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    Comparison of Conventional Methods, Automated Systems, and DNA Sequence Analysis Methods in the Identification of Corynebacterium afermentans and Corynebacterium mucifaciens Bacteria Isolated from Blood and Catheter Culture Samples
    (Mary Ann Liebert, Inc, 2021) Olmez, Serpil; Tuncer, Ozlem; Parlak, Mehmet; Bicakcigil, Asiye; Gursoy, Nafia Canan; Otlu, Baris; Guducuoglu, Huseyin
    The aim of this study is to compare different methods due to the difficulties in identifying coryneform bacteria to species level and to determine antibiotic resistance profiles. Isolates identified as Turicella otitidis (n:45) by VITEK 2 Compact and Corynebacterium mucifaciens (n:1) by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS), isolated from blood and catheter cultures between 2015 and 2017 were included in the study. For identification of the isolates, conventional tests and 16S rDNA sequence analysis were performed. Antibiotic susceptibilities of the isolates were determined by Etest. The isolates identified as T. otitidis with VITEK 2 Compact could not be identified by MALDI-TOF MS and described as C. mucifaciens/Corynebacterium afermentans spp. by 16S rDNA sequence analysis. One isolate identified as C. mucifaciens by MALDI-TOF MS could not be identified with VITEK 2 Compact and described as C. mucifaciens by 16S rDNA sequence analysis and conventional methods. All isolates (n:45) described as C. mucifaciens/C. afermentans spp. by 16S rDNA sequence analysis were identified as C. afermentans subsp. afermentans with conventional methods. All 45 isolates identified as C. afermentans subsp. afermentans were resistant to penicillin, erythromycin, and clindamycin and were susceptible to vancomycin and daptomycin, whereas 31 (69%) were resistant to trimethoprim-sulfamethoxazole (TMP-SXT). The isolate identified as C. mucifaciens was susceptible to penicillin, vancomycin, daptomycin, and TMP-SXT; it was resistant to erythromycin and clindamycin. In this study, we reported 45 C. afermentans isolates misidentified as T. otitidis in routine laboratory processes. To our knowledge, this is the first study to include the highest number of C. afermentans blood isolates.
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    Hospital Outbreak of a Colistin-Resistant, NDM-1-and OXA-48-Producing Klebsiella pneumoniae: High Mortality from Pandrug Resistance
    (Mary Ann Liebert, Inc, 2018) Guducuoglu, Huseyin; Gursoy, Nafia Canan; Yakupogullari, Yusuf; Parlak, Mehmet; Karasin, Gokhan; Sunnetcioglu, Mahmut; Otlu, Baris
    Colistin resistance causes substantial problems in the treatment of serious infections with carbapenem-resistant (CR) gram-negative bacteria. In this study, we report a fatal hospital outbreak from the spread of a pandrug-resistant Klebsiella pneumoniae clone. An outbreak investigation was conducted after consecutive isolation of nine CR-K. pneumoniae (CR-Kp) strains from eight patients in two intensive care units of a university hospital within 2 weeks. Carbapenem and colistin resistance genes were investigated with PCR, clonal relationships of isolates were studied with pulse-field gel electrophoresis, and multilocus sequence types were determined. The outcomes of the affected patients were analyzed. Genotyping showed a predominant CR-Kp clone consisting of seven strains from six patients. These strains were in ST11 type, an international high-risk clone. They were resistant to all antimicrobials, including colistin, and positive for NDM-1 and OXA-48 carbapenemases, but negative for plasmid-borne colistin resistance genes. One patient had colonization and the remaining five died due to the infection within mean 12 days. No environmental or staff links could be established, and the outbreak was stopped by augmenting infection-control measures. Colistin-resistant K. pneumoniae could clonally expand in the hospital setting, and this spread might be associated with high mortality due to the lack of an appropriate treatment option. Immediate implementation of infection-control measures may be the best way to limit fatal consequences of the spread of such incurable pathogens.