Biology subjects

Kramp, R. D.

Publications and source records attributed to Kramp, R. D..

4 recordsLinked to original sources

bioRxiv2026

Thermal variability interacts with infection load and the evolution of host-parasite defense

Rising temperatures and unpredictable weather patterns are directly linked to emerging infectious diseases that threaten global biodiversity. Thermal variability affects host-parasite interactions, and understanding how animal hosts respond to temperature variability and parasite infection is paramount for conservation and for predicting zoonotic spillover. Hosts employ two strategies to defend against parasites: resistance (inhibiting or limiting infection) and tolerance (limiting the negative effects of infection). This observation raises a fundamental question: How does thermal variability affect the expression and evolution of resistance versus tolerance? Subsequently, how does the evolution of resistance versus tolerance influence parasite load dynamics? Here, we first review why temperature may differentially affect resistance and tolerance mechanisms, thereby altering host selection and eco-evolutionary disease outcomes. Second, to highlight the importance of these interactions, we present a model that illustrates key potential effects of temperature variability on host defense mechanisms. Our model demonstrates that temperature variability alone could drive lower infection prevalence and loads, but it also selects for host tolerance, ultimately leading to higher net prevalence and loads. We also find widely divergent outcomes depending on how temperature impacts defense strategies. These results highlight key areas for future empirical and theoretical work on the interactions among temperature variability, infection load, and host defense evolution.

ecology↗

bioRxiv2024

Artificial Selection and the Skin Microbiome Independently Predict Parasite Resistance

Host responses to parasite infection involve several interacting systems. Host genetics determine much of the response, but it is increasingly clear that the host-associated microbiome also plays a role. Genetically determined systems and the microbiome can also interact; for example, the microbiome can modulate the immune response, and vice versa. However, it remains unclear how such interactions between the host immune system and the microbiome may influence the hosts overall response to parasites. To investigate how host genetics and the microbiome interact to shape responses to parasites, we imposed truncation selection on Trinidadian guppies (Poecilia reticulata) for low and high resistance to the specialist ectoparasite Gyrodactylus turnbulli. After 3-6 generations of breeding without parasites, we sampled the skin-associated microbiome and infected fish from each line. We applied Dirichlet Multinomial Modeling (DMM) machine-learning to identify bacterial community types across lines and evaluated how selection line and community type explained variations in infection severity. Our findings showed that among females, the resistant line had significantly lower infection severity, while the susceptible line had higher infection severity. Among males, only the susceptible line experienced higher infection severity compared to the other lines. Line did not explain skin microbial diversity, structure or composition. Our DMM analysis revealed three distinct bacterial community types, independent of artificial selection lines, which explained just as much variation in infection load as selection line. Overall, we found that the microbiome and host genetics independently predict infection severity, highlighting the microbiomes active role in host-parasite interactions.

ecology↗

bioRxiv2023

Infection affects guppy reproductive fitness and offspring parasite resistance

O_LIInfection imposes energetic costs on hosts. Hosts typically respond by shifting resources, potentially affecting the quantity and quality of offspring they produce. As the sexes differ in their optimal reproductive strategies, infection of mothers versus fathers may affect offspring quantity and quality in different ways. C_LIO_LIHere, we test how experimental infection of guppies Poecilia reticulata with the ectoparasite Gyrodactylus turnbulli affects parental reproductive fitness and offspring parasite resistance. We compared breeding pairs in which one or neither parent had previously been infected. C_LIO_LIIn terms of reproductive fitness, parental infection experience did not affect the size, body condition, or number of offspring produced, but fathers who experienced the heaviest infections produced offspring [~]55 days sooner than average. This result may represent terminal investment by the males most affected by infection, or may indicate that these males have a faster pace of life, investing in reproduction at the expense of parasite defence. C_LIO_LIWe found that offspring age, parental infection experience, and parental infection severity together strongly predicted offspring parasite resistance. Only among pairs in which one parent had been infected, older offspring, which were those born soonest after the parents infection, tended to experience heavier infections. This result may therefore reflect temporary infection-induced reductions in parental investment in offspring quality. Beyond this effect of offspring age, offspring of infected mothers experienced 105 fewer worm days than those of infected fathers: fathers, but not mothers, that experienced heavy infections themselves produced offspring that also experienced heavy infections. The parent-offspring regression for infected fathers is therefore consistent with previous evidence that parasite resistance is heritable in this system, and yields a narrow sense heritability estimate of 0.69{+/-}0.13. By contrast, the mother-offspring regression (slope: -0.13{+/-}0.17) provides novel insight that mothers may engage in transgenerational immune priming. C_LIO_LIOverall, our results suggest that the sexes strike a different balance between offspring quantity and quality when faced with infection, with potentially broad implications for disease and host-parasite coevolutionary dynamics in nature. C_LI

ecology↗

bioRxiv2021

Social hosts evade predation but have deadlier parasites

Parasites exploit hosts to replicate and transmit, but overexploitation kills host and parasite (1): predators may shift this cost-benefit balance by consuming hosts (2-4) or changing host behavior, but the strength of these effects remains unclear. Modeling both, we find a primary, strong effect: hosts group to defend against predators (5), increasing parasite transmission, thus multiple infections, and therefore favoring more exploitative, virulent, parasites (6). Indeed, among 18 Trinidadian Gyrodactyus spp. parasite lines, those collected from high predation guppy populations were more virulent in common garden than those from low predation populations. Our model accurately predicted this result when parametrized with our experimentally demonstrated virulence-transmission trade-off, implicating the behavioral effects of predation. Broadly, our results indicate that reduced social contact selects against parasite virulence. One-Sentence SummaryOur theory and data show predators cause increased host social grouping; the resulting transmission favors parasite virulence.

ecology↗