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At least 469 records · Page 26Linked to original sources

Detection, quantitation and identification of enteroviruses from surface waters and sponge tissue from the Florida Keys using real-time RT-PCR

A method was developed for the quantitative detection of pathogenic human enteroviruses from surface waters in the Florida Keys using Taqman (R) one-step Reverse transcription (RT)-PCR with the Model 7700 ABI Prism (R) Sequence Detection System. Viruses were directly extracted from unconcentrated grab samples of seawater, from seawater concentrated by vortex flow filtration using a 100kD filter and from sponge tissue. Total RNA was extracted from the samples, purified and concentrated using spin-column chromatography. A 192-196 base pair portion of the 5??? untranscribed region was amplified from these extracts. Enterovirus concentrations were estimated using real-time RT-PCR technology. Nine of 15 sample sites or 60% were positive for the presence of pathogenic human enteroviruses. Considering only near-shore sites, 69% were positive with viral concentrations ranging from 9.3viruses/ml to 83viruses/g of sponge tissue (uncorrected for extraction efficiency). Certain amplicons were selected for cloning and sequencing for identification. Three strains of waterborne enteroviruses were identified as Coxsackievirus A9, Coxsackievirus A16, and Poliovirus Sabin type 1. Time and cost efficiency of this one-step real-time RT-PCR methodology makes this an ideal technique to detect, quantitate and identify pathogenic enteroviruses in recreational waters. Copyright ?? 2002 Elsevier Science Ltd.

Water Research↗

Robotic environmental DNA bio-surveillance of freshwater health

Autonomous water sampling technologies may help to overcome the human resource challenges of monitoring biological threats to rivers over long time periods and large geographic areas. The Monterey Bay Aquarium Research Institute has pioneered a robotic Environmental Sample Processor (ESP) that overcomes some of the constraints associated with traditional sampling since it can automate water sample filtration and preservation of the captured material or homogenize it for immediate analyses in situ. The ESP was originally developed for marine environment applications. Here we evaluated whether the ESP can provide reliable, timely information on environmental (e)DNA detections of human and fish pathogens and introduced fishes at U.S. Geological Survey streamgage sites in freshwater rivers. We compared eDNA collected via ESP at high frequency (e.g., every 3 h) with manual eDNA collections collected at lower frequency (e.g., weekly). We found that water samples filtered and preserved by ESPs successfully detected the DNA of human pathogens, fish pathogens and introduced fishes. Both ESP and manually collected samples provided similar information about target DNA presence. We suggest that the greatest current benefit of the ESP is the cost savings of high frequency, bio-surveillance at remote or hard to access sites. The full potential of robotic technologies like the ESP will be realized when they can more easily execute in situ analyses of water samples and rapidly transmit results to decision-makers.

Idaho, Montana, Wyoming↗

Experimental inoculation trial to determine the effects of temperature and humidity on White-nose Syndrome in hibernating bats

Disease results from interactions among the host, pathogen, and environment. Inoculation trials can quantify interactions among these players and explain aspects of disease ecology to inform management in variable and dynamic natural environments. White-nose Syndrome, a disease caused by the fungal pathogen, Pseudogymnoascus destructans ( Pd ), has caused severe population declines of several bat species in North America. We conducted the first experimental infection trial on the tri-colored bat, Perimyotis subflavus , to test the effect of temperature and humidity on disease severity. We also tested the effects of temperature and humidity on fungal growth and persistence on substrates. Unexpectedly, only 37% (35/95) of bats experimentally inoculated with Pd at the start of the experiment showed any infection response or disease symptoms after 83 days of captive hibernation. There was no evidence that temperature or humidity influenced infection response. Temperature had a strong effect on fungal growth on media plates, but the influence of humidity was more variable and uncertain. Designing laboratory studies to maximize research outcomes would be beneficial given the high costs of such efforts and potential for unexpected outcomes. Understanding the influence of microclimates on host–pathogen interactions remains an important consideration for managing wildlife diseases, particularly in variable environments.

Scientific Reports↗

Host and viral ecology determine bat rabies seasonality and maintenance

Rabies is an acute viral infection that is typically fatal. Most rabies modeling has focused on disease dynamics and control within terrestrial mammals (e.g., raccoons and foxes). As such, rabies in bats has been largely neglected until recently. Because bats have been implicated as natural reservoirs for several emerging zoonotic viruses, including SARS-like corona viruses, henipaviruses, and lyssaviruses, understanding how pathogens are maintained within a population becomes vital. Unfortunately, little is known about maintenance mechanisms for any pathogen in bat populations. We present a mathematical model parameterized with unique data from an extensive study of rabies in a Colorado population of big brown bats (Eptesicus fuscus) to elucidate general maintenance mechanisms. We propose that life history patterns of many species of temperate-zone bats, coupled with sufficiently long incubation periods, allows for rabies virus maintenance. Seasonal variability in bat mortality rates, specifically low mortality during hibernation, allows long-term bat population viability. Within viable bat populations, sufficiently long incubation periods allow enough infected individuals to enter hibernation and survive until the following year, and hence avoid an epizootic fadeout of rabies virus. We hypothesize that the slowing effects of hibernation on metabolic and viral activity maintains infected individuals and their pathogens until susceptibles from the annual birth pulse become infected and continue the cycle. This research provides a context to explore similar host ecology and viral dynamics that may explain seasonal patterns and maintenance of other bat-borne diseases.

Proceedings of the National Academy of Sciences of↗

Genesis and spread of multiple reassortants during the 2016/2017 H5 avian influenza epidemic in Eurasia

Highly pathogenic avian influenza (HPAI) viruses of the H5 A/goose/Guangdong/1/96 lineage can cause severe disease in poultry and wild birds, and occasionally in humans. In recent years, H5 HPAI viruses of this lineage infecting poultry in Asia have spilled over into wild birds and spread via bird migration to countries in Europe, Africa, and North America. In 2016/2017, this spillover resulted in the largest HPAI epidemic on record in Europe and was associated with an unusually high frequency of reassortments between H5 HPAI viruses and cocirculating low-pathogenic avian influenza viruses. Here, we show that the seven main H5 reassortant viruses had various combinations of gene segments 1, 2, 3, 5, and 6. Using detailed time-resolved phylogenetic analysis, most of these gene segments likely originated from wild birds and at dates and locations that corresponded to their hosts’ migratory cycles. However, some gene segments in two reassortant viruses likely originated from domestic anseriforms, either in spring 2016 in east China or in autumn 2016 in central Europe. Our results demonstrate that, in addition to domestic anseriforms in Asia, both migratory wild birds and domestic anseriforms in Europe are relevant sources of gene segments for recent reassortant H5 HPAI viruses. The ease with which these H5 HPAI viruses reassort, in combination with repeated spillovers of H5 HPAI viruses into wild birds, increases the risk of emergence of a reassortant virus that persists in wild bird populations yet remains highly pathogenic for poultry.

PNAS↗

Phylogenetic escape from pests reduces pesticides on some crop plants

Pesticides are a ubiquitous component of conventional crop production but come with considerable economic and ecological costs. We tested the hypothesis that variation in pesticide use among crop species is a function of crop economics and the phylogenetic relationship of a crop to native plants because unrelated crops accrue fewer herbivores and pathogens. Comparative analyses of a dataset of 93 Californian crops showed that more valuable crops and crops with close relatives in the native plant flora received greater pesticide use, explaining roughly half of the variance in pesticide use among crops against pathogens and herbivores. Phylogenetic escape from arthropod and pathogen pests results in lower pesticides, suggesting that the introduced status of some crops can be leveraged to reduce pesticides.

Proceedings of the National Academy of Sciences↗

Identifying common decision problem elements for the management of emerging fungal diseases of wildlife

Emerging infectious diseases (EIDs) of wildlife have characteristics that make them difficult to manage, leading to reactive and often ineffective management strategies. Currently, two fungal pathogens, Pseudogymnoascus destructans (Pd) and Batrachochytrium salamandrivorans (Bsal), are causing declines in novel host species. To improve the application of management strategies addressing the risk of these pathogens to North American wildlife, we queried wildlife managers about their concerns regarding managing populations of bats and amphibians potentially impacted by Pd and Bsal. Using these responses, we identified aspects of each decision problem that were shared across pathogens, regions and agencies – and found similarities in decision-problem elements for disease management. Reframing management problems as decisions can enable managers to identify similarities across EIDs, i.e. uncertainties within management actions, and improve reactive responses if proactive management is not possible. Such an approach recognizes context-specific constraints and identifies relevant uncertainties that must be reduced in developing a response.

Society and Natural Resources↗

Sustaining transmission in different host species: The emblematic case of Sarcoptes scabiei

Some pathogens sustain transmission in multiple different host species, but how this epidemiologically important feat is achieved remains enigmatic. Sarcoptes scabiei is among the most host generalist and successful of mammalian parasites. We synthesize pathogen and host traits that mediate sustained transmission and present cases illustrating three transmission mechanisms (direct, indirect, and combined). The pathogen traits that explain the success of S. scabiei include immune response modulation, on-host movement capacity, off-host seeking behaviors, and environmental persistence. Sociality and host density appear to be key for hosts in which direct transmission dominates, whereas in solitary hosts, the use of shared environments is important for indirect transmission. In social den-using species, combined direct and indirect transmission appears likely. Empirical research rarely considers the mechanisms enabling S. scabiei to become endemic in host species—more often focusing on outbreaks. Our review may illuminate parasites’ adaptation strategies to sustain transmission through varied mechanisms across host species.

BioScience↗

Avian-associated Aspergillus fumigatus displays broad phylogenetic distribution, no evidence for host specificity, and multiple genotypes within epizootic events

Birds are highly susceptible to aspergillosis, which can manifest as a primary infection in both domestic and wild birds. Aspergillosis in wild birds causes mortalities ranging in scale from single animals to large-scale epizootic events. However, pathogenicity factors associated with aspergillosis in wild birds have not been examined. Specifically, it is unknown whether wild bird-infecting strains are host-adapted (i.e. phylogenetically related). Similarly, it is unknown whether epizootics are driven by contact with clonal strains that possess unique pathogenic or virulence properties, or by distinct and equally pathogenic strains. Here, we use a diverse collection of Aspergillus fumigatus isolates taken from aspergillosis-associated avian carcasses, representing 24 bird species from a wide geographic range, and representing individual bird mortalities as well as epizootic events. These isolates were sequenced and analyzed along with 130 phylogenetically diverse human clinical isolates to investigate the genetic diversity and phylogenetic placement of avian-associated A. fumigatus , the geographic and host distribution of avian isolates, evidence for clonal outbreaks among wild birds, and the frequency of azole resistance in avian isolates. We found that avian isolates were phylogenetically diverse, with no clear distinction from human clinical isolates, and no sign of host or geographic specificity. Avian isolates from the same epizootic events were diverse and phylogenetically distant, suggesting that avian aspergillosis is not contagious among wild birds and that outbreaks are likely driven by environmental spore loads or host comorbidities. Finally, all avian isolates were susceptible to Voriconazole and none contained the canonical azole resistance gene variants.

G3 Genes|Genomes|Genetics↗

Preliminary survey for entomopathogenic fungi associated with Ixodes scapularis (Acari: Ixodidae) in southern New York and New England, USA

Free-living larval, nymphal, and adult Ixodes scapularis Say were collected from scattered locales in southern New England and New York to determine infection rates with entomopathogenic fungi. Infection rates of larvae, nymphs, males, and females were 0% (571), 0% (272), 0% (57), and 4.3% (47), respectively. Two entomopathogenic fungi were isolated from field-collected I. scapularis females from Fire Island, NY. Isolates were identified as Verticillium lecanii (Zimmermann) Viegas and Verticillium sp. (a member of the Verticillium lecanii species complex). Ixodes scapularis Say is the principal vector of Borrelia burgdorferi Johnson, Schmid, Hyde, Steigerwalt & Brenner ( Burgdorfer et al. 1982 , Johnson et al. 1984 ), the etiologic agent of Lyme disease in the northeastern and upper-midwestern United States. Control of I. scapularis is based on chemical treatment ( Mather et al. 1987b ; Schulze et al. 1987 , 1991 ), environmental management ( Wilson et al. 1988 , Schulze et al. 1995 ), and habitat modification ( Wilson 1986 ). These methods have shown variable success, and some potentially have negative environmental effects ( Wilson and Deblinger 1993 , Ginsberg 1994 ). Studies concerning natural predators, parasitoids, and pathogens of I. scapularis are rare. The use of ground-dwelling birds as tick predators has had only limited success ( Duffy et al. 1992 ). Nymphal I. scapularis are often infected with the parasitic wasp Ixodiphagus hookeri (Howard) ( Mather et al. 1987a , Hu et al. 1993 , Stafford et al. 1996 , Hu and Hyland 1997 ), but this wasp does not effectively control I. scapularis populations ( Stafford et al. 1996 ). The entomopathogenic nematodes Steinernema carpocapsae (Weiser) and S. glaseri (Steiner) are pathogenic only to engorged female I. scapularis, and thus have limited applicability ( Zhioua et al. 1995 ). In contrast, the entomogenous fungus Metarhizium anisopliae (Metschnikoff) Sorokin is highly pathogenic to all stages of I. scapularis, unfed as well as engorged, and thus has considerable potential as a microbial control agent ( Zhioua et al. 1997 ). European studies have suggested that entomopathogenic fungi might serve as natural controls of of Ixodes ricinus L. populations ( Samsinakova et al. 1974 , Eilenberg et al. 1991 , Kalsbeek et al. 1995 ). In the current study, we describe the isolation of entomopathogenic fungi from field-collected I. scapularis.

Journal of Medical Entomology↗

Climate change can drive marine diseases

As an ultimate driver of marine ecosystem processes, climate change is expected to influence proximate disease drivers in marine systems. The observable effects of climate change, including changes in temperature, hypoxia, CO 2 accumulation, precipitation, and storm and cyclone frequencies and intensities, may directly act as proximate drivers of marine disease, especially in poikilotherms. These climate-driven changes are expected to result in the active and passive movement of pathogens and hosts into previously naïve geographical areas, thereby disrupting the long-evolved, stable host–pathogen relationships. Additionally, large-scale ecological changes stemming from climate change are expected to impact pathogen virulence and host susceptibilities. These real and anticipated changes present evolving challenges for resource managers who are charged with managing stochastic marine diseases in a constantly changing environment.

Book chapter↗

Utility of R0 as a predictor of disease invasion in structured populations

Early theoretical work on disease invasion typically assumed large and well-mixed host populations. Many human and wildlife systems, however, have small groups with limited movement among groups. In these situations, the basic reproductive number, R 0 , is likely to be a poor predictor of a disease pandemic because it typically does not account for group structure and movement of individuals among groups. We extend recent work by combining the movement of hosts, transmission within groups, recovery from infection and the recruitment of new susceptibles into a stochastic model of disease in a host metapopulation. We focus on how recruitment of susceptibles affects disease invasion and how population structure can affect the frequency of superspreading events (SSEs). We show that the frequency of SSEs may decrease with the reduced movement and the group sizes due to the limited number of susceptible individuals available. Classification tree analysis of the model results illustrates the hierarchical nature of disease invasion in host metapopulations. First, the pathogen must effectively transmit within a group ( R 0 >1), and then the pathogen must persist within a group long enough to allow for movement among the groups. Therefore, the factors affecting disease persistence—such as infectious period, group size and recruitment of new susceptibles—are as important as the local transmission rates in predicting the spread of pathogens across a metapopulation.

Journal of the Royal Society Interface↗

Host mating system and the prevalence of a disease in a plant population

A modified susceptible–infected–recovered (SIR) host–pathogen model is used to determine the influence of plant mating system on the outcome of a host–pathogen interaction. Unlike previous models describing how interactions between mating system and pathogen infection affect individual fitness, this model considers the potential consequences of varying mating systems on the prevalence of resistance alleles and disease within the population. If a single allele for disease resistance is sufficient to confer complete resistance in an individual and if both homozygote and heterozygote resistant individuals have the same mean birth and death rates, then, for any parameter set, the selfing rate does not affect the proportions of resistant, susceptible or infected individuals at equilibrium. If homozygote and heterozygote individual birth rates differ, however, the mating system can make a difference in these proportions. In that case, depending on other parameters, increased selfing can either increase or decrease the rate of infection in the population. Results from this model also predict higher frequencies of resistance alleles in predominantly selfing compared to predominantly outcrossing populations for most model conditions. In populations that have higher selfing rates, the resistance alleles are concentrated in homozygotes, whereas in more outcrossing populations, there are more resistant heterozygotes.

Proceedings of the Royal Society B↗

Systematic shifts in the variation among host individuals must be considered in climate-disease theory

To make more informed predictions of host–pathogen interactions under climate change, studies have incorporated the thermal performance of host, vector and pathogen traits into disease models to quantify effects on average transmission rates. However, this body of work has omitted the fact that variation in susceptibility among individual hosts affects disease spread and long-term patterns of host population dynamics. Furthermore, and especially for ectothermic host species, variation in susceptibility is likely to be plastic, influenced by variables such as environmental temperature. For example, as host individuals respond idiosyncratically to temperature, this could affect the population-level variation in susceptibility, such that there may be predictable functional relationships between variation in susceptibility and temperature. Quantifying the relationship between temperature and among-host trait variation will therefore be critical for predicting how climate change and disease will interact to influence host–pathogen population dynamics. Here, we use a model to demonstrate how short-term effects of temperature on the distribution of host susceptibility can drive epidemic characteristics, fluctuations in host population sizes and probabilities of host extinction. Our results emphasize that more research is needed in disease ecology and climate biology to understand the mechanisms that shape individual trait variation, not just trait averages.

Proceedings of the Royal Society B: Biological Sci↗

Confronting models with data: The challenges of estimating disease spillover

For pathogens known to transmit across host species, strategic investment in disease control requires knowledge about where and when spillover transmission is likely. One approach to estimating spillover is to directly correlate observed spillover events with covariates. An alternative is to mechanistically combine information on host density, distribution, and pathogen prevalence to predict where and when spillover events are expected to occur. We use several case studies at the wildlife-livestock disease interface to highlight the challenges, and potential solutions, to estimating spatio-temporal variation in spillover risk. Datasets on multiple host species often do not align in space, time or resolution, and may have no estimates of observation error. Linking these datasets requires they be related to a common spatial and temporal resolution and appropriately propagating errors in predictions can be difficult. Hierarchical models are one potential solution, but for fine-resolution predictions at broad spatial scales many models become computationally challenging. Despite these limitations, the confrontation of mechanistic predictions with observed events is an important avenue for developing a better understanding of pathogen spillover. Systems where data have been collected at all levels in the spillover process are rare, or non-existent, and require investment and sustained effort across disciplines.

Philosophical Transactions of the Royal Society B:↗

From understanding to action: Integrating new and old methodologies to manage marine infectious disease

Marine diseases can have far-reaching effects on population, community and ecosystem health; however, our ability to track, predict and manage these diseases has, historically, been poor. As a result, the fields of disease ecology and epidemiology have developed at a slower pace for marine than terrestrial systems [ 1 ]. New methodologies, including genomic tools for diagnostics [ 2 , 3 ], transcriptomic tools for measuring host and pathogen responses to infection (e.g. [ 4 , 5 ]), regional oceanic modelling systems that estimate environmental conditions influencing pathogen dispersal and disease progression [ 6 ], artificial intelligence methods for quantifying pathology from images (e.g. [ 7 ]) and advanced disease modelling techniques [ 8 , 9 ] are precipitating a rapid increase in our understanding of marine pathosystems. In 2016, these efforts led to the first special issue of Philosophical Transactions of the Royal Society B ( Marine diseases, volume 371, issue 1689) focused entirely on marine disease ecology and evolution, and in 2020, the first book, Marine disease ecology, was devoted to this topic [ 10 ]. This special issue, focused on marine disease management , is being published a decade after the first Philosophical Transactions special issue on marine diseases. The shift to a management focus reflects an urgent need for management strategies to address high-impact diseases and the rapid methodological advances that have resulted. The papers included in this issue demonstrate the value of combining classical approaches (e.g. routine disease surveillance, reductionistic pathogen challenge trials, rapid throughput diagnostics) with cutting-edge technologies (e.g. high-resolution oceanographic models, Bayesian models, replicated transcriptomic studies) to identify drivers of disease, quantify impacts and suggest management strategies.

Philosophical Transactions of the Royal Society, S↗

The roles of antimicrobial resistance, phage diversity, isolation source, and selection in shaping the genomic architecture of Bacillus anthracis

Bacillus anthracis, the causative agent of anthrax disease, is a worldwide threat to livestock, wildlife and public health. While analyses of genetic data from across the globe have increased our understanding of this bacterium’s population genomic structure, the influence of selective pressures on this successful pathogen is not well understood. In this study, we investigate the effects of antimicrobial resistance, phage diversity, geography and isolation source in shaping population genomic structure. We also identify a suite of candidate genes potentially under selection, driving patterns of diversity across 356 globally extant B. anthracis genomes. We report ten antimicrobial resistance genes and 11 different prophage sequences, resulting in the first large-scale documentation of these genetic anomalies for this pathogen. Results of random forest classification suggest genomic structure may be driven by a combination of antimicrobial resistance, geography and isolation source, specific to the population cluster examined. We found strong evidence that a recombination event linked to a gene involved in protein synthesis may be responsible for phenotypic differences between comparatively disparate populations. We also offer a list of genes for further examination of B. anthracis evolution, based on high-impact single nucleotide polymorphisms (SNPs) and clustered mutations. The information presented here sheds new light on the factors driving genomic structure in this notorious pathogen and may act as a road map for future studies aimed at understanding functional differences in terms of B. anthracis biogeography, virulence and evolution.

Microbial Genomics↗

Parsing the effects of demography, climate, and management on recurrent brucellosis outbreaks in elk

1. Zoonotic pathogens can harm human health and well-being directly or by impacting livestock. Pathogens that spillover from wildlife can also impair conservation efforts if humans perceive wildlife as pests. Brucellosis, caused by the bacterium Brucella abortus, circulates in elk and bison herds of the Greater Yellowstone Ecosystem and poses a risk to cattle and humans. Our goal was to understand the relative effects of climatic drivers, host demography, and management control programs on disease dynamics. 2. Using >20 years of serologic, demographic, and environmental data on brucellosis in elk, we built stochastic compartmental models to assess the influences of climate forcing, herd immunity, population turnover, and management interventions on pathogen transmission. Data were collected at feedgrounds visited in winter by free-ranging elk in Wyoming, USA. 3. Snowpack, hypothesized as a driver of elk aggregation and thus brucellosis transmission, was strongly correlated across feedgrounds. We expected this variable to drive synchronized disease dynamics across herds. Instead, we demonstrate asynchronous epizootics driven by variation in demographic rates. 4. We evaluated the effectiveness of test-and-slaughter of seropositive female elk at two feedgrounds. Test-and-slaughter temporarily reduced herd-level seroprevalence but likely reduced herd immunity while removing few infectious individuals, resulting in subsequent outbreaks once the intervention ceased. We simulated an alternative strategy of removing seronegative female elk and found it would increase herd immunity, yielding fewer infections. We evaluated a second experimental treatment wherein feeding density was reduced at one feedground, but we found no evidence for an effect despite a decade of implementation. 5. Synthesis and applications: Positive serostatus is often weakly correlated with infectiousness but is nevertheless used to make management decisions including lethal removal in wildlife disease systems. We show how this can have adverse consequences whereas efforts that maintain herd immunity can have longer-term protective effects. Climatic drivers may not result in synchronous disease dynamics across populations unless vital rates are also similar because demographic factors have a large influence on disease patterns.

Idaho, Montana, Wyoming↗