Emerging infectious diseases have caused population declines and biodiversity loss. The ability of pathogens to survive in the environment, independent of their host, can exacerbate disease impacts and increase the likelihood of species extinction. Control of pathogens with environmental stages remains a significant challenge for conservation and effective management strategies are urgently needed. We examined the effectiveness of managing environmental exposure to reduce the impacts of an emerging infectious disease of bats, white‐nose syndrome (WNS). We used a chemical disinfectant, chlorine dioxide (ClO2), to experimentally reduce ClO2was effective at killing The reduction in the environmental reservoir at treatment sites resulted in lower fungal loads on bats compared to untreated control populations. Survival following treatment was also higher in little brown bats (
Host abundance and heterogeneity in infectiousness determine extent of the environmental reservoir
Environmental pathogen reservoirs exist for many globally important diseases and can fuel disease outbreaks, affect pathogen evolution, and increase the threat of host extinction. Differences in pathogen shedding among hosts can create mosaics of infection risk across landscapes by increasing pathogen contamination in high use areas. However, how the environmental reservoir establishes in multi-host communities and the importance of factors like host-specific infection and abundance in environmental contamination and transmission remain important outstanding questions. Here we examine how Pseudogymnoascus destructans, the fungal pathogen that causes white-nose syndrome in bats, invades and establishes in the environment. We quantified dynamic changes in pathogen shedding, infection intensities, host abundance, and the subsequent propagule pressure imposed by each species within the community. We find that the initial establishment of the pathogen reservoir is driven by different species within the community than those that are responsible for maintaining the reservoir over time. Our results also show that highly shedding species do not always contribute the most to pathogen reservoirs. More broadly, we demonstrate how individual host shedding rates scale to influence landscape-level pathogen contamination.
more »
« less
- Award ID(s):
- 1911853
- NSF-PAR ID:
- 10425006
- Date Published:
- Journal Name:
- bioRxiv
- ISSN:
- 2692-8205
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
More Like this
-
more » « less
Abstract Pseudogymnoascus destructans , the fungal pathogen causing WNS, in the environment. We combined laboratory experiments with 3 years of field trials at four abandoned mines to determine whether ClO2could effectively removeP. destructans from the environment, reduce host infection and limit population impacts.P. destructans in vitro across multiple concentrations. In field settings, higher concentrations of ClO2treatment were needed to sufficiently reduce viableP. destructans conidia in the environment.Myotis lucifugus ), and trended higher for tricolored bats (Perimyotis subflavus ).Synthesis and applications . Our results highlight that targeted management of sources for environmental transmission can be an effective control strategy for wildlife disease. We found that successfully reducing pathogen in the environment decreased disease severity and increased survival, but required higher treatment exposure than was effective in laboratory experiments, and the effects varied among species. More broadly, our findings have implications for other emerging wildlife diseases with free‐living pathogen stages by highlighting how the degree of environmental contamination can have cascading impacts on hosts, presenting an opportunity for intervention. -
Abstract Understanding the community ecology of vector-borne and zoonotic diseases, and how it may shift transmission risk as it responds to environmental change, has become a central focus in disease ecology. Yet, it has been challenging to link the ecology of disease with reported human incidence. Here, we bridge the gap between local-scale community ecology and large-scale disease epidemiology, drawing from a priori knowledge of tick-pathogen-host ecology to model spatially-explicit Lyme disease (LD) risk, and human Lyme disease incidence (LDI) in California. We first use a species distribution modeling approach to model disease risk with variables capturing climate, vegetation, and ecology of key reservoir host species, and host species richness. We then use our modeled disease risk to predict human disease incidence at the zip code level across California. Our results suggest the ecology of key reservoir hosts—particularly dusky-footed woodrats—is central to disease risk posed by ticks, but that host community richness is not strongly associated with tick infection. Predicted disease risk, which is most strongly influenced by the ecology of dusky-footed woodrats, in turn is a strong predictor of human LDI. This relationship holds in the Wildland-Urban Interface, but not in open access public lands, and is stronger in northern California than in the state as a whole. This suggests peridomestic exposure to infected ticks may be more important to LD epidemiology in California than recreational exposure, and underlines the importance of the community ecology of LD in determining human transmission risk throughout this LD endemic region of far western North America. More targeted tick and pathogen surveillance, coupled with studies of human and tick behavior could improve understanding of key risk factors and inform public health interventions. Moreover, longitudinal surveillance data could further improve forecasts of disease risk in response to global environmental change.more » « less
-
Globally, zoonotic vector-borne diseases are on the rise and understanding their complex transmission cycles is pertinent to mitigating disease risk. In North America, Lyme disease is the most commonly reported vector-borne disease and is caused by transmission of Borrelia burgdorferi sensu lato (s.l.) from Ixodes spp. ticks to a diverse group of vertebrate hosts. Small mammal reservoir hosts are primarily responsible for maintenance of B. burgdorferi s.l. across the United States. Never- theless, birds can also be parasitized by ticks and are capable of infection with B. burgdorferi s.l. but their role in B. burgdorferi s.l. transmission dynamics is understudied. Birds could be important in both the maintenance and spread of B. burgdorferi s.l. and ticks because of their high mobility and shared habitat with important mammalian reservoir hosts. This study aims to better understand the role of avian hosts in tick-borne zoonotic disease transmission cycles in the western United States. We surveyed birds, mammals, and ticks at nine sites in northern California for B. burgdorferi s.l. infection and collected data on other metrics of host community composition such as abundance and diversity of birds, small mammals, lizards, predators, and ticks. We found 22.8% of birds infected with B. burgdorferi s.l. and that the likelihood of avian B. burgdorferi s.l. infection was significantly associated with local host community composition and pathogen prevalence in California. Addition- ally, we found an average tick burden of 0.22 ticks per bird across all species. Predator and lizard abundances were significant predictors of avian tick infestation. These results indicate that birds are relevant hosts in the local B. burgdorferi s.l. transmission cycle in the western United States and quantifying their role in the spread and maintenance of Lyme disease requires further research.more » « less
-
Atack, John M. (Ed.)ABSTRACT Buruli ulcer disease is a neglected tropical disease caused by the environmental pathogen Mycobacterium ulcerans . The M. ulcerans major virulence factor is mycolactone, a lipid cytotoxic compound whose genes are carried on a plasmid. Although an exact reservoir and mode(s) of transmission are unknown, data provide evidence of both. First, Buruli ulcer incidence and M. ulcerans presence have been linked to slow-moving water with low oxygen. M. ulcerans has also been suggested to be sensitive to UV due to termination in crtI , encoding a phytoene dehydrogenase, required for carotenoid production. Further, M. ulcerans has been shown to cause disease following puncture but not when introduced to open abrasion sites, suggesting that puncture is necessary for transmission and pathology. Despite these findings, the function and modulation of mycolactone and other genes in response to dynamic abiotic conditions such as UV, temperature, and oxygen have not been shown. In this study, we investigated modulation of mycolactone and other genes on exposure to changing UV and oxygen microenvironmental conditions. Mycolactone expression was downregulated on exposure to the single stress high temperature and did not change significantly with exposure to UV; however, it was upregulated when exposed to microaerophilic conditions. Mycolactone expression was downregulated under combined stresses of high temperature and low oxygen, but there was upregulation of several stress response genes. Taken together, results suggest that temperature shapes M. ulcerans metabolic response more so than UV exposure or oxygen requirements. These data help to define the environmental niche of M. ulcerans and metabolic responses during initial human infection. IMPORTANCE Buruli ulcer is a debilitating skin disease caused by the environmental pathogen Mycobacterium ulcerans . M. ulcerans produces a toxic compound, mycolactone, which leads to tissue necrosis and ulceration. Barriers to preventing Buruli ulcer include an incomplete understanding of M. ulcerans reservoirs, how the pathogen is transmitted, and under what circumstances mycolactone and other M. ulcerans genes are expressed and produced in its natural environment and in the host. We conducted a study to investigate M. ulcerans gene expression under several individual or combined abiotic conditions. Our data showed that mycolactone expression was downregulated under combined stresses of high temperature and low oxygen but there was upregulation of several stress response genes. These data are among only a few studies measuring modulation of mycolactone and other M. ulcerans genes that could be involved in pathogen fitness in its natural environment and virulence while within the host.more » « less
-
more » « less
Abstract Disease dynamics are governed by variation of individuals, species, and environmental conditions across space and time. In some cases, an alternate reservoir host amplifies pathogen loads and drives disease transmission to less competent hosts in a process called pathogen spillover. Spillover is frequently associated with multi‐host disease systems where a single species is more tolerant of infection and more competent in pathogen transmission compared to other hosts. Pathogen spillover must be driven by biotic factors, including host and community characteristics, yet biotic factors interact with the abiotic environment (e.g., temperature) to create disease. Despite its fundamental role in disease dynamics, the influence of the abiotic environment on pathogen spillover has seldom been examined. Improving our understanding of disease processes such as pathogen spillover hinges on disentangling the effects of interrelated biotic and abiotic factors over space and time. We applied 10 yr of fine‐scale microclimate, disease, and tree community data in a path analysis to investigate the relative influence of biotic and abiotic factors on pathogen spillover for the emerging infectious forest disease sudden oak death (
SOD ). Disease transmission inSOD is primarily driven by the reservoir host California bay laurel, which supports high foliar pathogen loads that spillover onto neighboring oak trees and create lethal canker infections. The foliar pathogen load and susceptibility of oaks is expected to be sensitive to forest microclimate conditions. We found that biotic factors of pathogen load and tree diversity had relatively stronger effects on pathogen spillover compared to abiotic microclimate factors, with pathogen load increasing oak infection and tree diversity reducing oak infection. Abiotic factors still had significant effects, with greater heat exposure during summer months reducing pathogen loads and optimal pathogen conditions during the wet season increasing oak infection. Our results offer clues to possible disease dynamics under future climate change where hotter and drier or warmer and wetter conditions could have opposing effects on pathogen spillover in theSOD system. Disentangling direct and indirect effects of biotic and abiotic factors affecting disease processes can provide key insights into disease dynamics including potential avenues for reducing disease spread and predicting future epidemics.
- Free Publicly Accessible Full Text
-
Accepted Manuscript1.0
- Journal Article:
- The DOI is not currently available.
