No abstract

A Shigella sonnei strain resistant to cefotaxime and aztreonam (but not ceftazidime) was isolated from the stool sample of a 7-y-old outpatient. Double disk synergy test, isoelectric focusing, polymerase chain reaction and sequence analysis confirmed that the isolate produced CTX-M-3, an extended-spectrum beta-lactamase (ESBL). This is the first report from Turkey of Shigella spp. producing an ESBL, and of CTX-M type enzyme.

Fecal specimens from 50 healthy volunteers living in Izmir, Turkey, were examined for the presence of beta-lactamase producing Escherichia coli by selection on agar plates containing ampicillin (10 mg/L). Thirty-nine (78%) of the strains were ampicillin-resistant and ampicillin MIC50 values for these isolates were > or =1024 microg/ml (range 32- > or =1024 microg/ml). Ampicillin MIC values remained above 64 microg/ml in 16 (41%) strains despite addition of clavulanic acid (2 mg/L). Beta-lactamase production of the clavulanate-resistant strains was further investigated by analytical isoelectric focusing (pI). Enzymes with pIs of 5.4, 5.6, 7.4, 7.6 and >8.5 were detected. Sixty-nine percent of the isolates produced a pI 5.4 enzyme that cofocused with TEM-1. Beta-lactamase assays revealed that hyperproduction of these enzymes was the predominant mechanism for clavulanate resistance. Twelve (75%) of the isolates were able to transfer their ampicillin resistance. The ampicillin and ampicillin plus clavulanic acid MIC values of all transconjugants were above 256 microg/ml. Transferable ampicillin resistance was associated with resistance to other antibacterials at the following frequencies: tetracycline 92%, trimethoprim 83%, streptomycin 50%, gentamicin 25%, and chloramphenicol 8%. In conclusion, it has been suggested that commensal bacteria in normal populations make up the largest reservoir of antibiotic-resistant genes. Although the exact molecular mechanisms could not be determined, the current study shows that the incidence of ampicillin and clavulanic acid resistance is also high in commensal fecal flora.

Sequence analysis of the pbp genes from 20 Streptococcus pneumoniae isolates from Turkey (eight with high-level penicillin-resistance, nine with low-level penicillin-resistance, and three that were penicillin-susceptible) was performed and phylogenetic trees were constructed. Most isolates clustered together within a single branch that was distinct from sequences deposited previously in GenBank, which suggests that these isolates have probably evolved following new recombination events. The most prominent active-site mutations, which have also been associated previously with resistance, were T371A in PBP1a, E481G followed by T451A in PBP2b, and T338A in PBP2x. All isolates also possessed a (570)SVES/TK(574) block in the PBP2b sequence, instead of the QLQPT sequence of R6, which is fairly uncommon in GenBank sequences. This is the first study to analyse alterations in the pbp sequences of pneumococci isolated in Turkey.

Carbapenem resistance due to OXA-type carbapenemases seriously limits therapeutic options in nosocomial infections caused by Acinetobacter baumannii. Previous studies have shown the presence of OXA-51, OXA-58, and OXA-23 carbapenemases but not OXA-24/40 in A. baumannii in Turkey. In this study, we investigated carbapenem-hydrolyzing class D b-lactamases (CHDLs) in A. baumannii and the molecular epidemiology of CHDL producers at the Dokuz Eylul Hospital, Izmir Turkey, and detected bla OXA-24/40 in a clinical isolate from a patient in the medical intensive care unit (ICU). The specific enzyme type was OXA-72. Additional studies revealed 22 more isolates from 20 patients and that the OXA-72-producing strain caused an outbreak in the medical ICU from September 2012 to March 2013, which still continues. To our knowledge, this is the first report of OXA-24/40 carbapenemases in A. baumannii in Turkey. Emergency infection control should be implemented following the arrival of a new OXA at a hospital where A. baumannii is highly endemic. Acinetobacter baumannii is an opportunistic pathogen, which causes nosocomial infections and outbreaks worldwide, particularly in the intensive care units (ICUs) (1,2). Although carbapenems are frequently used for the treatment of infections due to multidrugresistant (MDR) A. baumannii isolates, the increasing resistance to these antimicrobial agents has significantly limited treatment options (3,4). The underlying resistance mechanisms may be related to efflux pump overexpression, decreased permeability, and carbapenemase production. Among the carbapenemases, carbapenem-hydrolyzing class D b-lactamases (CHDLs) are considered the most prevalent cause of carbapenem resistance in A. baumannii (4-6). The CHDLs in A. baumannii can be grouped into six subclasses: chromosomal OXA-51-like, acquired OXA-23-like, OXA-24/40-like, OXA-58-like, OXA-143-like, and OXA-235-like b-lactamases (7,8). OXA-23-like enzymes are the most prevalent CHDLs and have been reported worldwide (1-9). In Turkey, data regarding CHDLs and their epidemiology in A. baumannii are limited. Outbreaks due to OXA-23-like and OXA-58-like enzyme-producing strains were reported in 2008-2010 (10-12). Previous reports have shown that OXA-58-like enzymes were the most prevalent b-lactamases in Turkish strains; however, a recent study reported that OXA-23-like enzymes have become more prevalent since 2010 (13). There is no report regarding OXA-24/40-like enzymes in A. baumannii isolates from Turkey. Here, we describe a small outbreak caused by MDR A. baumannii that produced OXA-72, a member of