Prevalence and Mechanisms of Carbapenem Resistance Among Acinetobacter baumannii Clinical Isolates in Egypt.

The increasing number of carbapenem-resistant Acinetobacter baumannii clinical isolates is a major concern, which restricts therapeutic options for treatment of serious infections caused by this emerging pathogen. The aim of this work is to assess the antimicrobial resistance profile and identify the molecular mechanisms involved in carbapenem resistance in A. baumannii isolated from different clinical sources in Mansoura University Hospitals, Egypt. Antimicrobial susceptibility testing has shown that resistance to carbapenem has dramatically increased (98%) with concomitant elevated levels of resistance to quinolones, trimethoprim/sulfamethoxazole, and aminoglycosides. Polymyxin B and colistin are considered the last resort. Random amplified polymorphic DNA (RAPD) typing method revealed great diversity among A. baumannii isolates. Coexistence of diverse intrinsic and acquired carbapenem-hydrolyzing ß-lactamases has been detected in the tested isolates: Ambler class A: blaKPC (56%) and blaGES (48%), and Ambler class B: blaNDM (30%), blaSIM (28%), blaVIM (20%), and blaIMP (10%). Most isolates (94%) carried blaOXA-23-like and blaOXA-51-like simultaneously. blaOXA-23-like was preceded by ISAba1 providing a potent promoter activity for its expression. Sequencing analysis revealed that ISAba1 has been also inserted in carbapenem resistance-associated outer membrane protein (OMP) (carO) gene in three isolates, two of which were clonal based on RAPD typing, leading to interruption of its expression as confirmed by SDS-PAGE analysis of OMP fractions. Carbapenem resistance genes are widely distributed among A. baumannii clinical isolates from different clinical sources. Therefore, enhanced infection control measures, effective barriers, and rational use of antimicrobials should be enforced in hospitals for minimizing the widespread resistance to carbapenems and all other antibiotics.

Co-production of AmpC and extended spectrum beta-lactamases in cephalosporin-resistant Acinetobacter baumannii in Egypt.

Acinetobacter baumannii is an opportunistic pathogen that has been held responsible for a lot of infections worldwide. Infections caused by this pathogen are difficult to control because of the widespread of antimicrobial resistance mechanisms. The aim of the present study is to assess the prevalence of extended spectrum ß-lactamases (ESBLs) and AmpC ß-lactamases among isolates of A. baumannii collected from different clinical sources in Mansoura University Hospitals, Egypt. Antimicrobial susceptibility testing has demonstrated elevated resistance level to ß-lactams, quinolones and aminoglycosides. All isolates were sensitive to colistin and polymyxin B. ESBL activity was detected in 86% of the isolates. Among the tested ESBL encoding genes, blaTEM gene was the most prevalent gene as it was detected in 52% of the isolates. While blaPER, blaSHV and blaVEB were detected in 12%, 4%, and 2%, respectively. AmpC activity and blaADC gene were detected in 90% of the tested isolates. Insertion sequence ISAba1 was located 9 bp upstream of blaADC gene in 88.9% of the ADC-expressing isolates providing a potent promoter activity for its expression. To our knowledge this is the first report of loss of intrinsic ADC activity, in 10% of the tested isolates, as a result of insertional inactivation by an element belonging to IS5 family transposase. Co-expression of both ESBLs and AmpC ß-lactamases was detected in 78% of the isolates. The study demonstrates high prevalence of resistance to ß-lactam antibiotics through ESBLs and AmpC ß-lactamases production among A. baumannii clinical isolates. Prevalence of ß-lactamases should be detected routinely and reported in hospitals to avoid inappropriate use of antibiotics and therapeutic failure.