scholarly journals Virulence factor profiles and genetic background of quinolone-resistant Escherichia coli isolated from hospital effluent

2016 ◽  
Vol 53 ◽  
pp. 37
Author(s):  
L. Anssour ◽  
Y. Messai ◽  
R. Bakour
Keyword(s):  
Escherichia Coli ◽  
Virulence Factor ◽  
Genetic Background ◽  
Hospital Effluent

scholarly journals Stand-alone ClpG disaggregase confers superior heat tolerance to bacteria

2017 ◽  
Vol 115 (2) ◽  
pp. E273-E282 ◽  
Author(s):  
Changhan Lee ◽  
Kamila B. Franke ◽  
Shady Mansour Kamal ◽  
Hyunhee Kim ◽  
Heinrich Lünsdorf ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Pseudomonas Aeruginosa ◽  
Gene Transfer ◽  
Horizontal Gene Transfer ◽  
Atpase Activity ◽  
Stationary Phase ◽  
Virulence Factor ◽  
Heat Tolerance ◽  
Molecular Features ◽  
Partner Proteins

AAA+ disaggregases solubilize aggregated proteins and confer heat tolerance to cells. Their disaggregation activities crucially depend on partner proteins, which target the AAA+ disaggregases to protein aggregates while concurrently stimulating their ATPase activities. Here, we report on two potent ClpG disaggregase homologs acquired through horizontal gene transfer by the species Pseudomonas aeruginosa and subsequently abundant P. aeruginosa clone C. ClpG exhibits high, stand-alone disaggregation potential without involving any partner cooperation. Specific molecular features, including high basal ATPase activity, a unique aggregate binding domain, and almost exclusive expression in stationary phase distinguish ClpG from other AAA+ disaggregases. Consequently, ClpG largely contributes to heat tolerance of P. aeruginosa primarily in stationary phase and boosts heat resistance 100-fold when expressed in Escherichia coli. This qualifies ClpG as a potential persistence and virulence factor in P. aeruginosa.

scholarly journals Multiple Insertional Events, Restricted by the Genetic Background, Have Led to Acquisition of Pathogenicity Island IIJ96-Like Domains among Escherichia coli Strains of Different Clinical Origins

2005 ◽  
Vol 73 (7) ◽  
pp. 4081-4087 ◽  
Author(s):  
Philippe Bidet ◽  
Stéphane Bonacorsi ◽  
Olivier Clermont ◽  
Caroline De Montille ◽  
Naima Brahimi ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Genetic Background ◽  
Pathogenicity Island ◽  
Neonatal Meningitis ◽  
Pcr Analysis ◽  
Ecological Niches ◽  
Class Iii ◽  
Phylogenetic Grouping ◽  
Flanking Sequences ◽  
Long Range Pcr

ABSTRACT We investigated the dissemination of pathogenicity island (PAI) IIJ96-like elements (hra, hly, cnf1, and pap) among 455 Escherichia coli isolates from children and adults with urinary tract infection (UTI), neonates with meningitis or colonized healthy neonates, and 74 reference strains by means of PCR phylogenetic grouping, ribotyping, and PCR analysis of virulence genes. Colocalization of these genes was documented by pulsed-field gel electrophoresis followed by Southern hybridization and long-range PCR (LRPCR) between the hra and the papG alleles. Site-specific insertion of the PAI was determined by LRPCR between hra and tRNA flanking sequences. hra, hly, and cnf1 were found in 113 isolates and consistently colocalized, constituting the backbone of PAI IIJ96-like domains. The prevalence of PAI IIJ96-like domains was significantly higher among UTI isolates than among neonatal meningitis and commensal isolates. These domains were restricted to a few ribotypes of group B2. In contrast to the consistent colocalization of hra, hly, and cnf1, the pap operon was varied: 12% of strains exhibited an allelic exchange of the papG class III allele (papGIII) for the papG class II allele (papGII) (only UTI isolates), and the pap operon was deleted in 23% of strains. No strains harbored papGIII outside the PAI, which appears to be the only source of this allele. PAI IIJ96-like domains were inserted in the vicinities of three different tRNAs—pheU (54%), leuX (29%), and pheV (15%)—depending on the genetic backgrounds and origins of the isolates. Multiple insertional events restricted by the genetic background have thus led to PAI IIJ96 acquisition. Specific genetic backgrounds and insertion sites may have played a role in additional recombination processes for E. coli adaptation to different ecological niches.

Molecular characterization and prevalence of virulence factor genes of Shiga toxin-producing Escherichia coli (STEC) isolated from diarrheic children

Gene Reports ◽  
2021 ◽  
pp. 101379
Author(s):  
Mohammad Moeinirad ◽  
Masoumeh Douraghi ◽  
Abbas Rahimi Foroushani ◽  
Rahimeh Sanikhani ◽  
Mohammad Mehdi Soltan Dallal
Keyword(s):  
Escherichia Coli ◽  
Molecular Characterization ◽  
Virulence Factor ◽  
Shiga Toxin ◽  
Virulence Factor Genes

scholarly journals SodA Contributes to the Virulence of Avian PathogenicEscherichia coliO2 Strain E058 in Experimentally Infected Chickens

2019 ◽  
Vol 201 (6) ◽  
Author(s):  
Qingqing Gao ◽  
Le Xia ◽  
Xiaobo Wang ◽  
Zhengqin Ye ◽  
Jinbiao Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
Hydrogen Peroxide ◽  
Virulence Factor ◽  
Infection Process ◽  
Strain Identification ◽  
Bacterial Disease ◽  
Wild Type ◽  
Content Type

ABSTRACTStrains of avian pathogenicEscherichia coli(APEC), the common pathogen of avian colibacillosis, encounter reactive oxygen species (ROS) during the infection process. Superoxide dismutases (SODs), acting as antioxidant factors, can protect against ROS-mediated host defenses. Our previous reports showed that thesodAgene (encoding a Mn-cofactor-containing SOD [MnSOD]) is highly expressed during the septicemic infection process of APEC.sodAhas been proven to be a virulence factor of certain pathogens, but its role in the pathogenicity of APEC has not been fully identified. In this study, we deleted thesodAgene from the virulent APEC O2 strain E058 and examined thein vitroandin vivophenotypes of the mutant. ThesodAmutant was more sensitive to hydrogen peroxide in terms of both its growth and viability than was the wild type. The ability to form a biofilm was weakened in thesodAmutant. ThesodAmutant was significantly more easily phagocytosed by chicken macrophages than was the wild-type strain. Chicken infection assays revealed significantly attenuated virulence of thesodAmutant compared with the wild type at 24 h postinfection. The virulence phenotype was restored by complementation of thesodAgene. Quantitative real-time reverse transcription-PCR revealed that the inactivation ofsodAreduced the expression of oxidative stress response geneskatE,perR, andosmCbut did not affect the expression ofsodBandsodC. Taken together, our studies indicate that SodA is important for oxidative resistance and virulence of APEC E058.IMPORTANCEAvian colibacillosis, caused by strains of avian pathogenicEscherichia coli, is a major bacterial disease of severe economic significance to the poultry industry worldwide. The virulence mechanisms of APEC are not completely understood. This study investigated the influence of an antioxidant protein, SodA, on the phenotype and pathogenicity of APEC O2 strain E058. This is the first report demonstrating that SodA plays an important role in protecting a specific APEC strain against hydrogen peroxide-induced oxidative stress and contributes to the virulence of this pathotype strain. Identification of this virulence factor will enhance our knowledge of APEC pathogenic mechanisms, which is crucial for designing successful strategies against associated infections and transmission.

Verotoxin-Producing Escherichia coli in Spain: Prevalence, Serotypes, and Virulence Genes of O157:H7 and Non-O157 VTEC in Ruminants, Raw Beef Products, and Humans

2003 ◽  
Vol 228 (4) ◽  
pp. 345-351 ◽  
Author(s):  
Jorge Blanco ◽  
Miguel Blanco ◽  
Jesus E. Blanco ◽  
Azucena Mora ◽  
Enrique A. Gonzalez ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Virulence Factor ◽  
Intestinal Mucosa ◽  
Virulence Genes ◽  
Chromosomal Gene ◽  
E Coli ◽  
Beef Products

In Spain, as in many other countries, verotoxin-producing Escherichia coli (VTEC) strains have been frequently isolated from cattle, sheep, and foods. VTEC strains have caused seven outbreaks in Spain (six caused by E. coli O157:H7 and one by E. coli O111:H– [nonmotile]) in recent years. An analysis of the serotypes indicated serological diversity. Among the strains isolated from humans, serotypes O26:H11, O111:H–, and O157:H7 were found to be more prevalent. The most frequently detected serotypes in cattle were O20:H19, O22:H8, O26:H11, O77:H41, O105:H18, O113:H21, O157:H7, O171:H2, and OUT (O untypeable):H19. Different VTEC serotypes (e.g., O5:H–, O6:H10, O91:H–, O117:H–, O128:H–, O128:H2, O146:H8, O146:H21, O156:H–, and OUT:H21) were found more frequently in sheep. These observations suggest a host serotype specificity for some VTEC. Numerous bovine and ovine VTEC serotypes detected in Spain were associated with human illnesses, confirming that ruminants are important reservoirs of pathogenic VTEC. VTEC can produce one or two toxins (VT1 and VT2) that cause human illnesses. These toxins are different proteins encoded by different genes. Another virulence factor expressed by VTEC is the protein intimin that is responsible for intimate attachment of VTEC and effacing lesions in the intestinal mucosa. This virulence factor is encoded by the chromosomal gene eae. The eae gene was found at a much less frequency in bovine (17%) and ovine (5%) than in human (45%) non-O157 VTEC strains. This may support the evidence that the eae gene contributes significantly to the virulence of human VTEC strains and that many animal non-O157 VTEC strains are less pathogenic to humans.

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