Acinetobacter baumannii has become a major concern for scientific attention due to extensive antimicrobial resistance. This resistance causes an increase in mortality rate because strains resistant to antimicrobial agents are a major challenge for physicians and healthcare workers regarding the eradication of either hospital or community-based infections. These strains with emerging resistance are a serious issue for patients in the intensive care unit (ICU). Antibiotic resistance has increased because of the acquirement of mobile genetic elements such as transposons, plasmids, and integrons and causes the prevalence of multidrug resistance strains (MDR). In addition, an increase in carbapenem resistance, which is used as last line antibiotic treatment to eliminate infections with multidrug-resistant Gram-negative bacteria, is a major concern. Carbapenems resistant A. baumannii (CR-Ab) is a worldwide problem. Because these strains are often resistant to all other commonly used antibiotics. Therefore, pathogenic multi-drug resistance A. baumannii (MDR-Ab) associated infections become hard to eradicate. Plasmid-mediated resistance causes outbreaks of extensive drug-resistant . A. baumannii (XDR-Ab). In addition, recent outbreaks relating to livestock and community settings illustrate the existence of large MDR-Ab strain reservoirs within and outside hospital settings. The purpose of this review, proper monitoring, prevention, and treatment are required to control (XDR-Ab) infections. Attachment, the formation of biofilms and the secretion of toxins, and low activation of inflammatory responses are mechanisms used by pathogenic A. baumannii strain. This review will discuss some aspects associated with antibiotics resistance in A. baumannii as well as cover briefly phage therapy as an alternative therapeutic treatment.
Background and Aim Recently, the extensive use of quinolones led to increased resistance to these antimicrobial agents, with different rates according to the organism and the geographical region. The aim of this study was to detect the resistance rate of Klebsiella pneumoniae Iraqi isolates toward quinolone antimicrobial agents, to determine genetic mutations in gyrA and parC , to screen for efflux-pump activity, and to screen the presence of plasmid-mediated quinolone resistance (PMQR) genes. Methods Forty-three K. pneumoniae isolates were confirmed phenotypically and genotypically by Vitek 2 system and species specific primers by PCR using the targeting rpo gene followed by sequencing. Antibiotic susceptibility test was carried out using disc diffusion method. Quinolone resistant isolates were subjected to ciprofloxacin MIC testing, and cartwheel method to screen for efflux pump activity. The presence of the plasmid mediated quinolone resistance genes qepA, qnrB, qnrS , and aac(6)Ib was tested by PCR. Sequencing of gyr A and par C was performed. Results We observed a high rate of resistance to ceftriaxone, gentamicin ciprofloxacin, and levofloxacin. Low rate of resistance was detected against amikacin and azithromycin. Ciprofloxacin MIC results revealed that 96.1% of the isolates had MICs >256 µg/mL, 83.4% had MICs >512 µg/mL while 34.6% had MIC >1024 µg/mL. Testing of isolates against ciprofloxacin mixed with EtBr at various concentrations resulted in decreased resistant. Sequencing results showed that Ser83Leu was the most common mutation in gyr A that was observed in all quinolone resistant isolates, followed by Asp87Asn. Ser80Ile mutation in par C was observed in 77.7% of the tested isolates. The prevalence of PMQR genes was 92.5% aac (6)-Ib , 51.8% qnr B, 40.7% qep A, and 37% qnr S. Conclusion Quinolone resistance is common in K. pneumoniae isolates in Baghdad. The frequent mutation in gyr A and par C, and the presence of PMQR genes is alarming.
Background and aim: Colistin is increasingly being used as a 'last-line' therapy to treat infections caused by multi-drug resistant Acinetobacter baumannii (A. baumannii) isolates, when essentially no other options are available in these days. The aim of this study was to detect genes associated with Colistin resistance in A. baumannii. Methods: 121 isolates of A. baumannii were collected from clinical and environmental samples during 2016 to 2018 in Baghdad. Isolates were diagnosed as A. baumannii by using morphological tests, Vitek-2 system, 16SrRNA PCR amplification and sequencing. Antibiotic susceptibility test was carried out using disc diffusion method. Phenotypic detection of colistin resistance was performed by CHROMagar TM COL-APSE medium and broth microdilution method for the determination of the minimal inhibitory concentration (MIC). Molecular detection of genes responsible for colistin resistance in A. baumannii was performed by PCR. Results: 92 (76%) out of 121 A. baumannii isolates were colistin resistant. 26 (21.5%) out of 121 isolates showed positive growth on CHROM agar Acinetobacter base for MDR. PCR detected mcr-1, mcr-2 and mcr-3 genes in 89 (73.5%), 78 (64.5%) and 82 (67.8%) in the A. baumannii isolates respectively. 78 (64.5%) out of 121 isolates harbored the integron intI2 gene and 81 (66.9%) contained intI3 gene. Moreover, 60 (49.6 %) out of 121 isolates were positive for the quorum sensing Iasl gene Conclusion: The presence of a large percentage of colistin resistant A. baumannii strains in Baghdad may be due to the presence of mobile genetic elements and it is urgent to avoid unnecessary clinical use of colistin.
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