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Abstract Host competence—the ability to acquire, harbour and transmit infections—drives pathogen spread and persistence in multi‐host communities. Evaluating species‐specific competence is critical for predicting transmission, particularly for generalist fungal pathogens likeBatrachochytrium dendrobatidis(Bd). Despite its central role in disease dynamics, we lack an epidemiologically grounded competence metric that rigorously accounts for how infection intensity affects a host's competence. This knowledge gap limits our ability to compare mechanisms across species and assess their roles in pathogen persistence. To address these challenges, we developed a novel, load‐dependent competence metric using host–pathogen Integral Projection Models (IPMs) that integrates variation in susceptibility, within‐host pathogen growth and pathogen shedding dynamics.We applied this metric to laboratory‐based challenge experiments with three common North American amphibians (Notophthalmus viridescens,Rana clamitansandRana catesbeianus) that persist endemically with Bd. Using dose–response assays and repeated pathogen shedding measurements across species, we asked: (i) is there a consistent, non‐linear relationship between infection intensity and pathogen shedding across species? and (ii) which load‐based traits best predict host competence? We quantified four of five components of host competence—susceptibility, pathogen growth, pathogen survival and load‐dependent shedding—and used these to parameterize species‐specific IPMs, integrating competence into a single relative metric across species.We found that Bd shedding increased non‐linearly with infection intensity, contradicting the standard assumption that Bd shedding is linearly related to infection intensity.Notophthalmus viridescensandR. catesbeianuswere the most competent hosts but through distinct pathways: high susceptibility inN. viridescensand elevated shedding rates inR. catesbeianus. In contrast, density‐dependent reductions in pathogen growth and shedding limitedR. clamitanscompetence. Thus, species‐level competence is not determined by a single trait, but emerges from interactions among multiple load‐based processes.Our results demonstrate that variation in competence emerges from distinct, species‐specific processes across multiple dimensions of competence. By linking individual infection dynamics to population‐level transmission potential, our integrative framework provides a more mechanistic approach to predicting host contributions to community‐level pathogen persistence. Read the freePlain Language Summaryfor this article on the Journal blog.
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This content will become publicly available on March 1, 2027
Cohorts of immature Pteropus bats show interannual variation in Hendra virus serology
Abstract Understanding the drivers of seasonal disease outbreaks remains a fundamental challenge in disease ecology. Periodic outbreaks can be driven by several seasonally varying factors, including pulses of susceptible individuals through births, changes in host behaviour and social aggregation and variation in host immunity. However, when these potential drivers overlap temporally, isolating their relative contributions to outbreak patterns becomes challenging.We studied Hendra virus, a zoonotic pathogen with seasonal spillovers from bats to horses and humans. Multiple seasonal factors have been hypothesized to drive Hendra virus transmission, including food shortages, birth pulses and changes in host aggregation, but their temporal overlap has made identifying primary drivers difficult.We conducted a 4‐year longitudinal study ofPteropusbats to test whether seasonal birth pulses and the resulting influx of susceptible juveniles drive Hendra virus transmission. Using a Bayesian ageing model, we aged sexually immature bats and placed them into birth cohorts. We used our age predictions to model how viral shedding and antibody responses changed as bats aged. We trackedBartonellaspp. Infection—a bacterial pathogen requiring close contact for transmission—as an indicator of transmission opportunities within each cohort for comparison.We found no evidence that seasonal birth pulses of immunologically naïve juveniles drove Hendra virus transmission. Two out of three cohorts showed substantially reduced maternal antibody transfer compared to the 2018 cohort, with seroprevalence near zero at our earliest sampling timepoints and showed no clear evidence of synchronized seroconversion. Furthermore,Bartonellainfection rates were consistent across cohorts, indicating that opportunities for pathogen transmission remained consistent across cohorts despite varying viral shedding patterns.Our findings demonstrate that birth pulses alone cannot explain observed patterns of Hendra virus outbreaks. These results highlight the importance of using multiple lines of evidence to evaluate competing mechanisms underlying seasonal disease dynamics, particularly when potential drivers coincide temporally.
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- PAR ID:
- 10674347
- Author(s) / Creator(s):
- ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; more »
- Publisher / Repository:
- Wiley Online Publishing
- Date Published:
- Journal Name:
- Journal of Animal Ecology
- Volume:
- 95
- Issue:
- 3
- ISSN:
- 0021-8790
- Page Range / eLocation ID:
- 521 to 537
- Format(s):
- Medium: X
- Associated Dataset(s):
- View Associated Dataset(s) >>
- Sponsoring Org:
- National Science Foundation
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