scholarly journals YaxAB, a Yersinia enterocolitica Pore-Forming Toxin Regulated by RovA

2013 ◽  
Vol 81 (11) ◽  
pp. 4208-4219 ◽  
Author(s):  
Nikki J. Wagner ◽  
Carolina P. Lin ◽  
Luke B. Borst ◽  
Virginia L. Miller
Keyword(s):  
Virulence Factors ◽  
Yersinia Enterocolitica ◽  
Mammalian Cells ◽  
Virulence Gene ◽  
Xenorhabdus Nematophila ◽  
Host Cell Membrane ◽  
Content Type ◽  
Membrane Pores ◽  
Osmotic Lysis

ABSTRACTThe transcriptional regulator RovA positively regulates transcription of theYersinia enterocoliticavirulence geneinv. Invasin, encoded byinv, is important for establishment ofY. enterocoliticainfection. However, arovAmutant is more attenuated for virulence than aninvmutant, implying that RovA regulates additional virulence genes. When theY. enterocoliticaRovA regulon was defined by microarray analysis, YE1984 and YE1985 were among the genes identified as being upregulated by RovA. Since these genes are homologous toXenorhabdus nematophilacytotoxin genesxaxAandxaxB, we named themyaxAandyaxB, respectively. In this work, we demonstrate the effects of YaxAB on the course of infection in the murine model. While ayaxABmutant (ΔyaxAB) is capable of colonizing mice at the same level as the wild type, it slightly delays the course of infection and results in differing pathology in the spleen. Further, we found thatyaxABencode a probable cytotoxin capable of lysing mammalian cells, that both YaxA and YaxB are required for cytotoxic activity, and that the two proteins associate. YaxAB-mediated cell death occurs via osmotic lysis through the formation of distinct membrane pores.In silicotertiary structural analysis identified predicted structural homology between YaxA and proteins in pore-forming toxin complexes fromBacillus cereus(HBL-B) andEscherichia coli(HlyE). Thus, it appears that YaxAB function as virulence factors by inducing cell lysis through the formation of pores in the host cell membrane. This characterization of YaxAB supports the hypothesis that RovA regulates expression of multiple virulence factors inY. enterocolitica.

scholarly journals Nutritional Regulation of the Sae Two-Component System by CodY inStaphylococcus aureus

2018 ◽  
Vol 200 (8) ◽  
Author(s):  
Kevin D. Mlynek ◽  
William E. Sause ◽  
Derek E. Moormeier ◽  
Marat R. Sadykov ◽  
Kurt R. Hill ◽  
...  
Keyword(s):  
Gene Expression ◽  
Virulence Factors ◽  
Virulence Gene ◽  
Nutrient Depletion ◽  
Global Regulator ◽  
Two Component System ◽  
Component System ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Two Component

ABSTRACTStaphylococcus aureussubverts innate defenses during infection in part by killing host immune cells to exacerbate disease. This human pathogen intercepts host cues and activates a transcriptional response via theS. aureusexoprotein expression (SaeR/SaeS [SaeR/S]) two-component system to secrete virulence factors critical for pathogenesis. We recently showed that the transcriptional repressor CodY adjusts nuclease (nuc) gene expression via SaeR/S, but the mechanism remained unknown. Here, we identified two CodY binding motifs upstream of thesaeP1 promoter, which suggested direct regulation by this global regulator. We show that CodY shares a binding site with the positive activator SaeR and that alleviating direct CodY repression at this site is sufficient to abrogate stochastic expression, suggesting that CodY repressessaeexpression by blocking SaeR binding. Epistasis experiments support a model that CodY also controlssaeindirectly through Agr and Rot-mediated repression of thesaeP1 promoter. We also demonstrate that CodY repression ofsaerestrains production of secreted cytotoxins that kill human neutrophils. We conclude that CodY plays a previously unrecognized role in controlling virulence gene expression via SaeR/S and suggest a mechanism by which CodY acts as a master regulator of pathogenesis by tying nutrient availability to virulence gene expression.IMPORTANCEBacterial mechanisms that mediate the switch from a commensal to pathogenic lifestyle are among the biggest unanswered questions in infectious disease research. Since the expression of most virulence genes is often correlated with nutrient depletion, this implies that virulence is a response to the lack of nourishment in host tissues and that pathogens likeS. aureusproduce virulence factors in order to gain access to nutrients in the host. Here, we show that specific nutrient depletion signals appear to be funneled to the SaeR/S system through the global regulator CodY. Our findings reveal a strategy by whichS. aureusdelays the production of immune evasion and immune-cell-killing proteins until key nutrients are depleted.

scholarly journals A Small Unstructured Region in Vibrio cholerae ToxT Mediates the Response to Positive and Negative Effectors and ToxT Proteolysis

2014 ◽  
Vol 197 (3) ◽  
pp. 654-668 ◽  
Author(s):  
Joshua J. Thomson ◽  
Sarah C. Plecha ◽  
Jeffrey H. Withey
Keyword(s):  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Unsaturated Fatty Acids ◽  
Diarrheal Disease ◽  
Virulence Gene ◽  
Site Directed Mutagenesis ◽  
Content Type ◽  
Terminal Domain ◽  
Virulence Gene Regulation ◽  
Host Signals

Vibrio choleraeis the causative agent of the severe diarrheal disease cholera. The production of the virulence factors that are required for human disease is controlled by a complex network of transcriptional and posttranscriptional regulators. ToxT is the transcription regulator that directly controls the production of the two major virulence factors, toxin-coregulated pilus (TCP) and cholera toxin (CT). The solved crystal structure of ToxT revealed an unstructured region in the N-terminal domain between residues 100 and 110. This region and the surrounding amino acids have been previously implicated in ToxT proteolysis, resistance to inhibition by negative effectors, and ToxT dimerization. To better characterize this region, site-directed mutagenesis was performed to assess the effects on ToxT proteolysis and bile sensitivity. This analysis identified specific mutations within this unstructured region that prevent ToxT proteolysis and other mutations that reduce inhibition by bile and unsaturated fatty acids. In addition, we found that mutations that affect the sensitivity of ToxT to bile also affect the sensitivity of ToxT to its positive effector, bicarbonate. These results suggest that a small unstructured region in the ToxT N-terminal domain is involved in multiple aspects of virulence gene regulation and response to human host signals.

scholarly journals The Acyl-Homoserine Lactone Synthase YenI from Yersinia enterocolitica Modulates Virulence Gene Expression in Enterohemorrhagic Escherichia coli O157:H7

2013 ◽  
Vol 81 (11) ◽  
pp. 4192-4199 ◽  
Author(s):  
Y N. Nguyen ◽  
Haiqing Sheng ◽  
Rambabu Dakarapu ◽  
John R. Falck ◽  
Carolyn J. Hovde ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Yersinia Enterocolitica ◽  
Virulence Gene ◽  
Acid Resistance ◽  
Homoserine Lactone ◽  
Enterohemorrhagic Escherichia Coli ◽  
Content Type ◽  
Fecal Shedding ◽  
Virulence Gene Expression

ABSTRACTThe human pathogen enterohemorrhagicEscherichia coli(EHEC) O157:H7 colonizes the rectoanal junction (RAJ) in cattle, its natural reservoir. Colonization at the RAJ poses a serious risk for fecal shedding and contamination of the environment. We previously demonstrated that EHEC senses acyl-homoserine lactones (AHLs) produced by the microbiota in the rumen to activate thegadacid resistance genes necessary for survival through the acidic stomachs in cattle and to repress the locus of enterocyte effacement (LEE) genes important for colonization of the RAJ, but unnecessary in the rumen. Devoid of AHLs, the RAJ is the prominent site of colonization of EHEC in cattle. To determine if the presence of AHLs in the RAJ could repress colonization at this site, we engineered EHEC to express theYersinia enterocoliticaAHL synthase geneyenI, which constitutively produces AHLs, to mimic a constant exposure of AHLs in the environment. TheyenI+EHEC produces oxo-C6-homoserine lactone (oxo-C6-HSL) and had a significant reduction in LEE expression, effector protein secretion, and attaching and effacing (A/E) lesion formationin vitrocompared to the wild type (WT). TheyenI+EHEC also activated expression of thegadgenes. To assess whether AHL production, which decreases LEE expression, would decrease RAJ colonization by EHEC, cattle were challenged at the RAJ with WT oryenI+EHEC. Although theyenI+EHEC colonized the RAJ with efficiency equal to that of the WT, there was a trend for the cattle to shed the WT strain longer than theyenI+EHEC.

scholarly journals Molecular evaluation of quorum quenching potential of vanillic acid against Yersinia enterocolitica through transcriptomic and in silico analysis

2020 ◽  
Vol 69 (11) ◽  
pp. 1319-1331
Author(s):  
Chandran Sivasankar ◽  
Nisha Kumari Jha ◽  
Satya Rajan Singh ◽  
Ayaluru Murali ◽  
Prathapkumar Halady Shetty
Keyword(s):  
Quorum Sensing ◽  
Rna Sequencing ◽  
Virulence Factors ◽  
Yersinia Enterocolitica ◽  
Vanillic Acid ◽  
In Silico ◽  
Type Species ◽  
Content Type ◽  
Link Type ◽  
Surfactant Production

Introduction. Yersinia enterocolitica is one of the leading food-borne entero-pathogens causing various illnesses ranging from gastroenteritis to systemic infections. Quorum sensing (QS) is one of the prime mechanisms that control the virulence in Y. enterocolitica . Hypothesis/Gap Statement. Vanillic acid inhibits the quorum sensing and other virulence factors related to Y. enterocolitica . It has been evaluated by transcriptomic and Insilico analysis. Therefore, it can be a prospective agent to develop a therapeutic combination against Y. enterocolitica . Aim. The present study is focused on screening natural anti-quorum-sensing agents against Y. enterocolitica . The effect of selected active principle on various virulence factors was evaluated. Methodology. In total, 12 phytochemicals were screened by swarming assay. MATH assay, EPS and surfactant production assay, SEM analysis, antibiotic and blood sensitivity assay were performed to demonstrate the anti-virulence activity. Further, RNA sequencing and molecular docking studies were carried out to substantiate the anti-QS activity. Results. Vanillic acid (VA) has exhibited significant motility inhibition, thus indicating the anti-QS activity with MQIC of 400 µg ml−1 without altering the cell viability. It has also inhibited the violacein production in Chromobacterium violaceum ATCC 12472, which further confirms the anti-QS activity. VA has inhibited 16 % of cell-surface hydrophobicity (CSH), 52 % of EPS production and 60 % of surfactant production. Moreover, it has increased the sensitivity of Y. enterocolitica towards antibiotics. It has also made the cells upto 91 % more vulnerable towards human immune cells. The transcriptomic analysis by RNA sequencing revealed the down regulation of genes related to motility, virulence, chemotaxis, siderophores and drug resistance. VA treatment has also positively regulated the expression of several stress response genes. In furtherance, the anti-QS potential of VA has been validated with QS regulatory protein YenR by in silico molecular simulation and docking study. Conclusion. The present study is possibly the first attempt to demonstrate the anti-QS and anti-pathogenic potential of VA against Y. enterocolitica by transcriptomic and in silico analysis. It also deciphers that VA can be a promising lead to develop biopreservative and therapeutic regimens to treat Y. enterocolitica infections.

scholarly journals Relationship between Vancomycin MIC and Virulence Gene Expression in Clonal Complexes of Methicillin-Susceptible Staphylococcus aureus Strains Isolated from Left-Sided Endocarditis

2020 ◽  
Vol 64 (3) ◽  
Author(s):  
Juan M. Pericàs ◽  
Carlos Cervera ◽  
Cristina Garcia-de-la-Mària ◽  
Batu K. Sharma-Kuinkel ◽  
Rachelle Gonzales ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Virulence Factors ◽  
Virulence Genes ◽  
Multivariable Analysis ◽  
Virulence Gene ◽  
Mortality Rates ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Vancomycin Mics ◽  
Genes Encoding

ABSTRACT Higher vancomycin MICs have been associated with more complicated courses and higher mortality rates in patients with Staphylococcus aureus bacteremia and infective endocarditis (IE). The aim of this study was to investigate whether the strains belonging to the cohort of 93 patients from a previously published study in which patients with strains with vancomycin MICs of ≥1.5 μg/ml presented higher mortality rates and systemic emboli than patients with strains with vancomycin MICs of <1.5 μg/ml had specific patterns of virulence factors, clonal complex (CC) types, or the ability to form biofilms. Vancomycin MICs were determined by Etest, and the isolates underwent spa typing to infer the CC, biofilm studies, a thrombin-induced platelet microbicidal assay, and multiplex PCR for the presence of virulence genes. We found no differences in genes encoding adhesins, toxins, or other putative virulence genes according to the vancomycin MIC group. CC30, CC34, and CC45 represented nearly half of the isolates, and there was no association with the vancomycin MIC. agr subgroups I and III predominated, with no association with the vancomycin MIC. Isolates with higher vancomycin MICs exhibited a poorer ability to form biofilms with and without the presence of vancomycin (2.03 versus 2.48 [P < 0.001], respectively, for isolates with higher vancomycin MICs and 2.60 versus 2.87 [P = 0.022], respectively, for isolates with lower vancomycin MICs). In the multivariable analysis, efb and V8 were risk factors for major emboli (adjusted odds ratio [aOR] = 7.5 and 95% confidence interval [CI] = 1.2 to 46.6 for efb, and aOR = 3.9 and 95% CI = 1.1 to 14.1 for V8), whereas no genotypic predictors of in-hospital mortality were found. No clear associations between genes encoding virulence factors, agr type, clonal complexes, mortality, and major embolic events according to vancomycin MIC group were found.

scholarly journals Characterization of a DHA-1-Producing Klebsiella pneumoniae Strain Involved in an Outbreak and Role of the AmpR Regulator in Virulence

2011 ◽  
Vol 56 (1) ◽  
pp. 288-294 ◽  
Author(s):  
Claire Hennequin ◽  
Frédéric Robin ◽  
Nadège Cabrolier ◽  
Richard Bonnet ◽  
Christiane Forestier
Keyword(s):  
Gastrointestinal Tract ◽  
Klebsiella Pneumoniae ◽  
Virulence Factors ◽  
Intestinal Epithelial ◽  
Content Type ◽  
Disk Diffusion Assay ◽  
Severe Infections ◽  
Type 3

ABSTRACTA clonal strain ofKlebsiella pneumoniaeproducing the plasmid-encoded cephalosporinase DHA-1 was isolated from four patients admitted to the teaching hospital of Clermont-Ferrand, France, in 2006. It was responsible for severe infections in three of the patients; the fourth was colonized only in the gastrointestinal tract. The strain had at least two plasmids encoding resistance to antibiotics (quinolones, aminoglycosides, chloramphenicol, sulfonamides, and trimethoprim), as shown by disk diffusion assay, and harbored only a few genes for virulence factors (wabGandmrkD), as shown by PCRs. DHA-1 synthesis is regulated by an upstream, divergently transcribed gene,ampR, which is also involved in the expression of virulence factors inPseudomonas aeruginosa. To investigate the role of AmpR inK. pneumoniae, we cloned the wild-typeampRgene from the DHA-1 clonal isolate into a previously characterizedK. pneumoniaebackground plasmid-cured strain, CH608.ampRwas also introduced into a CH608 isogenic mutant deleted ofampD, in which AmpR is present only in its activator form, resulting in constitutive hyperproduction of the β-lactamase. We showed thatampRwas involved in the upregulation of capsule synthesis and therefore in resistance to killing by serum. AmpR also modulated biofilm formation and type 3 fimbrial gene expression, as well as colonization of the murine gastrointestinal tract and adhesion to HT-29 intestinal epithelial cells. These results show the pleiotropic role ofampRin the pathogenesis process ofK. pneumoniae.

scholarly journals Characterization of a Mutant Escherichia coli Heat-Labile Toxin, LT(R192G/L211A), as a Safe and Effective Oral Adjuvant

2011 ◽  
Vol 18 (4) ◽  
pp. 546-551 ◽  
Author(s):  
Elizabeth B. Norton ◽  
Louise B. Lawson ◽  
Lucy C. Freytag ◽  
John D. Clements
Keyword(s):  
Escherichia Coli ◽  
Mammalian Cells ◽  
Oral Vaccines ◽  
Content Type ◽  
Intracellular Degradation ◽  
Heat Labile ◽  
Increased Sensitivity

ABSTRACTDespite the fact that the adjuvant properties of the heat-labile enterotoxins ofEscherichia coli(LT) andVibrio cholerae(CT) have been known for more than 20 years, there are no available oral vaccines containing these molecules as adjuvants, primarily because they are both very potent enterotoxins. A number of attempts with various degrees of success have been made to reduce or eliminate the enterotoxicity of LT and CT so they can safely be used as oral adjuvants or immunogens. In this report we characterize the structural, enzymatic, enterotoxic, and adjuvant properties of a novel mutant of LT, designated LT(R192G/L211A), or dmLT. dmLT was not sensitive to trypsin activation, had reduced enzymatic activity for induction of cyclic AMP in Caco-2 cells, and exhibited no enterotoxicity in the patent mouse assay. Importantly, dmLT retained the ability to function as an oral adjuvant for a coadministered antigen (tetanus toxoid) and to elicit anti-LT antibodies.In vitroandin vivodata suggest that the reduced enterotoxicity of this molecule compared to native LT or the single mutant, LT(R192G), is a consequence of increased sensitivity to proteolysis and rapid intracellular degradation in mammalian cells. In conclusion, dmLT is a safe and powerful detoxified enterotoxin with the potential to function as a mucosal adjuvant for coadministered antigens and to elicit anti-LT antibodies without undesirable side effects.

scholarly journals Metabolic Genetic Screens Reveal Multidimensional Regulation of Virulence Gene Expression in Listeria monocytogenes and an Aminopeptidase That Is Critical for PrfA Protein Activation

2017 ◽  
Vol 85 (6) ◽  
Author(s):  
Sivan Friedman ◽  
Marika Linsky ◽  
Lior Lobel ◽  
Lev Rabinovich ◽  
Nadejda Sigal ◽  
...  
Keyword(s):  
Gene Expression ◽  
Listeria Monocytogenes ◽  
Mammalian Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Virulence Gene ◽  
High Plasticity ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Protein Activation

ABSTRACT Listeria monocytogenes is an environmental saprophyte and intracellular bacterial pathogen. Upon invading mammalian cells, the bacterium senses abrupt changes in its metabolic environment, which are rapidly transduced to regulation of virulence gene expression. To explore the relationship between L. monocytogenes metabolism and virulence, we monitored virulence gene expression dynamics across a library of genetic mutants grown under two metabolic conditions known to activate the virulent state: charcoal-treated rich medium containing glucose-1-phosphate and minimal defined medium containing limiting concentrations of branched-chain amino acids (BCAAs). We identified over 100 distinct mutants that exhibit aberrant virulence gene expression profiles, the majority of which mapped to nonessential metabolic genes. Mutants displayed enhanced, decreased, and early and late virulence gene expression profiles, as well as persistent levels, demonstrating a high plasticity in virulence gene regulation. Among the mutants, one was noteworthy for its particularly low virulence gene expression level and mapped to an X-prolyl aminopeptidase (PepP). We show that this peptidase plays a role in posttranslational activation of the major virulence regulator, PrfA. Specifically, PepP mediates recruitment of PrfA to the cytoplasmic membrane, a step identified as critical for PrfA protein activation. This study establishes a novel step in the complex mechanism of PrfA activation and further highlights the cross regulation of metabolism and virulence.

scholarly journals Inhibition of Rho Activity Increases Expression of SaeRS-Dependent Virulence Factor Genes inStaphylococcus aureus, Showing a Link between Transcription Termination, Antibiotic Action, and Virulence

mBio ◽  
2018 ◽  
Vol 9 (5) ◽  
Author(s):  
Anna Nagel ◽  
Stephan Michalik ◽  
Michel Debarbouille ◽  
Tobias Hertlein ◽  
Manuela Gesell Salazar ◽  
...  
Keyword(s):  
Gene Expression ◽  
Staphylococcus Aureus ◽  
Virulence Factors ◽  
Transcription Termination ◽  
Virulence Gene ◽  
Antisense Transcription ◽  
Termination Factor ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Transcription Termination Factor

ABSTRACTStaphylococcus aureuscauses various diseases ranging from skin and soft tissue infections to life-threatening infections. Adaptation to the different host niches is controlled by a complex network of transcriptional regulators. Global profiling of condition-dependent transcription revealed adaptation ofS. aureusHG001 at the levels of transcription initiation and termination. In particular, deletion of the gene encoding the Rho transcription termination factor triggered a remarkable overall increase in antisense transcription and gene expression changes attributable to indirect regulatory effects. The goal of the present study was a detailed comparative analysis ofS. aureusHG001 and its isogenicrhodeletion mutant. Proteome analysis revealed significant differences in cellular and extracellular protein profiles, most notably increased amounts of the proteins belonging to the SaeR regulon in the Rho-deficient strain. The SaeRS two-component system acts as a major regulator of virulence gene expression in staphylococci. Higher levels of SaeRS-dependent virulence factors such as adhesins, toxins, and immune evasion proteins in therhomutant resulted in higher virulence in a murine bacteremia model, which was alleviated in arhocomplemented strain. Inhibition of Rho activity by bicyclomycin, a specific inhibitor of Rho activity, also induced the expression of SaeRS-dependent genes, at both the mRNA and protein levels, to the same extent as observed in therhomutant. Taken together, these findings indicate that activation of the Sae system in the absence of Rho is directly linked to Rho’s transcription termination activity and establish a new link between antibiotic action and virulence gene expression inS. aureus.IMPORTANCEThe major human pathogenStaphylococcus aureusis a widespread commensal bacterium but also the most common cause of nosocomial infections. It adapts to the different host niches through a complex gene regulatory network. We show here that the Rho transcription termination factor, which represses pervasive antisense transcription in various bacteria, includingS. aureus, plays a role in controlling SaeRS-dependent virulence gene expression. A Rho-deficient strain produces larger amounts of secreted virulence factorsin vitroand shows increased virulence in mice. We also show that treatment ofS. aureuswith the antibiotic bicyclomycin, which inhibits Rho activity and is effective against Gram-negative bacteria, induces the same changes in the proteome as observed in the Rho-deficient strain. Our results reveal for the first time a link between transcription termination and virulence regulation inS. aureus, which implies a novel mechanism by which an antibiotic can modulate the expression of virulence factors.

scholarly journals PCR Detection of Virulence Genes in Yersinia enterocolitica and Yersinia pseudotuberculosis and Investigation of Virulence Gene Distribution

2003 ◽  
Vol 69 (3) ◽  
pp. 1810-1816 ◽  
Author(s):  
P. Thoerner ◽  
C. I. Bin Kingombe ◽  
K. Bögli-Stuber ◽  
B. Bissig-Choisat ◽  
T. M. Wassenaar ◽  
...  
Keyword(s):  
Yersinia Enterocolitica ◽  
Virulence Genes ◽  
Yersinia Pseudotuberculosis ◽  
Virulence Gene ◽  
Virulence Plasmid ◽  
Calcium Dependent ◽  
Dependent Growth ◽  
Plasmid Genes ◽  
Phenotypic Tests

ABSTRACT PCR-based assays were developed for the detection of plasmid- and chromosome-borne virulence genes in Yersinia enterocolitica and Yersinia pseudotuberculosis, to investigate the distribution of these genes in isolates from various sources. The results of PCR genotyping, based on 5 virulence-associated genes of 140 strains of Y. enterocolitica, were compared to phenotypic tests, such as biotyping and serotyping, and to virulence plasmid-associated properties such as calcium-dependent growth at 37°C and Congo red uptake. The specificity of the PCR results was validated by hybridization. Genotyping data correlated well with biotype data, and most biotypes resulted in (nearly) homogeneous genotypes for the chromosomal virulence genes (ystA, ystB, and ail); however, plasmid-borne genes (yadA and virF) were detected with variable efficiency, due to heterogeneity within the bacterial population for the presence of the virulence plasmid. Of the virulence genes, only ystB was present in biotype 1A; however, within this biotype, pathogenic and apathogenic isolates could not be distinguished based on the detection of virulence genes. Forty Y. pseudotuberculosis isolates were tested by PCR for the presence of inv, yadA, and lcrF. All isolates were inv positive, and 88% of the isolates contained the virulence plasmid genes yadA and lcrF. In conclusion, this study shows that genotyping of Yersinia spp., based on both chromosome- and plasmid-borne virulence genes, is feasible and informative and can provide a rapid and reliable genotypic characterization of field isolates.

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