What is known and objective: Acinetobacter baumannii is one of the most important nosocomial pathogens with the ability to cause infections such as meningitis, pneumonia, urinary tract, septicaemia and wound infections. A wide range of virulence factors are responsible for pathogenesis and high mortality of A. baumannii including outer membrane proteins, lipopolysaccharide, capsule, phospholipase, nutrientacquisition systems, efflux pumps, protein secretion systems, quarom sensing and biofilm production. These virulence factors contribute in pathogen survival in stressful conditions and antimicrobial resistance. Comment: According to the World Health Organization (WHO), A. baumannii is one of the most resistant pathogens of ESKAPE group (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, A. baumannii, Pseudomonas aeruginosa and Enterobacter spp.). In recent years, resistance to a wide range of antibiotics in A. baumannii has significantly increased and the high emergence of extensively drug resistant (XDR) isolates is challenging. Among therapeutic antibiotics, resistance to tigecycline as a last resort antibiotic has become a global concern. Several mechanisms are involved in tigecycline resistance, the most important of which is RND (Resistance-Nodulation-Division) family efflux pumps overexpression. The development of new therapeutic strategies to confront A. baumannii infections has been very promising in recent years.What is new and conclusion: In the present review we highlight microbiological and virulence traits in A. baumannii and peruse the tigecycline resistance mechanisms and novel therapeutic options. Among the novel therapeutic strategies we focus on combination therapy, drug repurposing, novel antibiotics, bacteriophage therapy, antimicrobial peptides (AMPs), human monoclonal antibodies (Hu-mAbs), nanoparticles and gene editing.

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Background and Objectives:Urinary tract infection (UTI) is one of the most frequent infectious diseases and can occur in all age groups. Escherichia coli is the main cause of this infection. Multiple resistances to antimicrobial agents are increasing quickly in E. coli isolates and may complicate therapeutic strategies for UTI. The aim of this study was to determine the antibiotic resistance pattern and the multidrug-resistance (MDR) phenotypes in uropathogenic E. coli (UPEC).Materials and Methods:A total of 135 UPEC isolates were collected from both outpatients (91 isolates) and inpatients (44 isolates) between September, 2012 and February, 2013. In order to determine the MDR among UPEC isolates, we have tested 15 antimicrobial agents and antibiotic susceptibility was done by Kirby-Bauer disk diffusion method.Results:The percentage of MDR isolates (resistant to at least three drug classes such as aminoglycosides, fluoroquinolones, penicillins, cephalosporins, or carbapenems) was 68% in the inpatients and 61% in the outpatients. Antibiotic resistance to ampicillin, ceftazidim, nalidixic acid, and trimethoprim/sulfamethoxazole were higher than 50%. Amikacin, nitrofurantoin, and gentamicin showed markedly greater activity (89.1%, 85.9%, and 82.4% sensitivity, respectively) than other antimicrobial agents. Resistance to meropenem did show either in outpatients or in inpatients.Interpretation and Conclusions:The high prevalence of drug resistance among UTI patients calls for continuous monitoring of the incidence of drug resistance for appropriate empiric selection of antibiotic therapy. Empirical treatment of UTIs should be relied on susceptibility patterns from local studies.

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Background β-Lactam antibiotics have been broadly used for the treatment of Acinetobacter baumannii infections, resulting in development of β-lactam inactivating β-lactamases. Here, we described antibiotic resistance rate, prevalence of β-lactamase-encoding genes, and clonal relationships of A. baumannii strains isolated from children referred to Children’s Medical Center in Tehran, Iran, during 2019–2020. Methods A total of 60 non-replicate A. baumannii isolates were recovered from clinical specimens of pediatric patients. Antibiotic susceptibility testing was done by the disc diffusion method. Colistin susceptibility of isolates was performed by the broth microdilution method. β-lactamase-encoding genes were characterized by PCR. The presence of ISAba1 element upstream of the several oxacillinase genes was also checked. Genetic relatedness of isolates was determined by using random amplification of polymorphic DNA (RAPD) typing. Results The antimicrobial susceptibility tests showed that 83.3% of A. baumannii isolates were MDR, and 40% XDR. Both MDR and XDR A. baumannii isolates were susceptible to colistin. The frequency of blaOXA-51-like, blaOXA-23-like, blaTEM, blaOXA-24-like, blaPER, blaSHV, blaCTX-M, blaOXA-58-like, and blaIMP was 100, 93.33, 60, 36.67, 28.33, 8.33, 5, 3.33, and 1.67%, respectively. Coexistence of ISAba1/blaOXA-23-like and ISAba1/blaOXA-51-like was observed in 65% and 85% of isolates, respectively. RAPD analysis revealed 4 common types and 2 single types of A. baumannii isolates. Conclusions The multiple clones harboring blaOXA-23-like, ISAba1-blaOXA-51-like, and ISAba1-blaOXA-23-like were responsible for the spread of A. baumannii isolates in our clinical wards. Dissemination of the well-established clones is worrisome and would become therapeutic challenges due to the possible transferring genetic elements associated with resistance.