BackgroundThe ability of biofilm formation is an effective way for Acinetobacter baumannii survival from stressed conditions. This present study was aimed to evaluate the association between biofilm formation, structure, the expression levels of genes related to biofilm formation and biofilm-specific resistance of A. baumannii strains isolated from burn infections in Ahvaz, Iran.MethodsIn this study, we assessed the antibiotic susceptibilities, ERIC-PCR typing, capacity of biofilm formation and biofilm structure of 64 A. baumannii isolates collected from burn infections. The distribution and the expression levels of genes involved in the biofilm formation including bap, ompA, abaI, pgaA and csuE were assessed by PCR and real-time PCR, respectively.ResultsWe classified A. baumannii isolates in 14 clonal types of ERIC-PCR. Most A. baumannii isolates were resistant to all antibiotics tested except to tigecycline and colistin and had the biofilm formation capability but with different capacities. There was a significant inverse relationship between resistance to antibiotic agents and biofilm formation. The biofilm matrix of 50 strains consisted of polysaccharides together with DNA or proteins. The genes involved in the biofilm formation were detected in both biofilm-forming and non-biofilm forming; however, the expression levels of these genes were higher in biofilm producers compared with non-producers.ConclusionThe biofilm cells exhibited dramatically decreased susceptibility to antibiotic agents; hence, they have great significance for public health. Therefore, the determination of antibiotic susceptibilities in biofilm and planktonic mode, molecular typing, and capacity of biofilm formation in clinical setting is essential.

Background: Metallo-β-Lactamases (MBL) are usually encoded on the gene cassettes harboring integrons and disseminated easily among Acinetobacter baumannii isolates. This study was aimed to investigate the association of the genes encoding MBL with the presence of class 1 and 2 integrons among multidrug-resistant (MDR) A.baumannii isolates. Methodology: A total of 85 non-duplicated A.baumannii isolates were collected and evaluated for the amplification of bla OXA-51. The presence of genes encoding MBLs, including bla IMP , bla VIM , bla SIM , bla SPM , bla GIM , bla DIM and bla NDM , as well as intI 1 and intI 2 was evaluated by PCR. Also, the production of MBLs was screened phenotypically by the combination of EDTA and meropenem. Results: In this study, 77 out of 85 isolates were MDR. Also, 34 isolates had only intI 1 , 10 had only intI 2 and 15 had both intI 1 and intI 2 . The phenotypic detection of MBLs was found in 30 isolates, among which bla VIM was as the most common the gene encoding MBL followed by bla IMP , bla SPM and bla SIM . The gene cassettes analysis revealed that class 1 integron is often responsible for transferring the genes harboring MBLs. Conclusion: The production of MBLs among A. baumannii strains is one of the main mechanisms of resistance to carbapenems. Therefore, the development of inexpensive screening methods for the phenotypic detection of MBLs in clinical laboratories settings is essential. Also, our data revealed that the class 1 integron is often responsible for the dissemination of the MBL genes among A. baumannii isolates.

Aminoglycosides are widely recommended for treatment of Acinetobacter baumannii infections in combination with β-lactams or quinolones. This cross-sectional study was aimed to investigate the coexistence of aminoglycoside modifying enzyme (AME) genes among A. baumannii isolates from clinical samples in Ahvaz, Iran. A total of 85 clinical A. baumannii isolates typed by ERIC-PCR were investigated for the presence of AME genes, including ant(3″)-Ia, aac(6′)-Ib, aac(3′)-Ia, ant(2″)-Ia, and aph(3′)-VIa by PCR. The resistance rates to aminoglycoside agents were evaluated by disk diffusion. In this study, 84 out of 85 A. baumannii isolates were resistant to at least one of the aminoglycosides and harbored at least one AME gene. The most common gene encoding AMEs was aph (3′)VIa, followed by aac(3′)-Ia, ant(3″)-Ia, ant (2″)-Ia, and aac(6′)-Ib. The aminoglycoside-resistant genotypes were completely matched to resistant phenotypes to each one of the aminoglycoside agents. There was a clear association between AME gene types and the phenotype of resistance to aminoglycosides with their ERIC-PCR types. Our findings highlight the coexistence of AME genes and clonal dissemination of multiresistant A. baumannii in hospital setting.