High occurrence of cyclosporiasis in Istanbul, Turkey, during a dry and warm summer

We evaluated the incidence of Cyclospora cayetanensis in immunocompetent, diarrheic patients during the summers of 2006-2009 in Istanbul. Stools from 1876 patients were examined using microscopic techniques. Cyclospora oocysts were observed in wet preparations by light and epifluorescence microscopy and in fecal smears that were stained by Kinyoun's modified acid-fast stain. Characteristic Cyclospora oocysts were observed in 2 patients in 2006, 17 in 2007, and one in 2009. Samples positive for Cyclospora were further analyzed by a single step polymerase chain reaction (PCR) with Cyclospora-specific primers from the ITS-1 region of the genome

The mgrB gene as a key target for acquired resistance to colistin in Klebsiella pneumoniae

Objectives Alterations in the PhoPQ two-component regulatory system may be associated with colistin resistance in Klebsiella pneumoniae. MgrB is a small transmembrane protein produced upon activation of the PhoPQ signalling system, and acts as a negative regulator on this system. We investigated the role of the MgrB protein as a source of colistin resistance in a series of K. pneumoniae.Methods Colistin-resistant K. pneumoniae isolates were recovered from hospitalized patients worldwide (France, Turkey, Colombia and South Africa). The mgrB gene was amplified and sequenced. A wild-type mgrB gene was cloned and the corresponding recombinant plasmid was used for complementation assays. Clonal diversity was evaluated by MLST and Diversilab analysis.Results Of 47 colistin-resistant isolates, 12 were identified as having a mutated mgrB gene. Five clonally unrelated isolates had an mgrB gene truncated by an IS5-like IS, while one clone also harboured an insertional inactivation at the exact same position of the mgrB gene, but with ISKpn13. Another clone harboured an insertional inactivation due to ISKpn14 at another location of the mgrB gene. Two clonally related isolates harboured an IS (IS10R) in the promoter region of mgrB. Finally, three clonally unrelated isolates harboured substitutions leading to anticipated stop codon in the MgrB protein. Complementation assays with a wild-type MgrB protein restored full susceptibility to colistin for all colistin-resistant isolates identified with qualitative or quantitative MgrB modifications.Conclusion The inactivation or down-regulation of the mgrB gene was shown to be a source of colistin resistance in K. pneumoniae. Interestingly, identical genetic events were identified among clonally unrelated isolates

The mgrB gene as a key target for acquired resistance to colistin in Klebsiella pneumoniae

Objectives Alterations in the PhoPQ two-component regulatory system may be associated with colistin resistance in Klebsiella pneumoniae. MgrB is a small transmembrane protein produced upon activation of the PhoPQ signalling system, and acts as a negative regulator on this system. We investigated the role of the MgrB protein as a source of colistin resistance in a series of K. pneumoniae. Methods Colistin-resistant K. pneumoniae isolates were recovered from hospitalized patients worldwide (France, Turkey, Colombia and South Africa). The mgrB gene was amplified and sequenced. A wild-type mgrB gene was cloned and the corresponding recombinant plasmid was used for complementation assays. Clonal diversity was evaluated by MLST and Diversilab analysis. Results Of 47 colistin-resistant isolates, 12 were identified as having a mutated mgrB gene. Five clonally unrelated isolates had an mgrB gene truncated by an IS5-like IS, while one clone also harboured an insertional inactivation at the exact same position of the mgrB gene, but with ISKpn13. Another clone harboured an insertional inactivation due to ISKpn14 at another location of the mgrB gene. Two clonally related isolates harboured an IS (IS10R) in the promoter region of mgrB. Finally, three clonally unrelated isolates harboured substitutions leading to anticipated stop codon in the MgrB protein. Complementation assays with a wild-type MgrB protein restored full susceptibility to colistin for all colistin-resistant isolates identified with qualitative or quantitative MgrB modifications. Conclusion The inactivation or down-regulation of the mgrB gene was shown to be a source of colistin resistance in K. pneumoniae. Interestingly, identical genetic events were identified among clonally unrelated isolate

High occurrence of cyclosporiasis in Istanbul, Turkey, during a dry and warm summer

We evaluated the incidence of Cyclospora cayetanensis in immunocompetent, diarrheic patients during the summers of 2006-2009 in Istanbul. Stools from 1876 patients were examined using microscopic techniques. Cyclospora oocysts were observed in wet preparations by light and epifluorescence microscopy and in fecal smears that were stained by Kinyoun's modified acid-fast stain. Characteristic Cyclospora oocysts were observed in 2 patients in 2006, 17 in 2007, and one in 2009. Samples positive for Cyclospora were further analyzed by a single step polymerase chain reaction (PCR) with Cyclospora-specific primers from the ITS-1 region of the genome

Acute prostatitis as an uncommon presentation of brucellosis

The present report concerns a 46-year-old man who presented with acute prostatitis due to Brucella melitensis infection. He was first treated with doxycycline and ciprofloxacin, but after 3 months he was admitted again with the same diagnosis. The relapse was probably related to ciprofloxacin use, or the length of treatment not being sufficient. The patient was successfully treated with a combination of doxycycline and rifampin for 3 months. In conclusion, prostatitis due to Brucella, such as spondylitis, meningoencephalitis and endocarditis, should be treated for longer courses

In vitro activities of colistin, tigecycline and tobramycin, alone or in combination, against carbapenem-resistant Enterobacteriaceae strains

The aim of this study was to investigate the activities of various antibiotics, alone or in combination, against carbapenem-resistant Enterobacteriaceae (CRE). Minimum inhibitory concentrations (MICs) of meropenem, colistin, tigecycline and tobramycin were determined by microbroth dilution against 40 clinical strains. Carbapenemase-encoding genes were detected by PCR using specific primers. The in vitro synergistic activities of tigecycline, colistin and tobramycin in double antibiotic combinations were determined by the microbroth chequerboard technique, and results were interpreted using the fractional inhibitory concentration index (FICI). To confirm the results acquired by the chequerboard method, time-kill assays were performed on eight isolates representing four different susceptibility patterns. Based on MIC90 values, colistin was the most potent agent, followed by tigecycline and tobramycin. According to PCR studies, carbapenem resistance in tested Enterobacteriaceae isolates was most often mediated by OXA-48-type carbapenemases. With an FICI of <= 0.5 as the cut-off, synergistic interactions were most frequent with tigecycline + tobramycin (30%); other results for synergistic interactions were 23% for colistin + tobramycin and 9% for colistin + tigecycline. By time-kill assays, all tested antibiotic combinations demonstrated synergistic activity against at least three of the eight strains at 1x or 4x MIC. Overall, the combinations used in this study were effective regimens, demonstrating synergy or no interaction (indifference) against all tested strains. No antagonism was observed with either of the techniques. The findings of this study might play a useful role in selecting appropriate combinations when a single agent is inadequate against CRE strains. (C) 2015 International Society for Chemotherapy of Infection and Cancer. Published by Elsevier Ltd. All rights reserved