Sharing an environment with sick conspecifics alters odors of healthy animals

Body odors change with health status and the odors of sick animals can induce avoidance behaviors in healthy conspecifics. Exposure to sickness odors might also alter the physiology of healthy conspecifics and modify the odors they produce. We hypothesized that exposure to odors of sick (but non-infectious) animals would alter the odors of healthy cagemates. To induce sickness, we injected mice with a bacterial endotoxin, lipopolysaccharide. We used behavioral odor discrimination assays and analytical chemistry techniques followed by predictive classification modeling to ask about differences in volatile odorants produced by two types of healthy mice: those cohoused with healthy conspecifics and those cohoused with sick conspecifics. Mice trained in Y-maze behavioral assays to discriminate between the odors of healthy versus sick mice also discriminated between the odors of healthy mice cohoused with sick conspecifics and odors of healthy mice cohoused with healthy conspecifics. Chemical analyses paired with statistical modeling revealed a parallel phenomenon. Urine volatiles of healthy mice cohoused with sick partners were more likely to be classified as those of sick rather than healthy mice based on discriminant model predictions. Sickness-related odors could have cascading effects on neuroendocrine or immune responses of healthy conspecifics, and could affect individual behaviors, social dynamics, and pathogen spread

Closing the Gap in High-Risk Pregnancy Care Using Machine Learning and Human-AI Collaboration

Health insurers often use algorithms to identify members who would benefit from care and condition management programs, which provide personalized, high-touch clinical support. Timely, accurate, and seamless integration between algorithmic identification and clinical intervention depends on effective collaboration between the system designers and nurse care managers. We focus on a high-risk pregnancy (HRP) program designed to reduce the likelihood of adverse prenatal, perinatal, and postnatal events and describe how we overcome three challenges of HRP programs as articulated by nurse care managers; (1) early detection of pregnancy, (2) accurate identification of impactable high-risk members, and (3) provision of explainable indicators to supplement predictions. We propose a novel algorithm for pregnancy identification that identifies pregnancies 57 days earlier than previous code-based models in a retrospective study. We then build a model to predict impactable pregnancy complications that achieves an AUROC of 0.760. Models for pregnancy identification and complications are then integrated into a proposed user interface. In a set of user studies, we collected quantitative and qualitative feedback from nurses on the utility of the predictions combined with clinical information driving the predictions on triaging members for the HRP program

POND DESICCATION RATE AFFECTS LARVAL DEVELOPMENT AND POST-METAMORPHIC IMMUNE SYSTEM RESPONSIVENESS IN A TEMPORARY POND BREEDING AMPHIBIAN, THE WOOD FROG

Organisms that exploit variable habitats often display phenotypically plastic responses, contingent upon prevailing conditions. Amphibians that metamorphose in ephemeral ponds constitute excellent models for examining plasticity in temporally variable environments. One way in which amphibians cope with variation in the larval environment is through plasticity in the duration and timing of metamorphosis. Facultative acceleration of developmental rate may reduce mortality due to desiccation at the larval stage, but it may also entail long-term costs in overall fitness. Here, we investigate the potential tradeoff between desiccation-driven acceleration of developmental rate and immune system responsiveness in a species that breeds exclusively in temporary ponds. We exposed Rana sylvatica tadpoles to four possible desiccation regimes and then assayed the cell-mediated immune response to a standardized foreign antigen, (phytohemagglutinin-PHA), injected three weeks after metamorphosis. We also quantified total leukocyte numbers from hematological smears to obtain a secondary measure of individual immunological condition. Animals exposed to desiccation treatments had shorter developmental times, weaker cellular immune system responses to PHA, and lower total leukocyte numbers than animals from control groups. Both immune measures showed a decrease in immune responsiveness with increasing severity of the desiccation treatment. It is currently unclear whether the observed depression in immune response is transient or permanent. However, even temporary periods of immune system suppression shortly after metamorphosis may lead to increased opportunistic infection within an environment of ubiquitous pathogens. Although infectious diseases alone are a major factor contributing to global amphibian declines, environmental stressors that increase susceptibility to pathogens may further promote extinction episodes. Desiccation-driven effects on temporary pond breeding amphibians are additionally relevant given projected changes in global and local climate that may impact surface water availability.Master of ScienceSchool of Natural Resources and EnvironmentUniversity of Michiganhttp://deepblue.lib.umich.edu/bitstream/2027.42/50467/1/THESIS.do

Sharing an environment with sick conspecifics alters odors of healthy animals

Body odors change with health status and the odors of sick animals can induce avoidance behaviors in healthy conspecifics. Exposure to sickness odors might also alter the physiology of healthy conspecifics and modify the odors they produce. We hypothesized that exposure to odors of sick (but non-infectious) animals would alter the odors of healthy cagemates. To induce sickness, we injected mice with a bacterial endotoxin, lipopolysaccharide. We used behavioral odor discrimination assays and analytical chemistry techniques followed by predictive classification modeling to ask about differences in volatile odorants produced by two types of healthy mice: those cohoused with healthy conspecifics and those cohoused with sick conspecifics. Mice trained in Y-maze behavioral assays to discriminate between the odors of healthy versus sick mice also discriminated between the odors of healthy mice cohoused with sick conspecifics and odors of healthy mice cohoused with healthy conspecifics. Chemical analyses paired with statistical modeling revealed a parallel phenomenon. Urine volatiles of healthy mice cohoused with sick partners were more likely to be classified as those of sick rather than healthy mice based on discriminant model predictions. Sickness-related odors could have cascading effects on neuroendocrine or immune responses of healthy conspecifics, and could affect individual behaviors, social dynamics, and pathogen spread

Host competence: An organismal trait to integrate immunology and epidemiology

The new fields of ecological immunology and disease ecology have begun to merge, and the classic fields of immunology and epidemiology are beginning to blend with them. This merger is occurring because the integrative study of host-parasite interactions is providing insights into disease in ways that traditional methods have not. With the advent of new tools, mathematical and technological, we could be on the verge of developing a unified theory of infectious disease, one that supersedes the barriers of jargon and tradition. Here we argue that a cornerstone of any such synthesis will be host competence, the propensity of an individual host to generate new infections in other susceptible hosts. In the last few years, the emergence of systems immunology has led to novel insight into how hosts control or eliminate pathogens. Most such efforts have stopped short of considering transmission and the requisite behaviors of infected individuals that mediate it, and few have explicitly incorporated ecological and evolutionary principles. Ultimately though, we expect that the use of a systems immunology perspective will help link suborganismal processes (i.e., health of hosts and selection on genes) to superorganismal outcomes (i.e., community-level disease dynamics and host-parasite coevolution). Recently, physiological regulatory networks (PRNs) were cast as whole-organism regulatory systems that mediate homeostasis and hence link suborganismal processes with the fitness of individuals. Here, we use the PRN construct to develop a roadmap for studying host competence, taking guidance from systems immunology and evolutionary ecology research. We argue that PRN variation underlies heterogeneity in individual host competence and hence host-parasite dynamics

Data from: Sharing an environment with sick conspecifics alters odors of healthy animals

Body odors change with health status and the odors of sick animals can induce avoidance behaviors in healthy conspecifics. Exposure to sickness odors might also alter the physiology of healthy conspecifics and modify the odors they produce. We hypothesized that exposure to odors of sick (but non-infectious) animals would alter the odors of healthy cage mates. To induce sickness, we injected mice with a bacterial endotoxin, lipopolysaccharide. We used behavioral odor discrimination assays and analytical chemistry techniques followed by predictive classification modeling to ask about differences in volatile odorants produced by two types of healthy mice: those cohoused with healthy conspecifics and those cohoused with sick conspecifics. Mice trained in Y-maze behavioral assays to discriminate between the odors of healthy versus sick mice also discriminated between the odors of healthy mice cohoused with sick conspecifics and odors of healthy mice cohoused with healthy conspecifics. Chemical analyses paired with statistical modeling revealed a parallel phenomenon. Urine volatiles of healthy mice cohoused with sick partners were more likely to be classified as those of sick rather than healthy mice based on discriminant model predictions. Sickness-related odors could have cascading effects on neuroendocrine or immune responses of healthy conspecifics, and could affect individual behaviors, social dynamics, and pathogen spread

Sharing an environment with sick conspecifics alters odors of healthy animals

Abstract Body odors change with health status and the odors of sick animals can induce avoidance behaviors in healthy conspecifics. Exposure to sickness odors might also alter the physiology of healthy conspecifics and modify the odors they produce. We hypothesized that exposure to odors of sick (but non-infectious) animals would alter the odors of healthy cagemates. To induce sickness, we injected mice with a bacterial endotoxin, lipopolysaccharide. We used behavioral odor discrimination assays and analytical chemistry techniques followed by predictive classification modeling to ask about differences in volatile odorants produced by two types of healthy mice: those cohoused with healthy conspecifics and those cohoused with sick conspecifics. Mice trained in Y-maze behavioral assays to discriminate between the odors of healthy versus sick mice also discriminated between the odors of healthy mice cohoused with sick conspecifics and odors of healthy mice cohoused with healthy conspecifics. Chemical analyses paired with statistical modeling revealed a parallel phenomenon. Urine volatiles of healthy mice cohoused with sick partners were more likely to be classified as those of sick rather than healthy mice based on discriminant model predictions. Sickness-related odors could have cascading effects on neuroendocrine or immune responses of healthy conspecifics, and could affect individual behaviors, social dynamics, and pathogen spread

Cohort3_PhysicallySeparated_PeakResponses

Peak responses for cohort 3 mice (physically separated pairs). Note that peak responses are not continuous from 1-68 because of preprocessing (e.g., removal of peaks that were not related to mouse urine)

Y_maze_data

Responses of individual biosensor mice in the Y maze. Note that training trial performance is included in this file, but these data are not shown in the final manuscript file (Fig. 2)

Data from: Stress hormones predict a host superspreader phenotype in the West Nile virus system

Glucocorticoid stress hormones, such as corticosterone (CORT), have profound effects on the behaviour and physiology of organisms, and thus have the potential to alter host competence and the contributions of individuals to population- and community-level pathogen dynamics. For example, CORT could alter the rate of contacts among hosts, pathogens and vectors through its widespread effects on host metabolism and activity levels. CORT could also affect the intensity and duration of pathogen shedding and risk of host mortality during infection. We experimentally manipulated songbird CORT, asking how CORT affected behavioural and physiological responses to a standardized West Nile virus (WNV) challenge. Although all birds became infected after exposure to the virus, only birds with elevated CORT had viral loads at or above the infectious threshold. Moreover, though the rate of mortality was faster in birds with elevated CORT compared with controls, most hosts with elevated CORT survived past the day of peak infectiousness. CORT concentrations just prior to inoculation with WNV and anti-inflammatory cytokine concentrations following viral exposure were predictive of individual duration of infectiousness and the ability to maintain physical performance during infection (i.e. tolerance), revealing putative biomarkers of competence. Collectively, our results suggest that glucocorticoid stress hormones could directly and indirectly mediate the spread of pathogens