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The pathogenesis of Behçet's disease (BD) is not fully understood and immunological abnormalities and genetic factors have been investigated. Because serum concentrations of mainly T helper 1 (Th1) type cells have been reported to be increased in BD, we aimed to investigate whether certain cytokine polymorphisms might represent a risk factor for developing BD. We genotyped 80 patients with BD and 105 healthy controls for interleukin (IL)-1 alpha (T/C -889), IL-1 beta (C/T -511, T/C +3962), IL-1R (C/T pst11970), IL-1RA (T/C mspa111100), IL-2 (T/G -330), IL-12 (C/A -1188), interferon (IFN)-gamma (A/T UTR 5644), and TNF-alpha (G/A -238) polymorphisms. Analyses of cytokine polymorphisms were performed with PCR-SSP. The genotype and allele frequencies of the patients and controls were compared and the association between the polymorphisms of the cytokines with the clinical findings was investigated. Genotype distribution showed significant differences between the patients and the controls for the IL-1 alpha -889, IL-1 beta -511, IL-1 beta +3962, IL-1R, IL-12, IFN- gamma, and TNF-alpha cytokines. We didn't observe significant difference in genotypic frequencies of IL-1RA and IL-2 in our study. Comparison of the IL-1 alpha -889, IL 1 beta -511, and IL 1 beta +3962 genotype frequencies showed significant increase in CC genotype between the patients and the controls. The individuals with IL-1R TT polymorphism had a higher risk for BD compared to patients with CT/CC polymorphism. Comparison of IL-12, IFN- gamma, and TNF-alpha, genotype frequencies showed significant increase in CA, AA, and AA genotypes between the patients and controls, respectively. The frequencies of genotypes according to the clinical features of the patients with BD did not show a significant difference (p>0.05). Our study suggests that development of BD might be determined by various cytokine gene polymorphisms. However, further studies on larger numbers of cases are needed before definite conclusions can be drawn.

IntroductionMethicillin-resistant Staphylococcus aureus (MRSA) is one of the most important nosocomial pathogens and is also emerging in Turkish hospitals. The aim of this study was to determine the antimicrobial susceptibility profiles of MRSA isolated from Turkish hospitals.Materials and methodsA total of 397 MRSA strains isolated from 12 hospitals in Turkey were included to present study. Antimicrobial susceptibilities were tested using agar dilution method. Presence of ermA, ermB, ermC, msrA, tetM, tetK, linA and aac-aph genes were studied by PCR.ResultsAll strains were susceptible to vancomycin and linezolid. The susceptibility rates for fusidic acid, lincomycin, erythromycin, tetracyclin, gentamycin, kanamycin, and, ciprofloxacin were 91.9%, 41.1%, 27.2%, 11.8%, 8.5%, 8.3% and 6.8%, respectively. Lincomycin inactivation was positive for 3 isolates. Of 225 erythromycin resistant isolates 48 had ermA, 20 had ermC, and 128 had ermA-C. PCR was negative for 15 strains. Of 3 isolates with lincomycin inactivation one had linA and msrA. Of 358 gentamycin resistant isolates 334 had aac-aph and 24 were negatives. Among 350 tetracyclin resistant isolates 314 had tetM. Of 36 tetM negative isolates 10 had tetK.ConclusionMRSA isolates from Turkish hospitals were multiresistant to antimicrobials. Quinolone and gentamycin resistance levels were high and macrolide and lincosamide resistance were relatively low. Susceptibility rates for fusidic asid were high. Linezolide and vancomycin resistance are not emerged. The most common resistance genes were ermA, tetM and aac-aph. Evolution of antimicrobial susceptibilities and resistance genes profiles of MRSA isolates should be surveyed at regional and national level for accurate treatment of patients and to control dissemination of resistance genes.

In this study, we have evaluated the broth microdilution method (BMM) 100, 100, 96.9, and 90.2%, while specificity was 100, 85.7, 90.9, and 100% for INH, RIF, STR, and ETM, respectively

We developed two colorimetric methods for the detection of vancomycin-and oxacillin-resistant Staphylococcus aureus in <6 h: (i) a nitrate reductase assay and (ii) a resazurin microplate method. MICs agreed with results obtained by CLSI methods for oxacillin. However, detection of vancomycin resistance required a larger inoculum. These methods may be recommended for the detection of vancomycin-and oxacillin-resistant S. aureus.

In general, resistance to fluoroquinolones (FQs) in gram-negative bacteria is acquired either by mutations in DNA gyrase and topoisomerase IV or by active export of the agents via antibiotic efflux pumps. Reduced porin expression is also proposed to be another mechanism leading to resistance. In this study, interaction between levofloxacin, ofloxacin, and ciprofloxacin with MC-207,110 (multidrug efflux pump inhibitor) was investigated by a checkerboard assay using Pseudomonas aeruginosa. Levofloxacin, ofloxacin, and ciprofloxacin were tested at different concentrations (0.06–64 µg/ml) and MC-207,110 was tested at a concentration range of 4–128 µg/ml. In the presence of MC-207,110 (at 128, 64, 32, 16 µg/ml) resistance to FQs was inhibited significantly and MIC values were decreased, except at 8 and 4 µg/ml of MC-207,110. When MC-207,110 was used, resistance of P. aeruginosa to FQs in vitro was inhibited significantly, suggesting that MC-207,110 may be useful for use in clinical treatment protocols to overcome FQs resistance.

Treatment of multidrug resistant (MDR) Acinetobacter baumannii infections causes some problems as a result of possessing various antibacterial resistance mechanisms against available antibiotics. Combination of antibiotics, acting by different mechanisms, is used for the treatment of MDR bacterial infections. It is an important factor to determine synergy or antagonism between agents in the combination for the constitution of effective therapy. The study aimed to determine In vitro interactions interpreted according to calculated fractional inhibitory concentration (FIC) index between sulbactam and ceftazidime, ceftriaxone, cefepime, ciprofloxacin, gentamicin, meropenem, tigecycline, and colistin. Ten clinical isolates of A. baumannii were tested for determination of synergistic effects of sulbactam with different antimicrobial combinations. Minimal inhibitory concentration (MIC) values of both sulbactam and combined antibiotics decreased 2- to 128-fold. Synergy and partial synergy were determined in combination of sulbactam with ceftazidime and gentamicin (FIC index: ≤ 0.5 or >0.5 to <1) and MIC values of both ceftazidime and gentamicin for five isolates fell down below the susceptibility break point. Similarly, MIC value of ciprofloxacin for six ciprofloxacin resistant isolates was determined as below the susceptibility break point in combination. However, all isolates were susceptible to colistin and tigecycline, MIC values of both were decreased in combination with sulbactam. Although synergistic and partial synergistic effects were observed in the combination of sulbactam and ceftriaxone, all isolates remained resistant to ceftriaxone. The effect of cefepime-sulbactam combination was synergy in five, partial synergy in one and indifferent in four isolates. Meropenem and sulbactam showed a partial synergistic effect (FIC index: >0.5 to <1) in three, an additive effect (FIC index: 1) in one and an indifferent effect (FIC index: >1-2) in six isolates. Antagonism was not determined in any combination for clinical A. baumannii isolates in the study. In conclusion, sulbactam is a good candidate for combination treatment regimes for MDR A. baumannii infections.

In this study, we have evaluated the broth microdilution method (BMM) 100, 100, 96.9, and 90.2%, while specificity was 100, 85.7, 90.9, and 100% for INH, RIF, STR, and ETM, respectively