C. elegans against the bacterial parasite S. marcescens and tested for a correlation between them. We phenotyped a panel of 12 genetically divergent hosts using two distinct bacterial strains and multiple experimental contexts. We found no evidence of a correlation between avoidance and resistance. This result suggests that avoidance and resistance can covary independently. Moreover, we found strong genetic specificity not only for resistance, but also for a measure of avoidance, motivating further research to examine the coevolutionary dynamics of avoidance.

evolutionary biology↗

bioRxiv2019

The evolution of parasite host range in genetically diverse host populations

Parasites vary enormously in their host range. Why are some parasites specialists and others generalists? We tested the hypothesis that genetically diverse host populations select for parasites with broader host ranges than genetically homogeneous host populations. To do so, we selected for increased killing ability of the bacterial parasite Serratia marcescens in populations of the host Caenorhabditis elegans that were either diverse (50% mix of genotypes N2 and LTM1) or homogenous (100% N2 or LTM1). We found mixed support for the hypothesis. After 20 generations of selection, parasites selected in diverse host populations maintained a broad host range, as shown by the retention of high killing ability of a novel host genotype. Parasites selected in diverse populations killed N2 hosts equally well as parasites selected in homogenous populations of N2. However, N2-selected parasites lost killing ability against the novel host, consistent with the evolution of narrow host ranges in homogenous environments. In contrast, parasites selected in homogenous LTM1 populations did not specialize: they did not increase in their killing ability on LTM1 and did not lose killing ability against the novel host. Our results argue that the evolution of host range depends upon both the identity and diversity of hosts that a parasite encounters.

evolutionary biology↗