scholarly journals Continuous Genomic Surveillance Monitored the In Vivo Evolutionary Trajectories of Vibrio parahaemolyticus and Identified a New Virulent Genotype

mSystems ◽  
2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Songzhe Fu ◽  
Qian Yang ◽  
Qingyao Wang ◽  
Bo Pang ◽  
Ruiting Lan ◽  
...  
Keyword(s):  
Horizontal Transfer ◽  
Vibrio Parahaemolyticus ◽  
Insertion Sequence ◽  
Bacterial Pathogen ◽  
Evolutionary Strategies ◽  
Pathogenicity Islands ◽  
Content Type ◽  
Evolutionary Trajectories ◽  
Shrimp Farms

ABSTRACT Our ability to predict evolutionary trajectories of pathogens is one of the promising leverages to fight against the pandemic disease, yet few studies have addressed this question in situ, due to the difficulty in monitoring the milestone evolutionary events for a given pathogen and in understanding the evolutionary strategies. In this study, we monitored the real-time evolution of Vibrio parahaemolyticus in response to successive antibiotic treatment in three shrimp farms in North China from 2011 to 2018 by whole-genome sequencing. Results showed that the stepwise emergence of resistance was associated with the antibiotic usage. Genomic analysis of resistant isolates showed that the acquisition of the resistant mobile genetic elements flanked by an insertion sequence (ISVal1) closely mirrored the antibiotics used in shrimp farms since 2014. Next, we also identified 50 insertion sites of ISVal1 in the chromosome, which facilitated the formation of pathogenicity islands (PAIs) and fitness islands in the following years. Further, horizontal transfers of a virulent trh-nik-ure genomic island (GI) and two GIs improving the fitness have been observed in two farms since 2016. In this case study, we proposed that the insertion sequence triggered four major evolutionary events during the outbreaks of shrimp disease in three farms, including horizontal transfer of transposon (HTT) (stage 1), the formation of resistance islands (stage 2) and the PAIs (stage 3), and horizontal transfer of the PAIs (stage 4). This study presented the first in vivo evolutionary trajectories for a given bacterial pathogen, which helps us to understand the emergence mechanisms of new genotypes. IMPORTANCE Most human infectious diseases originate from animals. Thus, how to reduce or prevent pandemic zoonoses before they emerge in people is becoming a critical issue. Continuous genomic surveillance of the evolutionary trajectories of potential human pathogens on farms is a promising strategy to realize early warning. Here, we conducted an 8-year surveillance of Vibrio parahaemolyticus in three shrimp farms. The results showed that the use of antibiotics and horizontal transfer of transposons (HTT) drove the evolution of V. parahaemolyticus, which could be divided into four stages: HTT, formation of resistance islands, formation of pathogenicity islands (PAIs), and horizontal transfer of PAIs. This study presented the first in vivo monitoring of evolutionary trajectories for a given bacterial pathogen, providing valuable information for the prevention of pandemic zoonoses.

scholarly journals Genomic Features of Environmental and Clinical Vibrio parahaemolyticus Isolates Lacking Recognized Virulence Factors Are Dissimilar

2015 ◽  
Vol 82 (4) ◽  
pp. 1102-1113 ◽  
Author(s):  
J. Ronholm ◽  
N. Petronella ◽  
C. Chew Leung ◽  
A. W. Pightling ◽  
S. K. Banerjee
Keyword(s):  
Virulence Factors ◽  
Vibrio Parahaemolyticus ◽  
Bacterial Pathogen ◽  
Enteric Bacteria ◽  
Clinical Isolates ◽  
Type Vi Secretion System ◽  
Genomic Features ◽  
Content Type ◽  
Chemotaxis Proteins

ABSTRACTVibrio parahaemolyticusis a bacterial pathogen that can cause illness after the consumption or handling of contaminated seafood. The primary virulence factors associated withV. parahaemolyticusillness are thermostable direct hemolysin (TDH) and Tdh-related hemolysin (TRH). However, clinical strains lackingtdhandtrhhave recently been isolated, and these clinical isolates are poorly understood. To help understand the emergence of clinicaltdh- andtrh-negative isolates, a genomic approach was used to comprehensively compare 4 clinicaltdh- andtrh-negative isolates with 16 environmentaltdh- andtrh-negative isolates and 34 clinical isolates positive fortdhortrh, or both, with the objective of identifying genomic features that are unique to clinicaltdh- andtrh-negative isolates. The prevalence of pathogenicity islands (PAIs) common to clinical isolates was thoroughly examined in each of the clinicaltdh- andtrh-negative isolates. ThetdhPAI was not present in any clinical or environmentaltdh- andtrh-negative isolates. ThetrhPAI was not present in any environmental isolates; however, in clinicaltdh- andtrh-negative isolate 10-4238, the majority of thetrhPAI including a partialtrh1gene was present, which resulted in reclassification of this isolate as atdh-negative andtrh-positive isolate. In the other clinicaltdh- andtrh-negative isolates, neither thetrhgene nor thetrhPAI was present. We identified 862 genes in clinicaltdh- andtrh-negative isolates but not in environmentaltdh- andtrh-negative isolates. Many of these genes are highly homologous to genes found in common enteric bacteria and included genes encoding a number of chemotaxis proteins and a novel putative type VI secretion system (T6SS) effector and immunity protein (T6SS1). The availability of genome sequences from clinicalV. parahaemolyticustdh- andtrh-negative isolates and the comparative analysis may help provide an understanding of how this pathotype is able to survivein vivoduring clinical illness.

scholarly journals Edwardsiella tarda Ivy, a Lysozyme Inhibitor That Blocks the Lytic Effect of Lysozyme and Facilitates Host Infection in a Manner That Is Dependent on the Conserved Cysteine Residue

2013 ◽  
Vol 81 (10) ◽  
pp. 3527-3533 ◽  
Author(s):  
Chong Wang ◽  
Yong-hua Hu ◽  
Bo-guang Sun ◽  
Jun Li ◽  
Li Sun
Keyword(s):  
Bacterial Pathogen ◽  
Scophthalmus Maximus ◽  
Cysteine Residue ◽  
Edwardsiella Tarda ◽  
Broad Host Range ◽  
Content Type ◽  
Lytic Effect ◽  
Lysozyme Inhibitor

ABSTRACTEdwardsiella tardais a Gram-negative bacterial pathogen with a broad host range that includes fish and humans. In this study, we examined the activity and function of the lysozyme inhibitor Ivy (named IvyEt) identified in the pathogenicE. tardastrain TX01. IvyEtpossesses the Ivy signature motif CKPHDC in the form of82CQPHNC87and contains several highly conserved residues, including a tryptophan (W55). For the purpose of virulence analysis, an isogenic TX01 mutant, TXivy, was created. TXivy bears an in-frame deletion of theivyEtgene. A live infection study in a turbot (Scophthalmus maximus) model showed that, compared to TX01, TXivy exhibited attenuated overall virulence, reduced tissue dissemination and colonization capacity, an impaired ability to replicate in host macrophages, and decreased resistance against the bactericidal effect of host serum. To facilitate functional analysis, recombinant IvyEt(rIvy) and three mutant proteins, i.e., rIvyW55A, rIvyC82S, and rIvyH85D, which bear Ala, Ser, and Asp substitutions at W55, C82, and H85, respectively, were prepared.In vitrostudies showed that rIvy, rIvyW55A, and rIvyH85D were able to block the lytic effect of lysozyme on a Gram-positive bacterium, whereas rIvyC82S could not do so. Likewise, rIvy, but not rIvyC82S, inhibited the serum-facilitated killing effect of lysozyme onE. tarda.In vivoanalysis showed that rIvy, but not rIvyC82S, restored the lost pathogenicity of TXivy and enhanced the infectivity of TX01. Together these results indicate that IvyEtis a lysozyme inhibitor and a virulence factor that depends on the conserved C82 for biological activity.

scholarly journals Symbiotic Relationship between Streptococcus mutans and Candida albicans Synergizes Virulence of Plaque BiofilmsIn Vivo

2014 ◽  
Vol 82 (5) ◽  
pp. 1968-1981 ◽  
Author(s):  
Megan L. Falsetta ◽  
Marlise I. Klein ◽  
Punsiri M. Colonne ◽  
Kathleen Scott-Anne ◽  
Stacy Gregoire ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Dental Caries ◽  
Streptococcus Mutans ◽  
Bacterial Pathogen ◽  
Single Species ◽  
Content Type ◽  
3 Dimensional ◽  
Biofilm Development

ABSTRACTStreptococcus mutansis often cited as the main bacterial pathogen in dental caries, particularly in early-childhood caries (ECC).S. mutansmay not act alone;Candida albicanscells are frequently detected along with heavy infection byS. mutansin plaque biofilms from ECC-affected children. It remains to be elucidated whether this association is involved in the enhancement of biofilm virulence. We showed that the ability of these organisms together to form biofilms is enhancedin vitroandin vivo. The presence ofC. albicansaugments the production of exopolysaccharides (EPS), such that cospecies biofilms accrue more biomass and harbor more viableS. mutanscells than single-species biofilms. The resulting 3-dimensional biofilm architecture displays sizeableS. mutansmicrocolonies surrounded by fungal cells, which are enmeshed in a dense EPS-rich matrix. Using a rodent model, we explored the implications of this cross-kingdom interaction for the pathogenesis of dental caries. Coinfected animals displayed higher levels of infection and microbial carriage within plaque biofilms than animals infected with either species alone. Furthermore, coinfection synergistically enhanced biofilm virulence, leading to aggressive onset of the disease with rampant carious lesions. Ourin vitrodata also revealed that glucosyltransferase-derived EPS is a key mediator of cospecies biofilm development and that coexistence withC. albicansinduces the expression of virulence genes inS. mutans(e.g.,gtfB,fabM). We also found thatCandida-derived β1,3-glucans contribute to the EPS matrix structure, while fungal mannan and β-glucan provide sites for GtfB binding and activity. Altogether, we demonstrate a novel mutualistic bacterium-fungus relationship that occurs at a clinically relevant site to amplify the severity of a ubiquitous infectious disease.

scholarly journals The Genome Sequence of M228, a Chinese Isolate of Pseudomonas syringae pv. actinidiae, Illustrates Insertion Sequence Element Mobility

2019 ◽  
Vol 8 (1) ◽  
Author(s):  
Joycelyn Ho ◽  
George Taiaroa ◽  
Margi I. Butler ◽  
Russell T. M. Poulter
Keyword(s):  
Pseudomonas Syringae ◽  
Genome Sequence ◽  
Complete Genome Sequence ◽  
Insertion Sequence ◽  
Bacterial Pathogen ◽  
Chinese Isolate ◽  
Element Mobility ◽  
Sequence Element ◽  
Content Type ◽  
Insertion Sequence Element

We present here the complete genome sequence of M228, a Chinese biovar 3 strain of Pseudomonas syringae pv. actinidiae, a bacterial pathogen of kiwifruit.

scholarly journals Disruption of Francisella tularensis Schu S4iglI,iglJ, andpdpCGenes Results in Attenuation for Growth in Human Macrophages andIn VivoVirulence in Mice and Reveals a Unique Phenotype forpdpC

2012 ◽  
Vol 81 (3) ◽  
pp. 850-861 ◽  
Author(s):  
Matthew E. Long ◽  
Stephen R. Lindemann ◽  
Jed A. Rasmussen ◽  
Bradley D. Jones ◽  
Lee-Ann H. Allen
Keyword(s):  
Francisella Tularensis ◽  
Bacterial Pathogen ◽  
Human Monocyte ◽  
Pathogenicity Island ◽  
Intermediate Phenotype ◽  
Small Subset ◽  
Content Type ◽  
Isolation And Characterization ◽  
Schu S4

ABSTRACTFrancisella tularensisis a facultative intracellular bacterial pathogen and the causative agent of tularemia. After infection of macrophages, the organism escapes from its phagosome and replicates to high density in the cytosol, but the bacterial factors required for these aspects of virulence are incompletely defined. Here, we describe the isolation and characterization ofFrancisella tularensissubsp.tularensisstrain Schu S4 mutants that lack functionaliglI,iglJ, orpdpC, three genes of theFrancisellapathogenicity island. Our data demonstrate that these mutants were defective for replication in primary human monocyte-derived macrophages and murine J774 cells yet exhibited two distinct phenotypes. TheiglIandiglJmutants were similar to one another, exhibited profound defects in phagosome escape and intracellular growth, and appeared to be trapped in cathepsin D-positive phagolysosomes. Conversely, thepdpCmutant avoided trafficking to lysosomes, phagosome escape was diminished but not ablated, and these organisms replicated in a small subset of infected macrophages. The phenotype of each mutant strain was reversed bytranscomplementation.In vivovirulence was assessed by intranasal infection of BALB/c mice. The mutants appeared avirulent, as all mice survived infection with 108CFUiglJ-orpdpC-deficient bacteria. Nevertheless, thepdpCmutant disseminated to the liver and spleen before being eliminated, whereas theiglJmutant did not. Taken together, our data demonstrate that the pathogenicity island genes tested are essential forF. tularensisSchu S4 virulence and further suggest thatpdpCmay play a unique role in this process, as indicated by its distinct intermediate phenotype.

scholarly journals Alternative Sigma Factor RpoE Is Important for Vibrio parahaemolyticus Cell Envelope Stress Response and Intestinal Colonization

2014 ◽  
Vol 82 (9) ◽  
pp. 3667-3677 ◽  
Author(s):  
Brandy Haines-Menges ◽  
W. Brian Whitaker ◽  
E. Fidelma Boyd
Keyword(s):  
Stress Response ◽  
Vibrio Parahaemolyticus ◽  
Response Regulator ◽  
Cell Envelope ◽  
Polymyxin B ◽  
Content Type ◽  
Alternative Sigma Factors ◽  
Envelope Stress

ABSTRACTVibrio parahaemolyticusis a halophile that inhabits brackish waters and a wide range of hosts, including crustaceans, fish, mollusks, and humans. In humans, it is the leading cause of bacterial seafood-borne gastroenteritis. The focus of this work was to determine the role of alternative sigma factors in the stress response ofV. parahaemolyticusRIMD2210633, an O3:K6 pandemic isolate. Bioinformatics identified five putative extracytoplasmic function (ECF) family of alternative sigma factors: VP0055, VP2210, VP2358, VP2578, and VPA1690. ECF factors typically respond to cell wall/cell envelope stress, iron levels, and the oxidation state of the cell. We have demonstrated here that one such sigma factor, VP2578, a homologue of RpoE fromEscherichia coli, is important for survival under a number of cell envelope stress conditions and in gastrointestinal colonization of a streptomycin-treated adult mouse. In this study, we determined that anrpoEdeletion mutant strain BHM2578 compared to the wild type (WT) was significantly more sensitive to polymyxin B, ethanol, and high-temperature stresses. We demonstrated that inin vivocompetition assays between therpoEmutant and the WT marked with the β-galactosidase genelacZ(WBWlacZ), the mutant strain was defective in colonization compared to the WT. In contrast, deletion of therpoSstress response regulator did not affectin vivosurvival. In addition, we examined the role of the outer membrane protein, OmpU, which inV. choleraeis proposed to be the sole activator of RpoE. We found that anompUdeletion mutant was sensitive to bile salt stress but resistant to polymyxin B stress, indicating OmpU is not essential for the cell envelope stress responses or RpoE function. Overall, these data demonstrate that RpoE is a key cell envelope stress response regulator and, similar toE. coli, RpoE may have several factors that stimulate its function.

scholarly journals Superantigens Subvert the Neutrophil Response To Promote Abscess Formation and Enhance Staphylococcus aureus SurvivalIn Vivo

2014 ◽  
Vol 82 (9) ◽  
pp. 3588-3598 ◽  
Author(s):  
Stacey X. Xu ◽  
Kevin J. Gilmore ◽  
Peter A. Szabo ◽  
Joseph J. Zeppa ◽  
Miren L. Baroja ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Bacterial Pathogen ◽  
Staphylococcal Infection ◽  
Infection Process ◽  
Interleukin 12 ◽  
Bacterial Survival ◽  
Content Type ◽  
Knockout Strain ◽  
Neutrophil Response

ABSTRACTStaphylococcus aureusis a versatile bacterial pathogen that produces T cell-activating toxins known as superantigens (SAgs). Although excessive immune activation by SAgs can induce a dysregulated cytokine storm as a component of what is known as toxic shock syndrome (TSS), the contribution of SAgs to the staphylococcal infection process is not well defined. Here, we evaluated the role of the bacterial superantigen staphylococcal enterotoxin A (SEA) in a bacteremia model using humanized transgenic mice expressing SAg-responsive HLA-DR4 molecules. Infection withS. aureusNewman induced SEA-dependent Vβ skewing of T cells and enhanced bacterial survival in the liver compared with infection byseaknockout strain. SEA-induced gamma interferon, interleukin-12, and chemokine responses resulted in increased infiltration of CD11b+Ly6G+neutrophils into the liver, promoting the formation of abscesses that contained large numbers of viable staphylococci. Hepatic abscesses occurred significantly more frequently inS. aureusNewman-infected livers than in livers infected with the Newmanseaknockout strain, promoting the survival ofS. aureusin vivo. This represents a novel mechanism during infection wherebyS. aureusutilizes SAgs to form a specialized niche and manipulate the immune system.

scholarly journals Impact of the Listeria monocytogenes Protein InlC on Infection in Mice

2013 ◽  
Vol 81 (4) ◽  
pp. 1334-1340 ◽  
Author(s):  
Nelly Leung ◽  
Antonella Gianfelice ◽  
Scott D. Gray-Owen ◽  
Keith Ireton
Keyword(s):  
Listeria Monocytogenes ◽  
Mutant Strain ◽  
Type Strain ◽  
Wild Type Strain ◽  
Bacterial Pathogen ◽  
Adaptor Protein ◽  
Single Amino Acid ◽  
Wild Type ◽  
Content Type

ABSTRACTThe bacterial pathogenListeria monocytogenescauses serious food-borne illnesses in pregnant women and the immunocompromised.L. monocytogenespromotes its internalization into host epithelial cells and then uses an F-actin-dependent motility process to spread from infected cells to surrounding healthy cells. In cultured enterocytes, efficient spread ofL. monocytogenesrequires the secreted bacterial protein InlC. InlC promotes dissemination by physically interacting with and antagonizing the function of the human adaptor protein Tuba. Here we examine the role of InlC and its interaction with host Tuba during infection in mice. The study took advantage of a single-amino-acid substitution (K173A) in InlC that impairs binding to human Tuba but does not affect InlC-mediated inhibition of the NF-κB pathway. Mice were inoculated intravenously with the wild-typeL. monocytogenesstrain EGD, an isogenic strain deleted for theinlCgene (ΔinlC), or a strain expressing K173A mutant InlC (inlC.K173A). The 50% lethal doses (LD50) for the ΔinlCorinlC.K173Amutant strain were approximately 4- or 6-fold greater than that for the wild-type strain, indicating a role forinlCin virulence. Compared to the wild-type strain, theinlC.K173Amutant strain exhibited lower bacterial loads in the liver. Histological analysis of livers indicated that the twoinlCmutant strains produced smaller foci of infection than did the wild-type strain. These smaller foci are consistent with a role for InlC in cell-to-cell spreadin vivo. Taken together, these results provide evidence that interaction of InlC with host Tuba is important for full virulence.

scholarly journals Epinecidin-1 Has Immunomodulatory Effects, Facilitating Its Therapeutic Use in a Mouse Model of Pseudomonas aeruginosa Sepsis

2014 ◽  
Vol 58 (8) ◽  
pp. 4264-4274 ◽  
Author(s):  
Chieh-Yu Pan ◽  
Jian-Chyi Chen ◽  
Jenn-Feng Sheen ◽  
Tai-Lang Lin ◽  
Jyh-Yih Chen
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Mouse Model ◽  
Antimicrobial Properties ◽  
Bacterial Pathogen ◽  
Multidrug Resistant ◽  
Behavioral Effects ◽  
Immunomodulatory Effects ◽  
Kidney Toxicity ◽  
Content Type

ABSTRACTAntimicrobial peptides (AMPs) are garnering attention as possible alternatives to antibiotics. Here, we describe the antimicrobial properties of epinecidin-1 against a multidrug-resistant clinical isolate ofP. aeruginosa(P. aeruginosaR) and aP. aeruginosastrain from ATCC (P. aeruginosaATCC 19660)in vivo. The MICs of epinecidin-1 againstP. aeruginosaR andP. aeruginosaATCC 19660 were determined and compared with those of imipenem. Epinecidin-1 was found to be highly effective at combating peritonitis infection caused byP. aeruginosaR orP. aeruginosaATCC 19660 in mouse models, without inducing adverse behavioral effects or liver or kidney toxicity. Taken together, our results indicate that epinecidin-1 enhances the rate of survival of mice infected with the bacterial pathogenP. aeruginosathrough both antimicrobial and immunomodulatory effects.

scholarly journals Parallel Evolution of Two Clades of an Atlantic-Endemic Pathogenic Lineage of Vibrio parahaemolyticus by Independent Acquisition of Related Pathogenicity Islands

2017 ◽  
Vol 83 (18) ◽  
Author(s):  
Feng Xu ◽  
Narjol Gonzalez-Escalona ◽  
Kevin P. Drees ◽  
Robert P. Sebra ◽  
Vaughn S. Cooper ◽  
...  
Keyword(s):  
United States ◽  
Vibrio Parahaemolyticus ◽  
Phylogenetic Trees ◽  
Disease Incidence ◽  
Atlantic Coast ◽  
Parallel Evolution ◽  
Pathogenicity Islands ◽  
Human Pathogens ◽  
Content Type ◽  
Northeast United States

ABSTRACT Shellfish-transmitted Vibrio parahaemolyticus infections have recently increased from locations with historically low disease incidence, such as the Northeast United States. This change coincided with a bacterial population shift toward human-pathogenic variants occurring in part through the introduction of several Pacific native lineages (ST36, ST43, and ST636) to nearshore areas off the Atlantic coast of the Northeast United States. Concomitantly, ST631 emerged as a major endemic pathogen. Phylogenetic trees of clinical and environmental isolates indicated that two clades diverged from a common ST631 ancestor, and in each of these clades, a human-pathogenic variant evolved independently through acquisition of distinct Vibrio pathogenicity islands (VPaI). These VPaI differ from each other and bear little resemblance to hemolysin-containing VPaI from isolates of the pandemic clonal complex. Clade I ST631 isolates either harbored no hemolysins or contained a chromosome I-inserted island we call VPaIβ that encodes a type 3 secretion system (T3SS2β) typical of Trh hemolysin producers. The more clinically prevalent and clonal ST631 clade II had an island we call VPaIγ that encodes both tdh and trh and that was inserted in chromosome II. VPaIγ was derived from VPaIβ but with some additional acquired elements in common with VPaI carried by pandemic isolates, exemplifying the mosaic nature of pathogenicity islands. Genomics comparisons and amplicon assays identified VPaIγ-type islands containing tdh inserted adjacent to the ure cluster in the three introduced Pacific and most other emergent lineages that collectively cause 67% of infections in the Northeast United States as of 2016. IMPORTANCE The availability of three different hemolysin genotypes in the ST631 lineage provided a unique opportunity to employ genome comparisons to further our understanding of the processes underlying pathogen evolution. The fact that two different pathogenic clades arose in parallel from the same potentially benign lineage by independent VPaI acquisition is surprising considering the historically low prevalence of community members harboring VPaI in waters along the Northeast U.S. coast that could serve as the source of this material. This illustrates a possible predisposition of some lineages to not only acquire foreign DNA but also become human pathogens. Whereas the underlying cause for the expansion of V. parahaemolyticus lineages harboring VPaIγ along the U.S. Atlantic coast and spread of this element to multiple lineages that underlies disease emergence is not known, this work underscores the need to define the environment factors that favor bacteria harboring VPaI in locations of emergent disease.

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