27 research outputs found

    Dendrogram displaying the PFGE profiles of the 43 isolates.

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    <p>The strain number, origin, source, sequence type (ST), and H<sub>2</sub>S phenotype are shown for each strain. +, H<sub>2</sub>S-producing isolate; −, non-H<sub>2</sub>S-producing isolate.</p

    Sequence alignment of the <i>phs</i> gene and the protein.

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    <p>A nonsense mutation at position 208 of the <i>phsA</i> gene results in the replacement of a sense codon (CAG) with a termination codon (UAG) leading to the premature termination of <i>phsA</i>. The first sequence, <i>phsA</i>, is based on <i>S</i>. enterica serotype Typhimurium strain LT2 (GenBank AE006468). *, termination codon; +, H<sub>2</sub>S-producing isolate; −, non-H<sub>2</sub>S-producing isolate.</p

    Data_Sheet_1_A Novel mcr-1 Variant Carried by an IncI2-Type Plasmid Identified From a Multidrug Resistant Enterotoxigenic Escherichia coli.DOCX

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    <p>In this study, we discovered a novel mobilized colistin resistance (mcr-1) gene variant, named mcr-1.9, which was identified in a colistin-resistant enterotoxigenic Escherichia coli (ETEC) strain from a clinical diarrhea case. The mcr-1.9 gene differs from mcr-1 at position 1036 due to a single nucleotide polymorphism (G→A), which results in an aspartic acid residue being replaced by an asparagine residue (Asp346→Asn) in the MCR-1 protein sequence. Antimicrobial susceptibility testing showed that the mcr-1.9-harboring ETEC strain is resistant to colistin at a minimum inhibitory concentration of 4 μg/ml. Plasmid profiling and conjugation experiments also suggest that the mcr-1.9 variant can be successfully transferred into the E. coli strain J53, indicating that the gene is located on a transferable plasmid. Bioinformatics analysis of data obtained from genome sequencing indicates that the mcr-1.9 gene is located on a 64,005 bp plasmid which has been named pEC26. This plasmid was found to have high similarity to the mcr-1-bearing IncI2-type plasmids pWF-5-19C (99% identity and 99% coverage) and pmcr1-IncI2 (99% identity and 98% coverage). The mcr-1.9-harboring ETEC also shows multidrug resistance to nine classes of antibiotics, and contains several virulence and antimicrobial-resistance genes suggested by the genome sequence analysis. Our report is the first to identify a new mcr-1 variant in an ETEC isolated from a human fecal sample, raising concerns about the existence of more such variants in human intestinal flora. Therefore, we believe that an undertaking to identify new mcr-1 variants in the bacterial communities of human intestines is of utmost importance, and that measures need to be taken to control the spread of mcr-1 and its variants in human intestinal microflora.</p

    Dominant serotype distribution and antimicrobial resistance profile of <i>Shigella</i> spp. in Xinjiang, China

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    <div><p><i>Shigella</i> represents one of the major diarrhea-inducing pathogens threatening public health, but its prevalence and antimicrobial resistance profile in Xinjiang Uygur Autonomous region, China, remains unclear. We conducted comprehensive investigation of <i>Shigella</i> serotype distribution and antimicrobial resistance pattern in Xinjiang, identifying 458 <i>Shigella</i> isolates between 2008 to 2014. <i>Shigella flexneri</i> was identified as predominant species, and several <i>S</i>. <i>flexneri</i> serotypes were isolated, including atypical serotypes 1c, 2c, and 4s. Dominant <i>S</i>. <i>flexneri</i> serotypes were 2a, 1b, 2b, and Xv, different from those generally dominant in China. A hybrid serotype pattern was observed, which included the major Chinese serotypes (2a, Xv) and those predominant in Pakistan (1b, 2b). <i>Shigella sonnei</i> was shown to have a lower frequency compared with that generally observed in China, but an increasing trend of infections associated with this pathogen was observed. Furthermore, a high frequency of drug resistance and different <i>Shigella</i> antimicrobial resistance patterns were demonstrated as well, including very severe resistance phenotypes, such as multidrug resistance and resistance to frontline antibiotics. Seventy-five cephalosporin-resistant <i>Shigella</i> isolates were frequently identified with the resistance determinants that can undergo horizontal transfer, such as <i>bla</i><sub>OXA</sub>, <i>bla</i><sub>TEM</sub>, <i>bla</i><sub>CTX-M</sub>, and integrons, facilitating the development of cephalosporin resistance among <i>Shigella</i> subtypes. Additionally, genetic analyses demonstrated that all 86 quinolone-resistant <i>S</i>. <i>flexneri</i> isolates possess 3–4 mutation sites in quinolone resistance-determining regions, primarily contributing to their resistance to quinolone. However, <i>S</i>. <i>sonnei</i> isolates were not shown to be quinolone resistant. Co-resistance to cephalosporins and quinolones was detected in 17 <i>S</i>. <i>flexneri</i> isolates, and these isolates were additionally multidrug resistant and carried β-lactamase genes and quinolone-resistance determinants. As is demonstrated in this study, dominant serotypes of <i>Shigella</i> were distributed in unique trend with dangerous drug resistance patterns. Novel strategies are urgently required to prevent the development of drug resistance among diarrhea-inducing pathogens.</p></div

    An outbreak of acute respiratory disease caused by a virus associated RNA II gene mutation strain of human adenovirus 7 in China, 2015

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    <div><p>Human adenovirus 7 (HAdV-7) strains are a major cause of acute respiratory disease (ARD) among adults and children, associated with fatal pneumonia. An ARD outbreak caused by HAdV-7 that involved 739 college students was reported in this article. To better understand the underlying cause of this large-scale epidemic, virus strains were isolated from infected patients and sequence variations of the whole genome sequence were detected. Evolutionary trees and alignment results indicated that the major capsid protein genes hexon and fibre were strongly conserved among serotype 7 strains in China at that time. Instead, the HAdV-7 strains presented three thymine deletions in the virus associated RNA (VA RNA) II terminal region. We also found that the mutation might lead to increased mRNA expression of an adjacent gene, L1 52/55K, and thus promoted faster growth. These findings suggest that sequence variation of VA RNA II gene was a potential cause of such a severe HAdV-7 infection and this gene should be a new-emerging factor to be monitored for better understanding of HAdV-7 infection.</p></div

    Data_Sheet_2_A Novel mcr-1 Variant Carried by an IncI2-Type Plasmid Identified From a Multidrug Resistant Enterotoxigenic Escherichia coli.ZIP

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    <p>In this study, we discovered a novel mobilized colistin resistance (mcr-1) gene variant, named mcr-1.9, which was identified in a colistin-resistant enterotoxigenic Escherichia coli (ETEC) strain from a clinical diarrhea case. The mcr-1.9 gene differs from mcr-1 at position 1036 due to a single nucleotide polymorphism (G→A), which results in an aspartic acid residue being replaced by an asparagine residue (Asp346→Asn) in the MCR-1 protein sequence. Antimicrobial susceptibility testing showed that the mcr-1.9-harboring ETEC strain is resistant to colistin at a minimum inhibitory concentration of 4 μg/ml. Plasmid profiling and conjugation experiments also suggest that the mcr-1.9 variant can be successfully transferred into the E. coli strain J53, indicating that the gene is located on a transferable plasmid. Bioinformatics analysis of data obtained from genome sequencing indicates that the mcr-1.9 gene is located on a 64,005 bp plasmid which has been named pEC26. This plasmid was found to have high similarity to the mcr-1-bearing IncI2-type plasmids pWF-5-19C (99% identity and 99% coverage) and pmcr1-IncI2 (99% identity and 98% coverage). The mcr-1.9-harboring ETEC also shows multidrug resistance to nine classes of antibiotics, and contains several virulence and antimicrobial-resistance genes suggested by the genome sequence analysis. Our report is the first to identify a new mcr-1 variant in an ETEC isolated from a human fecal sample, raising concerns about the existence of more such variants in human intestinal flora. Therefore, we believe that an undertaking to identify new mcr-1 variants in the bacterial communities of human intestines is of utmost importance, and that measures need to be taken to control the spread of mcr-1 and its variants in human intestinal microflora.</p

    Table_1_A Novel mcr-1 Variant Carried by an IncI2-Type Plasmid Identified From a Multidrug Resistant Enterotoxigenic Escherichia coli.XLSX

    No full text
    <p>In this study, we discovered a novel mobilized colistin resistance (mcr-1) gene variant, named mcr-1.9, which was identified in a colistin-resistant enterotoxigenic Escherichia coli (ETEC) strain from a clinical diarrhea case. The mcr-1.9 gene differs from mcr-1 at position 1036 due to a single nucleotide polymorphism (G→A), which results in an aspartic acid residue being replaced by an asparagine residue (Asp346→Asn) in the MCR-1 protein sequence. Antimicrobial susceptibility testing showed that the mcr-1.9-harboring ETEC strain is resistant to colistin at a minimum inhibitory concentration of 4 μg/ml. Plasmid profiling and conjugation experiments also suggest that the mcr-1.9 variant can be successfully transferred into the E. coli strain J53, indicating that the gene is located on a transferable plasmid. Bioinformatics analysis of data obtained from genome sequencing indicates that the mcr-1.9 gene is located on a 64,005 bp plasmid which has been named pEC26. This plasmid was found to have high similarity to the mcr-1-bearing IncI2-type plasmids pWF-5-19C (99% identity and 99% coverage) and pmcr1-IncI2 (99% identity and 98% coverage). The mcr-1.9-harboring ETEC also shows multidrug resistance to nine classes of antibiotics, and contains several virulence and antimicrobial-resistance genes suggested by the genome sequence analysis. Our report is the first to identify a new mcr-1 variant in an ETEC isolated from a human fecal sample, raising concerns about the existence of more such variants in human intestinal flora. Therefore, we believe that an undertaking to identify new mcr-1 variants in the bacterial communities of human intestines is of utmost importance, and that measures need to be taken to control the spread of mcr-1 and its variants in human intestinal microflora.</p

    Image_1_A Novel mcr-1 Variant Carried by an IncI2-Type Plasmid Identified From a Multidrug Resistant Enterotoxigenic Escherichia coli.JPEG

    No full text
    <p>In this study, we discovered a novel mobilized colistin resistance (mcr-1) gene variant, named mcr-1.9, which was identified in a colistin-resistant enterotoxigenic Escherichia coli (ETEC) strain from a clinical diarrhea case. The mcr-1.9 gene differs from mcr-1 at position 1036 due to a single nucleotide polymorphism (G→A), which results in an aspartic acid residue being replaced by an asparagine residue (Asp346→Asn) in the MCR-1 protein sequence. Antimicrobial susceptibility testing showed that the mcr-1.9-harboring ETEC strain is resistant to colistin at a minimum inhibitory concentration of 4 μg/ml. Plasmid profiling and conjugation experiments also suggest that the mcr-1.9 variant can be successfully transferred into the E. coli strain J53, indicating that the gene is located on a transferable plasmid. Bioinformatics analysis of data obtained from genome sequencing indicates that the mcr-1.9 gene is located on a 64,005 bp plasmid which has been named pEC26. This plasmid was found to have high similarity to the mcr-1-bearing IncI2-type plasmids pWF-5-19C (99% identity and 99% coverage) and pmcr1-IncI2 (99% identity and 98% coverage). The mcr-1.9-harboring ETEC also shows multidrug resistance to nine classes of antibiotics, and contains several virulence and antimicrobial-resistance genes suggested by the genome sequence analysis. Our report is the first to identify a new mcr-1 variant in an ETEC isolated from a human fecal sample, raising concerns about the existence of more such variants in human intestinal flora. Therefore, we believe that an undertaking to identify new mcr-1 variants in the bacterial communities of human intestines is of utmost importance, and that measures need to be taken to control the spread of mcr-1 and its variants in human intestinal microflora.</p
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