OXA-Carbapenemases Present in ClinicalAcinetobacter baumannii-calcoaceticusComplex Isolates from Patients in Kurdistan Region, Iraq

Abstract

In addition to intrinsic resistance in Acinetobacter baumannii, many different types of acquired resistance mechanisms have been reported, including the presence of VIM and IMP metallo β-lactamases and also of bla and bla enzymes. In the Kurdistan region of Iraq, the multiresistant A. baumannii-calcoaceticus complex is prevalent. We characterized the different mechanisms of resistance present in clinical isolates collected from different wards and different hospitals from the Kurdistan region. One hundred twenty clinical nonduplicate A. baumannii-calcoaceticus complex isolates were collected from four hospitals between January 2012 and October 2013. The identification of the isolates was confirmed by MALDI-TOF. The susceptibility to different antibiotics was determined by disk diffusion and analyzed in accordance to EUCAST guidelines. By PCR, the presence of bla, bla, bla, and bla genes was determined as well as the presence of the insertion element ISAba1. Clonal diversity was analyzed by pulsed-field gel electrophoresis (PFGE) using the restriction enzyme ApaI and, in addition, multilocus sequence typing (MLST) was performed on a selected subset of 15 isolates. All 120 A. baumannii isolates harbored bla genes. One hundred one out of 110 (92%) imipenem (IMP)-resistant A. baumannii-calcoaceticus complex isolates additionally carried the bla gene and four isolates (3%) were positive for bla All 101 bla-positive isolates had the ISAba1 insertion sequence, 1,600 bp upstream of the bla gene. The bla gene was not detected in any of the 110 IMP-resistant strains. Eight different PFGE clusters were identified and distributed over the different hospitals. MLST analysis performed on a subset of 15 representative isolates revealed the presence of the international clone ST2 (Pasteur). Besides ST2 (Pasteur), also many other STs (Pasteur) were encountered such as ST136, ST94, ST623, ST792, and ST793, all carrying the bla gene. In clinical A. baumannii-calcoaceticus complex isolates from Kurdistan-Iraq, the bla gene in combination with the upstream ISAba1 insertion element is largely responsible for carbapenem resistance. Several small clusters of identical genotypes were found from patients admitted to the same ward and during overlapping time periods, suggesting transmission within the hospital. Identification of source(s) and limiting the transmission of these strains to patients needs to be prioritized.

A Prevalence of infections with antibiotic-resistant Acinetobacter baumannii in different clinical samples from hospitals in Erbil

“…Further studies are needed to elucidate the cause of these differences. The resistant of A. baumannii to carbapenem in clinical isolates is a serious threat, suggesting that if carbapenem is overused, early interruption of treatment, lead to rapid increase in resistance and treatment failure are likely to happen (Ganjo et al, 2016). For carbapenem-resistant A. baumannii, colistin is one of the most persistently used alternative agents according to the Behera (Behera et al, 2017).…”

Investigation of multidrug-resistant ST2 Acinetobacter baumannii isolated from Saint George hospital in Lebanon

“…In addition, in the United States, the OXA-23 has been described as the major mechanism responsible to the resistance of A. baumannii. These outbreaks are mostly associated to the worldwide spread of the international clones I and II [37]. The ST2 clone has also been reported in several Mediterranean countries.…”

Understanding the Epidemiology of Multi-Drug Resistant Gram-Negative Bacilli in the Middle East Using a One Health Approach

“…In Iraq, the most common carbapenemase producers are the non-fermenters including OXA-23/OXA-24 A. baumannii (Kusradze et al, 2011; Ganjo et al, 2016) and NDM (NDM-1, NDM-2), IMP and SPM P. aeruginosa (Al-Charrakh et al, 2016; Ismail and Mahmoud, 2018). According to Al-Charrakh et al (2016), the high resistance of carbapenem resistant P. aeruginosa to non-beta lactams such as ciprofloxacin and gentamicin, can be attributed to the over-use of these antimicrobial agents in Iraqi clinical practices.…”