In vitro activity of ceftolozane-tazobactam and ceftazidime-avibactam against clinical isolates of meropenem-non-susceptible Pseudomonas aeruginosa: A two-centre study.

OBJECTIVES: This study aimed to compare the activity of ceftazidime-avibactam (C/A), ceftolozane-tazobactam (C/T) and three anti-pseudomonal ß-lactams (piperacillin-tazobactam, ceftazidime and cefepime) against a collection of meropenem-non-susceptible Pseudomonas aeruginosa (P. aeruginosa) clinical isolates recovered from two centres in Turkey. METHODS: A total of 102 unique patient isolates of meropenem-non-susceptible P. aeruginosa were included in the study. MICs of antimicrobials were determined by the gradient diffusion method. RESULTS: Overall susceptibility rates for C/A and C/T were 83.3% and 82.4%, respectively. Both C/A and C/T had better activity than any one of the three anti-pseudomonal ß-lactams. According to the MIC50 values, C/T was the most potent agent against isolates. Although the susceptibility rates of isolates to C/T and C/A were similar, C/T (MIC50, 1 µg/mL) was four-fold more potent than C/A (MIC50, 4 µg/mL). The MIC50 values of C/A and C/T for the isolates that were non-susceptible to three ß-lactams were significantly higher than those for isolates that were non-susceptible to zero, one or two ß-lactams. Also, the C/A MIC50 value for the isolates that were non-susceptible to two ß-lactams was higher than that for isolates which were non-susceptible to one ß-lactam. CONCLUSIONS: C/A and C/T showed good activity against meropenem-non-susceptible P. aeruginosa isolates. However, resistance to these agents was not uncommon among these isolates. The overall ß-lactam susceptibility profile of isolates seems to have an effect on the probability of susceptibility to C/A and C/T. Antimicrobial susceptibility testing should be performed for C/A and C/T if these agents are considered for treatment of infections caused by meropenem-non-susceptible P. aeruginosa.

Aminoglycoside resistance determinants in multiresistant Escherichia coli and Klebsiella pneumoniae clinical isolates from Turkish and Syrian patients.

Escherichia coli and Klebsiella pneumoniae are frequently found resistance to aminoglycosides in Turkey. The aim of this study was to investigate aminoglycoside resistance in clinical isolates of E. coli and K. pneumoniae from Turkey using both phenotypic and genotypic methods and screening for the prevalence of gene coding for common aminoglycoside-modifying enzymes (AMEs) and 16S rRNA methylase genes. A total of 88 consecutive, non-duplicated E. coli (n = 65) and K. pneumoniae (n = 23) isolates showing resistance or intermediate resistance to amikacin and/or gentamicin were collected between October 2013 and May 2015 from clinical samples received at Gaziantep Dr. Ersin Arslan Training and Research Hospital. Seventeen isolates were obtained from Syrian patients. Isolates resistant to any of the two aminoglycosides were tested by PCR for seven AME genes, and 22 isolates with amikacin MIC ≥16 mg/L were also tested for 16S rRNA methylase genes. In E. coli isolates, the most frequent genes were aac(6')-Ib (50 strains; 76.9%) and aac(3)-IIa (40 strains; 70.7%), followed by aph(3')-Ia (5 strains; 7.6%) and ant(2″)-Ia (2 strains; 3.1%). Among the 23 resistant K. pneumoniae isolates, the most prevalent gene was aac(3')-IIa (87.0%) followed by aac(6')-Ib (73.9%) and aph(3')-Ia (8.6%). The rmtC gene was detected in one K. pneumoniae isolate. Resistance to aminoglycosides in clinical isolates of E. coli and K. pneumoniae from our center is predominantly caused by AAC(6')-Ib and AAC(3)-II enzymes, while the occurrence of 16S rRNA methylases is so far limited.

[Investigation of mupirocin resistance in nosocomial methicillin-resistant Staphylococcus aureus isolates by phenotypic and genotypic methods]. / Nozokomiyal kökenli metisiline dirençli Staphylococcus aureus izolatlarinda mupirosin direncinin fenotipik ve genotipik yöntemlerle arastirilmasi.

Since methicillin-resistant Staphylococcus aureus (MRSA) has become one of the most prevalent nosocomial pathogens and a frequent cause of mortality and morbidity, there is an increasing tendency to use topical mupirocin for eradication of MRSA carriage. However, there have been recent reports of resistance against mupirocin among MRSA isolates. This study was conducted to investigate the presence of mupirocin resistance in a population of 595 nosocomial MRSA isolates by phenotypic and genotypic methods. In 35 (5.9%) of 595 isolates, mupirocin resistance was detected by disc diffusion and E-test methods. High-level mupirocin resistance was detected in 23 (65.8%) isolates and low-level mupirocin resistance in 12 (34.2%) isolates by E-test method. The molecular analysis of 35 mupirocin resistant MRSA isolates showed the presence of both mecA and mupA genes by polymerase chain reaction. While in 23 high-level mupirocin resistant MRSA isolates a 38 kb plasmid was detected, none of the low-level mupirocin-resistant MRSA isolates revealed the presence of this plasmid. Thirty-two of 35 mupirocin resistant MRSA isolates were genotyped with pulsed-field gel electrophoresis and 24 isolates were typed as identical (genotype A) and 8 as genetically-related (genotype A1), according to Tenover criteria. These data revealed that mupirocin resistant MRSA isolates in our hospital were of the same genotype or closely related.