[Detection of plasmid-mediated AmpC beta-lactamase production in Escherichia coli and Klebsiella spp. isolates]. / Escherichia coli ve Klebsiella spp. izolatlarinda plazmid kaynakli AmpC beta-laktamaz üretiminin arastirilmasi

This study was conducted to obtain data about prevalence of plasmid-mediated AmpC (pAmpC), efficacy of various phenotypic tests applied for the detection of pAmpC-mediated resistance and the enzyme types responsible for this resistance. A total of 1316 isolates (1030 Escherichia coli and 286 Klebsiella spp.) obtained from the clinical samples sent to our laboratory between 2008-2011 period, from various inpatient and outpatient clinics and intensive care units, were included in this study. Antimicrobial susceptibility profiles of the isolates were determined by using Kirby-Bauer disk diffusion method. Production of pAmpC was phenotypically investigated by Boronic Acid Inhibition Test (BAIT), Cefoxitin Hodge Test (CHT) and AmpC Disk Test (ACDT) in a total of 36 (2.7%) cefoxitin-resistant isolates (77% were E.coli, 23% were K.pneumoniae); and by synergy tests with or without AmpC inhibitors in a total of 165 (88% were E.coli, 12% were K.pneumoniae) cefoxitin-susceptible, third generation cephalosporin-resistant (S3R) isolates. For the detection of pAmpC genes a multiplex-PCR protocol was applied to the isolates found positive at least by one of the phenotypic tests. CHT, ACDT and BAIT were found positive in 21 (58%), 18 (50%) and 7 (19%) of the 36 cefoxitin-resistant isolates, respectively. In only 10 (27.7%) of these isolates (all were E.coli strains), pAmpC presence was detected by PCR; and the enzyme produced was assessed as CMY-2. Based on the positive PCR results; specificity rates of the phenotypic tests, BAIT, ACDT and CHT were 97%, 69% and 58%; while the sensitivity rates were 50%, 100% and 100%, respectively. Our data indicated that, pAmpC prevalence (10/1316, 0.8%) detected in this study, did not seem to be an important problem yet, in the population screened. However, since the first detection of this resistance was in 2010, it should be considered as a sign to get necessary precautions preventing its spread. In conclusion, none of the phenotypic methods were satisfactory alone for the detection of pAmpC-mediated resistance; and BAIT was superior in terms of specificity while the others were superior in terms of sensitivity. Thus, combined application of these phenotypic tests are necessary to screen and confirm the presence of pAmpC-mediated resistance.

[Antibiotic resistance profiles of Acinetobacter species isolated from several clinical samples between 2007-2010]. / Çesitli klinik örneklerden 2007-2010 yillarinda izole edilen acinetobacter türlerinin antibiyotik direnç profilleri.

This study was aimed to investigate the changes in antibiotic resistance profiles of Acinetobacter spp. in our hospital during a four-year period. The study included a total of 465 non-duplicate Acinetobacter spp. isolated from various samples sent from intensive care (n= 274, 58.9%), inpatient (n= 141, 30.3%) and outpatient (n= 49, 10.5%) units of our hospital between 2007 and 2010. Sample distribution was as follows: 184 tracheal aspirates (39.5%), 70 blood (15.3%), 92 (19.8%) wound, 40 urine (8.6%), 24 sputum (5.1%), 22 (4.7%) bronchial lavage and 22 (4.7%) other (catheter tip, cerebrospinal fluid, thorasynthesis material) samples. The isolates were identified as A.baumannii (n= 340, 73.1%), A.lwoffii (n= 64, 13.7%) and Acinetobacter spp. (n= 61, 13.1%). The susceptibility profiles were investigated by Kirby-Bauer disc diffusion method. Overall, the results indicated an increase in resistance against all tested drugs since 2007. A steady increase of resistance from 2007 to 2009, followed by a tendency to decrease in 2010 was also noted for all drugs, except for ceftazidime (CAZ), trimethoprim-sulfomethoxazole (SXT), netilmicin (NET), imipenem (IPM), meropenem (MER) and gentamicin (CN). NET, IPM, cefepime and MER resistance rates increased regularly from 2007 to 2010. CAZ resistance followed a fluctuating course, while CN resistance displayed a decreasing trend since 2009. According to the statistical analyses (X2 and Fisher’s exact test), there was a regular resistance increase between 2007-2009 except for amikacin (AK), SXT and PIP. Resistance rates were also increased for AK and PIP, but only between 2007 and 2009; as well as for piperacillin-tazobactam, ticarcilin-clavulanate, NET, MER and IPM between 2008 and 2009. A significant increase from 2008 to 2010 was observed for NET; and a significant resistance decrease in 2010 was noted for only sultamicillin, cefotaxime, CN and tobramycin (TOB) (p< 0.05). As of 2010, the results indicated high resistance rates against ciprofloxacin [resistance rate (RR): 79%], NET (RR: 60%) and all beta-lactam drugs, including carbapenems (mean RR: 80%). Moreover, there was a progressive increase in resistance to carbapenems and NET, two very important treatment alternatives. Tigecycline (RR: 5.5%), TOB (RR: 19%), CN (RR: 34%) and cefoperazone-sulbactam (RR: 38%) appeared to remain as relatively effective treatment choices. The resistance rates of inpatient and outpatient isolates which were usually lower than those of the intensive care unit isolates, also displayed a noteworthy increase over the past four years. Evidently, pan-resistant Acinetobacter spp. will become a serious health problem in the near future, unless efficient and appropriate precautions are taken.