Testing The Multiple Stressor Hypothesis: Chlorothalonil Exposure Alters Transmission Potential Of A Bumble Bee Pathogen But Not Individual Host Health

Numerous threats are putting pollinator health and essential ecosystem pollination services in jeopardy. Although individual threats are widely studied, their co-occurrence may exacerbate negative effects, as posited by the multiple stressor hypothesis. A prominent branch of this hypothesis concerns pesticide–pathogen co-exposure. A landscape analysis demonstrated a positive association between local chlorothalonil fungicide use and microsporidian pathogen ( Nosema bombi ) prevalence in declining bumblebee species ( Bombus spp.), suggesting an interaction deserving further investigation. We tested the multiple stressor hypothesis with field-realistic chlorothalonil and N. bombi exposures in worker-produced B. impatiens microcolonies. Chlorothalonil was not avoided in preference assays, setting the stage for pesticide–pathogen co-exposure. However, contrary to the multiple stressor hypothesis, co-exposure did not affect survival. Bees showed surprising tolerance to Nosema infection, which was also unaffected by chlorothalonil exposure. However, previously fungicide-exposed infected bees carried more transmission-ready spores. Our use of a non-declining bumblebee and potential higher chlorothalonil exposures under some scenarios could mean stronger individual or interactive effects in certain field settings. Yet, our results alone suggest consequences of pesticide co-exposure for pathogen dynamics in host communities. This underlies the importance of considering both within- and between-host processes when addressing the multiple stressor hypothesis in relation to pathogens.

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Transient disease dynamics across ecological scales

Theoretical Ecology ◽

10.1007/s12080-021-00514-w ◽

2021 ◽

Author(s):

Yun Tao ◽

Jessica L. Hite ◽

Kevin D. Lafferty ◽

David J. D. Earn ◽

Nita Bharti

Keyword(s):

Disease Transmission ◽

Movement Ecology ◽

Pathogen Transmission ◽

Disease Spread ◽

Transient Dynamics ◽

Transmission Potential ◽

Movement Dynamics ◽

Individual Host ◽

Ecological Hierarchy ◽

The Individual

AbstractAnalyses of transient dynamics are critical to understanding infectious disease transmission and persistence. Identifying and predicting transients across scales, from within-host to community-level patterns, plays an important role in combating ongoing epidemics and mitigating the risk of future outbreaks. Moreover, greater emphases on non-asymptotic processes will enable timely evaluations of wildlife and human diseases and lead to improved surveillance efforts, preventive responses, and intervention strategies. Here, we explore the contributions of transient analyses in recent models spanning the fields of epidemiology, movement ecology, and parasitology. In addition to their roles in predicting epidemic patterns and endemic outbreaks, we explore transients in the contexts of pathogen transmission, resistance, and avoidance at various scales of the ecological hierarchy. Examples illustrate how (i) transient movement dynamics at the individual host level can modify opportunities for transmission events over time; (ii) within-host energetic processes often lead to transient dynamics in immunity, pathogen load, and transmission potential; (iii) transient connectivity between discrete populations in response to environmental factors and outbreak dynamics can affect disease spread across spatial networks; and (iv) increasing species richness in a community can provide transient protection to individuals against infection. Ultimately, we suggest that transient analyses offer deeper insights and raise new, interdisciplinary questions for disease research, consequently broadening the applications of dynamical models for outbreak preparedness and management.

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Population-Level Disease Dynamics Reflect Individual Heterogeneities in Transmission

10.1101/735480 ◽

2019 ◽

Author(s):

Jonathon A. Siva-Jothy ◽

Lauren A. White ◽

Meggan E. Craft ◽

Pedro F. Vale

Keyword(s):

Social Network ◽

Disease Transmission ◽

Network Connectivity ◽

Population Level ◽

Disease Dynamics ◽

Virus Shedding ◽

Transmission Potential ◽

Social Aggregation ◽

Individual Host ◽

Host Heterogeneity

AbstractHost heterogeneity in disease transmission is widespread and presents a major hurdle to predicting and minimizing pathogen spread. Using the Drosophila melanogaster model system infected with Drosophila C virus, we integrate experimental measurements of individual host heterogeneity in social aggregation, virus shedding, and disease-induced mortality into an epidemiological framework that simulates outbreaks of infectious disease. We use these simulations to calculate individual variation in disease transmission and apportion this variation to specific components of transmission: social network degree distribution, infectiousness, and infection duration. The experimentally-observed variation produces substantial differences in individual transmission potential, providing evidence for genetic and sex-specific effects on disease dynamics at a population level. Manipulating variation in social network connectivity, infectiousness, and infection duration in simulated populations reveals that these components affect disease transmission in clear and distinct ways. We consider the implications of this genetic and sex-specific variation in disease transmission and discuss implications for appropriate control methods given the relative contributions made by social aggregation, virus shedding, and infection duration to transmission in other host-pathogen systems.

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Interhost dispersal alters microbiome assembly and can overwhelm host innate immunity in an experimental zebrafish model

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1702511114 ◽

2017 ◽

Vol 114 (42) ◽

pp. 11181-11186 ◽

Cited By ~ 51

Author(s):

Adam R. Burns ◽

Elizabeth Miller ◽

Meghna Agarwal ◽

Annah S. Rolig ◽

Kathryn Milligan-Myhre ◽

...

Keyword(s):

Large Scale ◽

Ecological Theory ◽

Host Factors ◽

Wild Type ◽

Zebrafish Model ◽

Individual Host ◽

Host Health ◽

Host Innate Immunity ◽

Metacommunity Dynamics ◽

Microbiome Assembly

The diverse collections of microorganisms associated with humans and other animals, collectively referred to as their “microbiome,” are critical for host health, but the mechanisms that govern their assembly are poorly understood. This has made it difficult to identify consistent host factors that explain variation in microbiomes across hosts, despite large-scale sampling efforts. While ecological theory predicts that the movement, or dispersal, of individuals can have profound and predictable consequences on community assembly, its role in the assembly of animal-associated microbiomes remains underexplored. Here, we show that dispersal of microorganisms among hosts can contribute substantially to microbiome variation, and is able to overwhelm the effects of individual host factors, in an experimental test of ecological theory. We manipulated dispersal among wild-type and immune-deficient myd88 knockout zebrafish and observed that interhost dispersal had a large effect on the diversity and composition of intestinal microbiomes. Interhost dispersal was strong enough to overwhelm the effects of host factors, largely eliminating differences between wild-type and immune-deficient hosts, regardless of whether dispersal occurred within or between genotypes, suggesting dispersal can independently alter the ecology of microbiomes. Our observations are consistent with a predictive model that assumes metacommunity dynamics and are likely mediated by dispersal-related microbial traits. These results illustrate the importance of microbial dispersal to animal microbiomes and motivate its integration into the study of host–microbe systems.

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Neurotropic enteroviruses co-opt “fair-weather-friend” commensal gut microbiota to drive host infection and central nervous system disturbances

Behavioral and Brain Sciences ◽

10.1017/s0140525x18002741 ◽

2019 ◽

Vol 42 ◽

Author(s):

Kevin B. Clark

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Gut Bacteria ◽

Infection Cycle ◽

Fair Weather ◽

Host Health ◽

Microbe Interactions ◽

Animal Hosts ◽

Host Infection ◽

Neuropsychiatric Conditions

Abstract Some neurotropic enteroviruses hijack Trojan horse/raft commensal gut bacteria to render devastating biomimicking cryptic attacks on human/animal hosts. Such virus-microbe interactions manipulate hosts’ gut-brain axes with accompanying infection-cycle-optimizing central nervous system (CNS) disturbances, including severe neurodevelopmental, neuromotor, and neuropsychiatric conditions. Co-opted bacteria thus indirectly influence host health, development, behavior, and mind as possible “fair-weather-friend” symbionts, switching from commensal to context-dependent pathogen-like strategies benefiting gut-bacteria fitness.

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