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Helicobacter pylori exists in two morphologic forms: spiral shaped and coccoid. The nonculturable coccoid forms were believed to be the morphologic manifestations of cell death for a long time. However, recent studies indicate the viability of such forms. This form of H. pylori is now suspected to play a role in the transmission of the bacteria and is partly responsible for relapse of infection after antimicrobial treatment. Urease activity of H. pylori is an important maintenance factor. Determination of urease activity and possible mutations in the DNA sequences of coccoid bacteria will hence contribute to the understanding of pathogenesis of infections, which these forms might be responsible for. In this study, our aim was to analyze the urease activity and investigate the urease gene sequences of coccoid H. pylori forms induced by different factors with respect to the spiral form. For this purpose, the urease activities of H. pylori NCTC 11637 standard strain and two clinical isolates were examined before and after transformation of the cells to coccoid forms by different methods such as exposure to amoxicillin, aerobiosis, cold starvation, and aging. The effects of these conditions on the urease gene were examined by the amplification of 411-bp ureA gene and 115-bp ureB gene regions by PCR technique and sequencing of the ureA gene. The urease activities of coccoid cells were found to be lower than those of the spiral form. ureA and ureB gene regions were amplified in all coccoid cells by PCR. Inducing the change to coccoid form by different methods was found to have no effect on the nucleotide sequence of the ureA gene. These results show that the urease gene region of coccoid H. pylori is highly protected under various mild environmental conditions.

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We have documented the characteristics of the dominant MRSA clone in our hospital, which was a PVL (-), sasX (-) ST239 clone carrying sea (+) with type-III SCCmec, and type-1 agr locus.

E.coli ST131 is a global concern because of its high multi-drug resistance and several virulence factors. In this study, the contribution of acrAB-TolC efflux system of E.coli ST131 to fluoroquinolone resistance was evaluated. A total of non-repetitive 111 ciprofloxacin resistant E.coli isolates were included in the study. Multi-locus sequence typing (MLST) was used for genotyping. Expressions of acrA, acrB and tolC efflux pump genes were measured by RT-PCR. Mutations in marA, gyrA, parC, and aac(6')-lb-cr positivity were studied by Sanger sequencing. Sixty-four (57.7%) of the isolates were classified as ST131 and 52(81.3%) of the ST131 isolates belonged to H30-Rx subclone. In ST131, CTX-M 15 positivity (73%) and aac(6')-lb-cr carriage (75%) were significantly higher than non-ST131 (12.8% and 51%, respectively) (p<0.05). The ampicillin-sulbactam (83%) resistance was higher, gentamicin resistance (20%) was lower in ST131 than non-ST131 (64% and 55%, respectively) (p=0.001 and p=0.0002). Number of the isolates with MDR or XDR profiles did not differ in both groups. Multiple in-dels (up to 16) were recorded in all quinolone resistant isolates. However, marA gene was more overexpressed in ST131 compared to non-ST131 (median 5.98 vs 3.99; P=0.0007). Belonging to H30-Rx subclone, isolation site, ciprofloxacin MIC values did not correlate with efflux pump expression. In conclusion, the marA regulatory gene of AcrAB-TolC efflux pump system has a significant impact on quinolone resistance and progression to MDR profile in ST131 clone. Efflux pump inhibitors might be alternative drugs for the treatment of infections caused by E.coli ST131 if used synergistically in combination with antibiotics.