Biology subjects

Sauer, E. L.

Publications and source records attributed to Sauer, E. L..

8 recordsLinked to original sources

bioRxiv2026

A shared pathogen reservoir can tip widespread infection into mass mortality

Pathogens that persist subclinically across many wildlife populations can drive mass mortality in others. Mass mortality is often abrupt, and the timing can be difficult to predict from host or habitat features alone. In a recent field study tracking ranavirus epizootics in wood frog (Rana sylvatica) breeding ponds, we found that no environmental or biotic feature reliably predicted die-off occurrence or timing. Instead, the trajectory of viral accumulation in the water column was the strongest dynamic predictor of mass mortality. Infected hosts shed virus throughout epizootics, but the influence of waterborne viral concentration on disease progression was apparent only near die-off onset. This pattern suggests a potential threshold-dependent feedback operating through the shared viral environment. Here, we develop a compartmental model linking waterborne viral concentration to the rate at which subclinical infections progress to clinical, high-shedding states within already-infected hosts. We show that a dose-dependent progression model generates the two-phase epizootic trajectory observed in natural die-offs: prolonged subclinical circulation followed by abrupt clinical transition after environmental virus crosses an escalation threshold. The model exhibits a sharp phase transition between subclinical circulation and mass mortality, governed mainly by the clinical-to-subclinical shedding ratio, host density, and pond volume. Existing explanations for die-off variation emphasize individual-level susceptibility, but our model demonstrates that dose-dependent environmental feedback, a mechanism not previously formalized at the population level, can generate the transition from subclinical infection to mass mortality without invoking individual variation in host susceptibility. This mechanism may apply in any system where hosts share a bounded environment, pathogen dose influences disease severity, and pathogen shedding increases with disease progression.

ecology↗

bioRxiv2026

Epizootic tipping points: Environmental viral feedbacks predict amphibian die-offs

Virulent pathogens commonly circulate in wildlife populations without causing mass mortality, but the processes driving die-offs remain poorly understood. Prevailing frameworks emphasize individual-level susceptibility, although susceptibility factors often fail to predict population-level outcomes. We tracked ranavirus epizootics across 40 wood frog breeding ponds over three years, comparing models based on lagged viral state variables with those based on abiotic and host conditions. Models based on lagged viral-state variables received greater support for subsequent infection spread, intensification, and viral accumulation. Prevalence predicted later environmental viral concentration throughout epizootics, whereas relationships between environmental viral concentration and subsequent infection spread and intensification were substantially weakened when die-off onsets were excluded, consistent with phase-dependent feedback. Viral accumulation rates differentiated die-off from non-die-off pond-years while static pond and host features did not, suggesting that die-offs may be associated with pathogen accumulation in shared environments rather than being predictable from static pond and host features alone.

ecology↗

bioRxiv2026

A dedicated brain circuit controls forward walking in Drosophila

Neural circuits in the brain control high-level parameters of movement, including the initiation, speed, and direction of locomotion. How specific cell types are organized into circuits to compute these control signals and enable context-appropriate behavior remains unclear. Here, we identify central brain neurons in Drosophila that can initiate walking and exert graded control over walking speed. Connectome analyses position the neurons on top of a layered brain circuit, which recruits a specific population of descending neurons to control forward walking independently of turning and other parameters. As predicted by the connectome, the circuit enforces straight walking when activated unilaterally, and the activity of the central brain neurons represents a high-level walking drive. This drive is suppressed during flight but flexibly integrated with other control signals to enable complex movement sequences during obstacle negotiation. Together, our findings elucidate a dedicated brain circuit that enables efficient computation, selection, and integration of forward-walking signals for context-appropriate motor control.

neuroscience↗

bioRxiv2025

The nutritional content of anthropogenic resources affects wildlife disease dynamics

Wildlife have become increasingly reliant on human-supplemented food, affecting interactions between individuals and subsequently disease transmission. Much of the research investigating the impact of human-supplemented food has focused on host behavioral changes and food availability. However, the nutritional quality of food can significantly impact disease transmission depending on whether it boosts or hinders immunity. Few studies have investigated links between nutrition, immunity, and pathogen transmission, which weakens efforts to guide and manage infectious disease at the wildlife-human interface. We investigate these interactions using a data-driven transmission model that explicitly incorporates feedback between nutrition, immunity, and pathogen transmission in the bacterial pathogen, Mycoplasma gallisepticum and its avian hosts which are heavily dependent on supplemental food sources. We also examine the nutritional content and sales frequency of one of, if not the, most common source of anthropogenic food supplementation, bird feeder food. We find that food with lower nutritional quality is purchased for wild bird supplementation far more frequently than food with high nutritional quality. Further, our transmission model demonstrates that these lower quality food sources result in large epidemics that cause destabilizing population declines. Our results suggest that nutritional quality plays an important role in disease transmission and provide insight into the ecological and immunological consequences of human behavior on infectious disease in wildlife.

ecology↗

bioRxiv2025

Prior infection induces long-lasting partial immunity to reduce transmission within flocks in an avian host-pathogen system.

Population-level differences in the ability to maintain immunity can lead to contrasting survival outcomes between groups and determine how future outbreaks will spread. Pathology and infectiousness during subsequent infections can be influenced by immunity and an increase in resistance or tolerance of individuals. However, determining the longevity and effectiveness of immunity in wildlife population is challenging due to lack of infrastructure for long term monitoring of populations and individuals and host-pathogen specific tests. Further, predicting wildlife disease dynamics requires an understanding of individual-level heterogeneity in pathology and behavior as well as a knowledge of how populations with differing partial immunity will transmit disease, which is currently limited. Using an avian host-pathogen system, we ran two experiments to determine if previously exposed birds had immunity to MG after three years and if Mycoplasma gallisepticum (MG) transmission differed between first and second infection index birds. Birds retained partial immunity to MG for three years after their original infection and showed signs of being resistant to infection. The transmission experiment revealed that although first and second-infection index birds experienced pathology and pathogen growth, only first infection birds transmitted MG. Three years could represent lifetime protection for individuals who survive their first infection and a reduction in risk for other members of their flock. Our research has important implications for understanding MG epidemics in wild populations of birds as well as disease in wildlife more broadly.

ecology↗

bioRxiv2024

Diet driven differences in host tolerance are linked to shifts in global gene expression in a common avian host-pathogen system

As humans alter the landscape, wildlife have become increasingly dependent on anthropogenic resources, altering interactions between individuals and subsequently disease transmission dynamics. Further, nutritional quantity and quality greatly impact an individual hosts immune capacity and ability to mitigate damage caused by infectious disease. Thus, understanding the impact of dietary nutrition on immune function is critical for predicting disease severity and transmission as human activity both facilitates the dispersal of pathogens and alters dietary options for wildlife. Here, we use transcriptomics to explore the previously unstudied molecular mechanisms underpinning diet-driven differences in pathogen tolerance using a widespread avian bacterial pathogen, Mycoplasma gallisepticum (MG). MG is an ideal model for understanding the dietary drivers of disease as the human supplementation that wild birds commonly rely on, bird feeders, are also an important source for MG transmission. Significant diet-driven differences in the expression of many genes encoding immune response and translational machinery proteins are seen both in the absence of MG and during the recovery period. Prior to infection, protein-fed birds are more transcriptionally primed for infection than lipid-fed birds which translates to greater tolerance in protein-fed birds during the recovery period. Given the significant importance of human supplemented food in wildlife disease systems, the molecular mechanisms by which interactions between diet and infection emerge provide insight into the ecological and immunological consequences of human behavior and wildlife disease.

ecology↗

bioRxiv2023

Male pathology regardless of behaviour drives transmission in an avian host-pathogen system

Host sex is an important source of heterogeneity in the severity of epidemics. Pinpointing the mechanisms causing this heterogeneity can be difficult because differences in behaviour among sexes (e.g. greater territorial aggression in males) can bias exposure risk, obfuscating the role of immune function, which can lead to differences in pathology, in driving differential susceptibility between sexes. Thus, sex-biased transmission driven by differences in immune function independent of behaviour is poorly understood, especially in non-mammalian systems. Here we examine the previously unexplored potential for male-biased pathology to affect transmission using an avian host-pathogen system. We employ a sex-dependent multistate transmission model parameterized with isolated, individual-based experimental exposures of domestic canaries and experimental transmission data of house finches. The experiment revealed that male birds have shorter incubation periods, longer recovery periods, higher pathogen burdens, and greater disease pathology, than females. Our model revealed that male-biased pathology led to epidemic size rapidly increasing with the proportion of male birds, with a nearly 16-fold increase in total epidemic size from an all-female to an all-male simulation. Our results demonstrate that female-biased resistance, independent of male behaviour, can drive sex-dependent transmission in wildlife, indicating that sex-based differences in immune function, not just differences in exposure risk, can shape epidemic dynamics.

ecology↗

bioRxiv2019

A meta-analysis reveals temperature, dose, life stage, and taxonomy influence host susceptibility to a fungal parasite

Complex ecological relationships, such as host-parasite interactions, are often modeled with laboratory experiments. However, some experimental laboratory conditions, such as temperature or infection dose, are regularly chosen based on convenience or convention and it is unclear how these decisions systematically affect experimental outcomes. Here, we conducted a meta-analysis of 58 laboratory studies that exposed amphibians to the pathogenic fungus Batrachochytrium dendrobatidis (Bd) to better understand how laboratory temperature, host life stage, infection dose, and host species affect host mortality. We found that host mortality was driven by thermal mismatches: hosts native to cooler environments experienced greater Bd-induced mortality at relatively warm experimental temperatures and vice versa. We also found that Bd dose positively predicted Bd-induced host mortality and that the superfamilies Bufonoidea and Hyloidea were especially susceptible to Bd. Finally, the effect of Bd on host mortality varied across host life stages, with larval amphibians experiencing lower risk of Bd-induced mortality than adults or metamorphs. Metamorphs were especially susceptible and experienced mortality when inoculated with much smaller Bd doses than the average dose used by researchers. Our results suggest that when designing experiments on species interactions, researchers should carefully consider the experimental temperature, and inoculum dose, and life stage and taxonomy of the host species.

ecology↗