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Results for “Virulence”

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At least 127 records · Page 7Linked to original sources

USGS2002

Dieback of Acacia koa in Hawaii: Ecological and pathological characteristics of affected stands

Koa (Acacia koa) is an endemic Hawaiian tree that serves as a keystone species in the upper elevation forests of all the main islands. In the Mauna Loa Strip area of Hawaii Volcanoes National Park, mature koa stands are suffering from an unexplained dieback that has increased in severity since it was first noticed approximately 25 years ago. The dieback is often evident in patches, and generally spreads within stands in a radial fashion from a localized infection center. Entire crowns of affected trees become wilted, with foliage gradually progressing from an apparent healthy to a completely chlorotic condition. Although most trees die soon after the onset of symptoms, some trees are able to survive crown death by producing epicormic shoots on the lower portions of the trunk. Previously published studies reported that a vascular wilt fungus (Fusarium oxysporum f. sp. koae) was associated with koa seeds and the rhizosphere of healthy and dieback-affected koa stands. The purpose of this study was to characterize the stand structure, soil conditions, and physiological condition of dieback-affected trees, and to assess the possible role of F. oxysporum f. sp. koae in the current dieback stands. This fungus was isolated from branches of symptomatic koa in dieback-affected stands and roots from healthy and dieback-affected stands. Possible differences in the pathogenicity and virulence of F. oxysporum f. sp. koae isolates obtained from the roots of healthy koa in unaffected stands and those from branches of dieback-affected koa were determined by greenhouse inoculations of koa seedlings. Healthy koa saplings in stands unaffected by dieback were also inoculated to determine if disease symptoms could be induced by inoculation of injured roots in the field. Both branch and root isolates were pathogenic; with the percent mortality of inoculated seedlings ranging from 30 to 60% for all isolates. Disease severity between branch and root isolates was not significantly different. Wilt symptoms were not observed in field inoculations of koa saplings after 8 months. Investigation of the dieback stand structure determined that the larger size classes (i.e., DBH > 3 cm) were all affected equally, with the smallest size class (i.e., 0-3 cm DBH) having the lowest percentage of dieback at each site. Soil from dieback stands had higher water content and was more acidic than that from neighboring unaffected stands. Phyllodes on epicormic shoots of dieback trees had a reduced area, mass, and mass to area ratio. Phyllodes on dieback trees also had reduced stomatal conductance and higher (less negative) leaf water potential. Results from the greenhouse inoculations demonstrated that F. oxysporum f. sp. koae is pathogenic to koa, but the pathogen's activity in the field may be influenced by predisposing factors such as temperature fluctuations, water availability, soil type, and interactions with other soil organisms. F. oxysporum f. sp. koae appears to play an important role in regulating koa stand dynamics, growth, and physiology under environmental and edaphic conditions favorable for disease development. ?? 2002 Elsevier Science B.V. All rights reserved.

Forest Ecology and Management↗

USGS2006

Modeling the transport and inactivation of E. coli and enterococci in the near-shore region of Lake Michigan

To investigate the transport and fate of fecal pollution at Great Lakes beaches and the health risks associated with swimming, the near-shore waters of Lake Michigan and two tributaries discharging into it were examined for bacterial indicators of human fecal pollution. The enterococcus human fecal pollution marker, which targets a putative virulence factor the enterococcal surface protein (esp) in Enterococcus faecium , was detected in 2/28 samples (7%) in the tributaries draining into Lake Michigan and in 6/30 samples (20%) in Lake Michigan beaches. This was indicative of human fecal pollution being transported in the tributaries and occurrence at Lake Michigan beaches. To understand the relative importance of different processes influencing pollution transport and inactivation, a finite-element model of surf-zone hydrodynamics (coupled with models for temperature, E. coli and enterococci) was used. Enterococci appear to survive longer than E. coli , which was described using an overall first-order inactivation coefficient in the range 0.5−2.0 per day. Our analysis suggests that the majority of fecal indicator bacteria variation can be explained based on loadings from the tributaries. Sunlight is a major contributor to inactivation in the surf-zone and the formulation based on sunlight, temperature and sedimentation is preferred over the first-order inactivation formulation.

Environmental Science & Technology↗

USGS2001

How are climate and marine biological outbreaks functionally linked?

Since the mid-1970s, large-scale episodic events such as disease epidemics, mass mortalities, harmful algal blooms and other population explosions have been occurring in marine environments at an historically unprecedented rate. The variety of organisms involved (host, pathogens and other opportunists) and the absolute number of episodes have also increased during this period. Are these changes coincidental? Between 1972 and 1976, a global climate regime shift took place, and it is manifest most clearly by a change in strength of the North Pacific and North Atlantic pressure systems. Consequences of this regime shift are: (1) prolonged drought conditions in the Sahel region of Africa; (2) increased dust supply to the global atmosphere, by a factor of approximately four; (3) increased easterly trade winds across the Atlantic; (4) increased eolian transport of dust to the Atlantic and Caribbean basins; and (5) increased deposition of iron-rich eolian dust to typically iron-poor marine regions. On the basis of well-documented climate and dust observations and the widely accepted increase in marine outbreak rates, this paper proposes that the increased iron supply has altered the micronutrient factors limiting growth of opportunistic organisms and virulence of pathogenic microbes, particularly in macronutrient-rich coastal systems.

Hydrobiologia↗

USGS2017

Pathogenic lineage of Perkinsea associated with mass mortality of frogs across the United States

Emerging infectious diseases such as chytridiomycosis and ranavirus infections are important contributors to the worldwide decline of amphibian populations. We reviewed data on 247 anuran mortality events in 43 States of the United States from 1999–2015. Our findings suggest that a severe infectious disease of tadpoles caused by a protist belonging to the phylum Perkinsea might represent the third most common infectious disease of anurans after ranavirus infections and chytridiomycosis. Severe Perkinsea infections (SPI) were systemic and led to multiorganic failure and death. The SPI mortality events affected numerous anuran species and occurred over a broad geographic area, from boreal to subtropical habitats. Livers from all PCR-tested SPI-tadpoles (n = 19) were positive for the Novel Alveolate Group 01 (NAG01) of Perkinsea, while only 2.5% histologically normal tadpole livers tested positive (2/81), suggesting that subclinical infections are uncommon. Phylogenetic analysis demonstrated that SPI is associated with a phylogenetically distinct clade of NAG01 Perkinsea. These data suggest that this virulent Perkinsea clade is an important pathogen of frogs in the United States. Given its association with mortality events and tendency to be overlooked, the potential role of this emerging pathogen in amphibian declines on a broad geographic scale warrants further investigation.

Scientific Reports↗

USGS2015

Assessing threats from coral and crustose coralline algae disease on the reefs of New Caledonia

The present study reports the results of the first quantitative survey of lesions on coral and crustose coralline algae (CCA) on reefs in the lagoon of New Caledonia. Surveys on inshore and offshore reefs were conducted at 13 sites in 2010, with 12 sites resurveyed in 2013. Thirty coral diseases affecting 15 coral genera were found, with low overall disease prevalence (<1%). This study extends the known distribution of growth anomalies to the coral genera Platygyra and Hydnophora , endolithic hypermycosis to Platygyra , Leptoria and Goniastrea and extends the geographic range of three CCA diseases. We found the first trematode infection in Porites outside of Hawaii. Disease prevalence differed among coral genera, with Porites having more lesions, and Acropora and Montipora fewer lesions, than expected on the basis of field abundance. Inshore reefs had a lower coral-colony density, species diversity and reduced CCA cover than did the offshore reefs. Disease prevalence was significantly higher on inshore reefs in 2013 than in 2010, but did not change on offshore reefs. The potential ecological impact of individual coral diseases was assessed using an integrative-scoring and relative-ranking scheme based on average frequency of occurrence, prevalence and estimated degree of virulence. The top-five ranked diseases were all tissue-loss diseases.

Marine and Freshwater Research↗

USGS2010

Consumption of baits containing raccoon pox-based plague vaccines protects black-tailed prairie dogs (Cynomys ludovicianus)

Baits containing recombinant raccoon poxvirus (RCN) expressing plague antigens (fraction 1 [F1] and a truncated form of the V protein-V307) were offered for voluntary consumption several times over the course of several months to a group of 16 black-tailed prairie dogs ( Cynomys ludovicianus ). For comparison, another group of prairie dogs ( n = 12) was injected subcutaneously (SC) (prime and boost) with 40 μg of F1-V fusion protein absorbed to alum, a vaccine-adjuvant combination demonstrated to elicit immunity to plague in mice and other mammals. Control animals received baits containing RCN without the inserted antigen ( n = 8) or injected diluent ( n = 7), and as there was no difference in their survival rates by Kaplan–Meier analysis, all of them were combined into one group in the final analysis. Mean antibody titers to Yersinia pestis F1 and V antigen increased ( p < 0.05) in the vaccinated groups compared to controls, but titers were significantly higher ( p < 0.0001) in those receiving injections of F1-V fusion protein than in those orally vaccinated with RCN-based vaccine. Interestingly, upon challenge with approximately 70,000 cfu of virulent Y. pestis , oral vaccination resulted in survival rates that were significantly higher ( p = 0.025) than the group vaccinated by injection with F1-V fusion protein and substantially higher ( p < 0.0001) than the control group. These results demonstrate that oral vaccination of prairie dogs using RCN-based plague vaccines provides significant protection against challenge at dosages that simulate simultaneous delivery of the plague bacterium by numerous flea bites.

Vector-Borne and Zoonotic Diseases↗

USGS2022

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↗

USGS2012

Variation in clinical phenotype of human infection among genetic groups of Blastomyces dermatitidis

Background. Blastomyces dermatitidis, the etiologic agent of blastomycosis, has 2 genetic groups and shows varied clinical presentation, ranging from silent infections to fulminant respiratory disease and dissemination. The objective of this study was to determine whether clinical phenotype and outcomes vary based on the infecting organism's genetic group. Methods. We used microsatellites to genotype 227 clinical isolates of B. dermatitidis from Wisconsin patients. For each isolate, corresponding clinical disease characteristics and patient demographic information were abstracted from electronic health records and Wisconsin Division of Health reportable disease forms and questionnaires. Results. In univariate analysis, group 1 isolates were more likely to be associated with pulmonary-only infections ( P < .0001) and constitutional symptoms such as fever ( P < .0001). In contrast, group 2 isolates were more likely to be associated with disseminated disease ( P < .0001), older patient age ( P < .0001), and comorbidities ( P = .0019). In multivariate analysis, disease onset to diagnosis of >1 month ( P < .0001), older age at diagnosis ( P < .0001), and current smoking status ( P = .0001) remained predictors for group 2 infections. Conclusions. This study identified previously unknown associations between clinical phenotype of human infection and genetic groups of B. dermatitidis and provides a framework for further investigations of the genetic basis for virulence in B. dermatitidis .

Journal of Infectious Diseases↗

USGS2025

Identical sequence types of Yersinia ruckeri associated with lethal disease in wild-caught invasive Blue Catfish and cultured hybrid catfish (Channel Catfish ♀ × Blue Catfish ♂) from disparate aquatic ecosystems

Objective The Blue Catfish Ictalurus furcatus is commonly raised in warmwater aquaculture in the United States to produce Channel Catfish I. punctatus × Blue Catfish hybrids. It is also a prominent aquatic invasive species of concern in the mid-Atlantic region of the United States. Here, Yersina ruckeri was isolated from moribund Blue Catfish and hybrid catfish from disparate regions of the USA. The goal of the research here was to compare these Y. ruckeri strains to each other and other known strains for which adequate sequence data was available. In addition, we sought to determine if the strain from Blue Catfish was pathogenic to Rainbow Trout Oncorhynchus mykiss . Methods Moribund hybrid catfish from culture ponds in Mississippi were processed for diagnostic evaluation in March 2016. In April 2022, a moribund Blue Catfish specimen was collected from a tributary of the Nanticoke River in Maryland. Bacterial isolates were identified and characterized using biochemical tests, antimicrobial sensitivity screening, serotyping, and complete or partial genome sequencing. Disease pathology was described via histology. The isolate from Blue Catfish was used in challenge experiments to determine if it was pathogenic to Rainbow Trout. Multilocus sequencing typing was conducted using the PubMLST database. Results Biochemical testing was consistent with Y. ruckeri . A draft genome of the Y. ruckeri isolate was assembled based on Oxford Nanopore Technology sequencing and identified a single genomic replicon (3,791,418 bp) consistent in size to other Y. ruckeri genomes and a pLT plasmid (60, 933 bp). The challenge study demonstrated no significant virulence of this isolate for Rainbow Trout ( Y. ruckeri ). This isolate was most similar to other strains isolated from ictalurids. Notably, the gyrase B gene from this isolate was identical to that of archived strains isolated from moribund Mississippi hybrid catfish aquaculture during 2016 and these isolates share identical PubMLST sequence type profiles. Similarly, they shared a pLT plasmid that differed by only 6 bp. This plasmid has never been reported from trout isolates and appears to be unique to ictalurids. Conclusions Analyses here provide preliminary genetic evidence that geographically distant (Maryland and Mississippi, USA) isolates of Y. ruckeri from ictalurids are genetically similar to each other and Y. ruckeri (strain SC09) that infects ictalurids in China. This strain is not a biothreat to Rainbow Trout at typical culture temperatures.

Journal of Aquatic Animal Health↗

USGS2021

Insect pathogenic fungi for biocontrol of plague vector fleas: A review

Bubonic plague is a lethal bacterial disease of great historical importance. The plague organism, Yersinia pestis , is primarily transmitted by fleas (Siphonaptera). In natural settings, where its range expands, Y. pestis resides in association with wild rodents and their fleas (sylvatic plague). While chemical insecticides are used against plague vector fleas, biological approaches have not been as critically evaluated. Benign and cost-effective control methods are sorely needed, particularly where imperiled species are at risk. Here we explore the potential of two representative insect pathogenic fungi, Beauveria bassiana Vuillemin 1912 (Hypocreales: Cordycipitaceae) and Metarhizium anisopliae Metschnikoff 1879 (Hypocreales: Clavicipitaceae), each already used commercially worldwide in large-scale agricultural applications, as candidate biopesticides for application against fleas. We review the life cycles, flea virulence, commercial production, and field application of these fungi, and ecological and safety considerations. Pathogenic fungi infections among natural flea populations suggest that conditions within at least some rodent burrows are favorable, and laboratory studies demonstrate lethality of these fungi to at least some representative flea species. Continued study and advancements with these fungi, under appropriate safety measures, may allow for effective biocontrol of plague vector fleas to protect imperiled species, decrease plague outbreaks in key rodent species, and limit plague in humans.

Journal of Integrated Pest Management↗

USGS2020

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↗

USGS2022

Variation in within-host replication kinetics among virus genotypes provides evidence of specialist and generalist infection strategies across three salmonid host species

Theory of the evolution of pathogen specialization suggests that a specialist pathogen gains high fitness in one host, but this comes with fitness loss in other hosts. By contrast, a generalist pathogen does not achieve high fitness in any host, but gains ecological fitness by exploiting different hosts, and has higher fitness than specialists in nonspecialized hosts. As a result, specialist pathogens are predicted to have greater variation in fitness across hosts, and generalists would have lower fitness variation across hosts. We test these hypotheses by measuring pathogen replicative fitness as within-host viral loads from the onset of infection to the beginning of virus clearance, using the rhabdovirus infectious hematopoietic necrosis virus (IHNV) in salmonid fish. Based on field prevalence and virulence studies, the IHNV subgroups UP, MD, and L are specialists, causing infection and mortality in sockeye salmon, steelhead, and Chinook salmon juveniles, respectively. The UC subgroup evolved naturally from a UP ancestor and is a generalist infecting all three host species but without causing severe disease. We show that the specialist subgroups had the highest peak and mean viral loads in the hosts in which they are specialized, and they had low viral loads in nonspecialized hosts, resulting in large variation in viral load across hosts. Viral kinetics show that the mechanisms of specialization involve the ability to both maximize early virus replication and avoid clearance at later times, with different mechanisms of specialization evident in different host–virus combinations. Additional nuances in the data included different fitness levels for nonspecialist interactions, reflecting different trade-offs for specialist viruses in other hosts. The generalist UC subgroup reached intermediate viral loads in all hosts and showed the smallest variation in fitness across hosts. The evolution of the UC generalist from an ancestral UP sockeye specialist was associated with fitness increases in steelhead and Chinook salmon, but only slight decreases in fitness in sockeye salmon, consistent with low- or no-cost generalism. Our results support major elements of the specialist–generalist theory, providing evidence of a specialist–generalist continuum in a vertebrate pathogen. These results also quantify within-host replicative fitness trade-offs resulting from the natural evolution of specialist and generalist virus lineages in multi-host ecosystems

Virus Evolution↗

USGS2024

A meta-analysis highlights the idiosyncratic nature of tradeoffs in laboratory models of virus evolution

Different theoretical frameworks have been invoked to guide the study of virus evolution. Three of the more prominent ones are (i) the evolution of virulence, (ii) life history theory, and (iii) the generalism–specialism dichotomy. All involve purported tradeoffs between traits that define the evolvability and constraint of virus-associated phenotypes. However, as popular as these frameworks are, there is a surprising paucity of direct laboratory tests of the frameworks that support their utility as broadly applicable theoretical pillars that can guide our understanding of disease evolution. In this study, we conduct a meta-analysis of direct experimental evidence for these three frameworks across several widely studied virus–host systems: plant viruses, fungal viruses, animal viruses, and bacteriophages. We extracted 60 datasets from 28 studies and found a range of relationships between traits in different analysis categories (e.g., frameworks, virus–host systems). Our work demonstrates that direct evidence for relationships between traits is highly idiosyncratic and specific to the host–virus system and theoretical framework. Consequently, scientists researching viral pathogens from different taxonomic groups might reconsider their allegiance to these canons as the basis for expectation, explanation, or prediction. Future efforts could benefit from consistent definitions, and from developing frameworks that are compatible with the evidence and apply to particular biological and ecological contexts.

Virus Evolution↗

USGS2025

Identification of novel hepaciviruses and Sylvilagus-associated viruses via metatranscriptomics in North American lagomorphs

Cottontails ( Sylvilagus spp.) and jackrabbits ( Lepus spp.) within the Leporidae family are native to North America and are found in a wide range of habitats, including deserts, forests, and grasslands. Although there is a growing body of research describing the arrival of the highly virulent rabbit haemorrhagic disease virus 2 (RHDV2, GI.2) on this continent, and its impact on native lagomorphs, information about the natural virome and microbiome of healthy and deceased American lagomorphs is relatively limited. In this study, we used a meta-transcriptomics approach to conduct whole pathogen profiling on healthy and deceased animals in the USA. We analysed 48 matched liver and lung sample pools from apparently healthy cottontails and jackrabbits in Texas and an additional 48 liver samples from deceased animals from nine other US states. This approach enabled the discovery of three distinct new viruses and revealed additional new insights into the lung and liver microbiomes of North American lagomorphs. Of the three new viruses, a tetnovirus and a novel picorna-like virus were likely of insect origin and therefore considered environmental contaminants. Of particular interest was a new species of hepacivirus, with around 50% sequence identity to a known hepacivirus from a xeric four-striped grass rat ( Rhabdomys pumilio ). Phylogenetic analysis from 41 individual hepacivirus genomes recovered from our lagomorph samples revealed two distinct clades, corresponding with different cottontail species. No hepaciviruses were detected in any of the jackrabbit samples. This is the first description of a hepacivirus in lagomorphs. Our findings extend the Hepacivirus genus, provide new insights into its evolution, and describe the first baseline on microbial diversity in North American lagomorphs, an important step towards understanding the role of potential pathogens for population management and conservation.

Arizona, California, Iowa, Massachusetts, Montana,↗

USGS2016

When environmentally persistent pathogens transform good habitat into ecological traps

Habitat quality plays an important role in the dynamics and stability of wildlife metapopulations. However, the benefits of high-quality habitat may be modulated by the presence of an environmentally persistent pathogen. In some cases, the presence of environmental pathogen reservoirs on high-quality habitat may lead to the creation of ecological traps, wherein host individuals preferentially colonize high-quality habitat, but are then exposed to increased infection risk and disease-induced mortality. We explored this possibility through the development of a stochastic patch occupancy model, where we varied the pathogen’s virulence, transmission rate and environmental persistence as well as the distribution of habitat quality in the host metapopulation. This model suggests that for pathogens with intermediate levels of spread, high-quality habitat can serve as an ecological trap, and can be detrimental to host persistence relative to low-quality habitat. This inversion of the relative roles of high- and low-quality habitat highlights the importance of considering the interaction between spatial structure and pathogen transmission when managing wildlife populations exposed to an environmentally persistent pathogen.

Royal Society Open Science↗

USGS2024

Season of death, pathogen persistence and wildlife behaviour alter number of anthrax secondary infections from environmental reservoirs

An important part of infectious disease management is predicting factors that influence disease outbreaks, such as R , the number of secondary infections arising from an infected individual. Estimating R is particularly challenging for environmentally transmitted pathogens given time lags between cases and subsequent infections. Here, we calculated R for Bacillus anthracis infections arising from anthrax carcass sites in Etosha National Park, Namibia. Combining host behavioural data, pathogen concentrations and simulation models, we show that R is spatially and temporally variable, driven by spore concentrations at death, host visitation rates and early preference for foraging at infectious sites. While spores were detected up to a decade after death, most secondary infections occurred within 2 years. Transmission simulations under scenarios combining site infectiousness and host exposure risk under different environmental conditions led to dramatically different outbreak dynamics, from pathogen extinction ( R < 1) to explosive outbreaks ( R > 10). These transmission heterogeneities may explain variation in anthrax outbreak dynamics observed globally, and more generally, the critical importance of environmental variation underlying host–pathogen interactions. Notably, our approach allowed us to estimate the lethal dose of a highly virulent pathogen non-invasively from observational studies and epidemiological data, useful when experiments on wildlife are undesirable or impractical.

Etosha National Park↗

USGS2021

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↗

USGS2014

Global phylogeography of the avian malaria pathogen Plasmodium relictum based on MSP1 allelic diversity

Knowing the genetic variation that occurs in pathogen populations and how it is distributed across geographical areas is essential to understand parasite epidemiology, local patterns of virulence, and evolution of host-resistance. In addition, it is important to identify populations of pathogens that are evolutionarily independent and thus ‘free’ to adapt to hosts and environments. Here, we investigated genetic variation in the globally distributed, highly invasive avian malaria parasite Plasmodium relictum , which has several distinctive mitochondrial haplotyps (cyt b lineages, SGS1, GRW11 and GRW4). The phylogeography of P. relictum was accessed using the highly variable nuclear gene merozoite surface protein 1 (MSP1), a gene linked to the invasion biology of the parasite. We show that the lineage GRW4 is evolutionarily independent of GRW11 and SGS1 whereas GRW11 and SGS1 share MSP1 alleles and thus suggesting the presence of two distinct species (GRW4 versus SGS1 and GRW11). Further, there were significant differences in the global distribution of MSP1 alleles with differences between GRW4 alleles in the New and the Old World. For SGS1, a lineage formerly believed to have both tropical and temperate transmission, there were clear differences in MSP1 alleles transmitted in tropical Africa compared to the temperate regions of Europe and Asia. Further, we highlight the occurrence of multiple MSP1 alleles in GRW4 isolates from the Hawaiian Islands, where the parasite has contributed to declines and extinctions of endemic forest birds since it was introduced. This study stresses the importance of multiple independent loci for understanding patterns of transmission and evolutionary independence across avian malaria parasites.

Ecography↗