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  • American Society for Microbiology  (13)
  • Medicine  (13)
  • 1
    Online Resource
    Online Resource
    American Society for Microbiology ; 2010
    In:  Journal of Clinical Microbiology Vol. 48, No. 10 ( 2010-10), p. 3532-3538
    In: Journal of Clinical Microbiology, American Society for Microbiology, Vol. 48, No. 10 ( 2010-10), p. 3532-3538
    Abstract: We determined the groESL sequences of three species of nutritionally variant streptococci ( Abiotrophia defectiva , Granulicatella adiacens , and Granulicatella elegans ) and three Gemella species ( Gemella morbillorum , Gemella haemolysans , and Gemella sanguinis ). The nucleotide sequence similarities between the groES and groEL genes of the above genera were 41.7 to 85.9% and 63.7 to 84.3%, respectively. The intraspecies similarities of groESL sequences for the isolates of Abiotrophia and Granulicatella species were 94.4 to 97.8% for groES and 94.0 to 98.2% for groEL . For Ge. morbillorum and Ge. sanguinis , all strains showed the same groESL spacer length (8 bp), and sequence identities within species were 〉 97.8% for groES and 〉 96.1% for groEL . However, higher intraspecies heterogeneity was observed in Ge. haemolysans . Phylogenetic analysis of groEL sequences separated the 6 isolates of Ge. haemolysans into two subgroups. Among these isolates, three isolates with the same groESL spacer region length (45 bp) clustered together but were distant from the ATCC reference strain (with a spacer length of 8 bp). The remaining three isolates, with a spacer length of 50 or 8 bp, clustered together. Although 16S rRNA gene sequence analysis did not provide enough discrimination for the 6 Ge. haemolysans isolates, rpoB gene sequence analysis supported the subgrouping. Based on the obtained groESL sequences, we developed a multiplex PCR that enables simple, rapid, and accurate identification of Abiotrophia , Granulicatella , and Gemella at the genus level. This assay would be helpful for identifying these fastidious and slow-growing organisms in clinical laboratories.
    Type of Medium: Online Resource
    ISSN: 0095-1137 , 1098-660X
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2010
    detail.hit.zdb_id: 1498353-9
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  • 2
    Online Resource
    Online Resource
    American Society for Microbiology ; 2013
    In:  Antimicrobial Agents and Chemotherapy Vol. 57, No. 11 ( 2013-11), p. 5737-5739
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 57, No. 11 ( 2013-11), p. 5737-5739
    Abstract: Nucleotide sequencing of the fusB -flanking regions in two fusidic acid-resistant Staphylococcus epidermidis isolates with the type IV aj1 -leader peptide (LP)- fusB structure (lacking aj1 ) revealed that their fusB gene was located on novel phage-related islands inserted downstream of smpB and are here referred to as SeRI fusB -3692 and SePI fusB -857 . The novel SePI fusB -857 structure was followed by SeCI 857 , forming a composite pathogenicity island which contained a putative virulence gene, vapE . The linkage of fusB and vapE may contribute to bacterial adaption.
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2013
    detail.hit.zdb_id: 1496156-8
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  • 3
    Online Resource
    Online Resource
    American Society for Microbiology ; 2010
    In:  Antimicrobial Agents and Chemotherapy Vol. 54, No. 12 ( 2010-12), p. 4985-4991
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 54, No. 12 ( 2010-12), p. 4985-4991
    Abstract: A total of 71 fusidic acid-resistant Staphylococcus aureus (45 methicillin-resistant and 26 methicillin-susceptible) isolates were examined for the presence of resistance determinants. Among 45 fusidic acid-resistant methicillin-resistant S. aureus (MRSA), isolates, 38 (84%) had fusA mutations conferring high-level resistance to fusidic acid (the MIC was ≥128 μg/ml for 22/38), none had fusB , and 7 (16%) had fusC . For 26 fusidic acid-resistant methicillin-susceptible S. aureus (MSSA), only 3 possessed fusA mutations, but 15 (58%) had fusB and 8 (31%) had fusC . Low-level resistance to fusidic acid (MICs ≤ 32 μg/ml) was found in most fusB - or fusC -positive isolates. For 41 isolates (38 MRSA and 3 MSSA), with fusA mutations, a total of 21 amino acid substitutions in EF-G ( fusA gene) were detected, of which R76C, E444K, E444V, C473S, P478S, and M651I were identified for the first time. The nucleotide sequencing of fusB and flanking regions in an MSSA isolate revealed the structure of partial IS 257 - aj1 -LP- fusB - aj2 - aj3 -IS 257 -partial blaZ , which is identical to the corresponding region in pUB101, and the rest of fusB -carrying MSSA isolates also show similar structures. On the basis of spa and staphylococcal cassette chromosome mec element (SCC mec ) typing, two major genotypes, spa type t037-SCC mec type III (t037-III; 28/45; 62%) and t002-II (13/45; 29%), were predominant among 45 MRSA isolates. By pulsed-field gel electrophoresis analysis, 45 MRSA isolates were divided into 12 clusters, while 26 MSSA isolates were divided into 15 clusters. Taken together, the distribution of fusidic acid resistance determinants ( fusA mutations, fusB , and fusC ) was quite different between MRSA and MSSA groups.
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2010
    detail.hit.zdb_id: 1496156-8
    SSG: 12
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    American Society for Microbiology ; 2014
    In:  Antimicrobial Agents and Chemotherapy Vol. 58, No. 2 ( 2014-02), p. 1224-1227
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 58, No. 2 ( 2014-02), p. 1224-1227
    Abstract: A high prevalence of fusC (16/46, 59%) was found in fusidic acid-resistant methicillin-resistant Staphylococcus aureus isolates collected from 2008 to 2010. Nucleotide sequencing of fusC and flanking regions revealed a novel staphylococcal cassette chromosome (SCC) structure, SCC fusC , which was integrated into rlmH and located upstream from SCC mec . The SCC fusC element contained speG , which may contribute to the polyamine resistance.
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2014
    detail.hit.zdb_id: 1496156-8
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  • 5
    Online Resource
    Online Resource
    American Society for Microbiology ; 2011
    In:  Antimicrobial Agents and Chemotherapy Vol. 55, No. 12 ( 2011-12), p. 5842-5849
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 55, No. 12 ( 2011-12), p. 5842-5849
    Abstract: To understand the high prevalence of fusB genes in fusidic acid-resistant Staphylococcus epidermidis , analysis of resistance elements in 34 isolates was performed. First, sequence analysis of the aj1 -LP- fusB region indicated that at least three types were present. Type I contained full-length aj1 , type II contained a partial aj1 truncated from nucleotide position 93 to 421, and type III contained a more truncated aj1 that retained only the last 37 bp. Isolates with type I or type II aj1 displayed slightly higher levels of resistance to fusidic acid (MICs, 8 to 32 μg/ml) than did those with type III aj1 (MICs, 4 to 16 μg/ml). Subsequent sequencing of the flanking regions of fusB from four selected isolates carrying different types of aj1 -LP- fusB regions revealed that the fusB genes were all located on phage-related resistance islands (RIs), referred to as SeRI fusB -2793 , SeRI fusB -704 , SeRI fusB -5907 , and SeRI fusB -7778 , respectively. Among them, three islands (SeRI fusB -2793 , SeRI fusB -704 , and SeRI fusB -5907 ) were located downstream of groEL (corresponding to the 44-min position based on Staphylococcus aureus whole genomic sequences), and one (SeRI fusB -7778 ) was located downstream of rpsR (corresponding to the 8-min position). All of the RIs were inserted into integrase-recognized att sites. Among 34 isolates, the insertion sites of fusB RIs were mostly (28/34, 82%) located downstream of groEL and two were located downstream of rpsR , but four remained unidentified. The pulsotype distribution indicated that fusB -containing S. epidermidis isolates were heterogeneous. In conclusion, the fusB resistance determinant in S. epidermidis was highly associated with phage-related RIs. This is the first report of fusB RI in S. epidermidis .
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2011
    detail.hit.zdb_id: 1496156-8
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    SSG: 15,3
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  • 6
    In: Journal of Clinical Microbiology, American Society for Microbiology, Vol. 48, No. 8 ( 2010-08), p. 2975-2977
    Abstract: A total of 274 Streptococcus dysgalactiae subsp. equisimilis isolates was analyzed by emm typing and by determining the organization of their mgrC loci. Three of the most frequent emm types were stG485.0 (45/274, 16.4%), stG6.1 (43/274, 15.7%), and stC839.0 (32/274, 11.7%), in decreasing order. The cpdB -positive mgrC locus appears to be predominant in some emm types.
    Type of Medium: Online Resource
    ISSN: 0095-1137 , 1098-660X
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2010
    detail.hit.zdb_id: 1498353-9
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  • 7
    Online Resource
    Online Resource
    American Society for Microbiology ; 2016
    In:  Antimicrobial Agents and Chemotherapy Vol. 60, No. 10 ( 2016-10), p. 6108-6114
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 60, No. 10 ( 2016-10), p. 6108-6114
    Abstract: We determined the resistance determinants in 274 erythromycin-resistant methicillin-susceptible Staphylococcus aureus (MSSA) isolates during a 13-year period, 2000 to 2012. The resistance phenotypes, inducible macrolide-lincosamide-streptogramin (iMLS), constitutive MLS (cMLS), and macrolide-streptogramin (MS) resistance phenotypes, were examined by a double-disk diffusion D test. The ermB gene was more frequent (35%; 97/274) than ermC (27%; 75/274) or ermA (21%; 58/274). All 97 ermB -positive isolates harbored Tn 551 and IS 1216V . The majority (89/97) of ermB -positive isolates displayed the cMLS phenotype and carried mobile element structure (MES)-like structures, which has been previously reported in sequence type 59 (ST59) methicillin-resistant S. aureus (MRSA). The remaining 8 ermB -carrying isolates, belonging to ST7 ( n = 4), ST5 ( n = 3), and ST59 ( n = 1), were sasK intact and did not carry MES-like structures. Unlike a MES-like structure that was located on the chromosome, the ermB elements on sasK -intact isolates were located on plasmids by S1 nuclease pulsed-field gel electrophoresis (PFGE) analysis and conjugation tests. Sequence data for the ermB -containing region (14,566 bp) from ST59 NTUH_3874 revealed that the best match was a Tn 1546 -like element in plasmid pMCCL2 DNA (GenBank accession number AP009486 ) of Macrococcus caseolyticus . Tn 1546 is recognized as an enterococcal transposon and was known from the vancomycin resistance gene cluster in vancomycin-resistant Enterococcus (VRE). So far, acquisitions of Tn 1546 in S. aureus have occurred in clonal complex 5 (CC5) MRSA, but not in MSSA. This is the first report that MSSA harbors an Enterococcus faecium -originated ermB -positive Tn 1546 -like element located on a plasmid.
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
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    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2016
    detail.hit.zdb_id: 1496156-8
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  • 8
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 60, No. 8 ( 2016-08), p. 5006-5009
    Abstract: We analyzed the staphylococcal cassette chromosome mec (SCC mec ) types of 143 fusidic acid- and methicillin-resistant Staphylococcus epidermidis isolates. The most frequent SCC mec type was SCC mec III/SCC Hg (53%), followed by SCC mec IV (29%). Clonal spreading of SCC mec III/SCC Hg strains contributed to the increased prevalence of SCC mec III. A novel non- mec SCC structure, SCC 7684 , adjacent to SCC mec III, which carries a new ccrC allotype ( ccrC3 allele 1) and contains heavy metal resistance genes, was identified in 14 isolates.
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2016
    detail.hit.zdb_id: 1496156-8
    SSG: 12
    SSG: 15,3
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  • 9
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 55, No. 3 ( 2011-03), p. 1123-1129
    Abstract: The accuracy of genotypic resistance to levofloxacin ( gyrA mutations) and its agreement with treatment outcomes after levofloxacin-based therapy have not been reported. We aimed to assess the correlation. Helicobacter pylori strains isolated from patients who received levofloxacin-based and clarithromycin-based triple therapies in a previous randomized trial were analyzed for point mutations in gyrA and 23S rRNA. PCR followed by direct sequencing was used to assess the gyrA and 23S rRNA mutations. An agar dilution test was used to determine the MICs of clarithromycin and levofloxacin. We found that the agreement between genotypic and phenotypic resistance to levofloxacin was best when the MIC breakpoint was 〉 1 μg/ml (kappa coefficient, 0.754). The eradication rates in patients with and without gyrA mutations were 41.7% and 82.7%, respectively ( P = 0.003). The agreement between genotypic and phenotypic resistance to clarithromycin was best when the MIC breakpoint was 〉 2 μg/ml (kappa, 0.694). The eradication rates in patients with and without 23S rRNA mutations were 7.7% and 93.5%, respectively ( P 〈 0.001). The agreements (kappa coefficient) between therapeutic outcomes after clarithromycin-based triple therapy and genotypic and phenotypic resistance were 0.671 and 0.356, respectively. The agreements (kappa coefficient) between therapeutic outcomes after levofloxacin-based triple therapy and genotypic and phenotypic resistance were 0.244 and 0.190, respectively. In conclusion, gyrA and 23S rRNA mutations in H. pylori strains appeared to be better markers than phenotypic resistance in the prediction of treatment outcomes. The optimal breakpoints for levofloxacin and clarithromycin resistance appeared to be 〉 1 μg/ml and 〉 2 μg/ml, respectively.
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2011
    detail.hit.zdb_id: 1496156-8
    SSG: 12
    SSG: 15,3
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  • 10
    In: Journal of Clinical Microbiology, American Society for Microbiology, Vol. 49, No. 3 ( 2011-03), p. 1083-1089
    Abstract: An outbreak of human immunodeficiency virus (HIV) infection occurred among injecting drug users (IDU) in Taiwan between 2003 and 2006, when an extremely high prevalence of hepatitis C virus (HCV) infection was also detected. To determine whether clusters of hepatitis D virus (HDV) infection occurred in this outbreak, 4 groups of subjects were studied: group 1, HIV-infected IDU ( n = 904); group 2, HIV-infected non-IDU ( n = 880); group 3, HIV-uninfected IDU ( n = 211); and group 4, HIV-uninfected non-IDU ( n = 1,928). The seroprevalence of hepatitis B virus (HBV) was 19.8%, 18.4%, 17.1%, and 6.7%, and HDV seroprevalence among HBV carriers was 75.4%, 9.3%, 66.7%, and 2.3%, for groups 1, 2, 3, and 4, respectively. Ninety-nine of 151 (65.6%) HDV-seropositive IDU had HDV viremia: 5 were infected with HDV genotype I, 41 with genotype II, 51 with genotype IV, and 2 with genotypes II and IV. In the phylogenetic analysis, only one cluster of 4 strains within the HDV genotype II was identified. Among patients with HCV viremia, a unique cluster within genotype 1a was observed; yet, patients within this cluster did not overlap with those observed in the HDV phylogenetic analysis. In summary, although IDU had a significantly higher HDV seroprevalence, molecular epidemiologic investigations did not support that HDV was introduced at the same time as HCV among IDU.
    Type of Medium: Online Resource
    ISSN: 0095-1137 , 1098-660X
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2011
    detail.hit.zdb_id: 1498353-9
    SSG: 12
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