The emergence and increasing prevalence of multidrug-resistant pathogens has become a major global healthcare problem. According to the World Health Organization if these trends continue, mortality from infection in 2050 will be higher than that from cancer. Microorganisms have various resistance mechanisms against different classes of antibiotics that emphasize the need for discovery of new antimicrobial compounds to treat bacterial infections. An interesting and new strategy for disarming pathogens is antivirulence therapy by blocking bacterial virulence factors or pathogenicity. Therefore, the use of these new pathoblockers could reduce the administration of broad-spectrum antimicrobials and prevalence of resistant strains.

Acinetobacter baumannii (A. baumannii) is an important opportunistic pathogen responsible for nosocomial infections worldwide at recent decades. Biofilm formation by A. baumannii leads to antibiotic resistance and survives on abiotic and biotic surfaces. In the present study we aimed to assess the ability of biofilm formation in clinical and environmental isolates of A. baumannii by phenotypic methods and to detect the presence of genes involving in the biofilm development; bap, ompA, csuE, abaI, and bla_PER-1by PCR method. Totally 120 A. baumanniin isolates, 98 clinical, and 22 environmental were evaluated for biofilm formation using the modified Microtiter plate method, Congo red agar methods, and the existence of genes related to biofilm by standard PCR. The phenotypic results showed that the biofilm formation rate was 10.8% isolates that in environmental A. baumannii isolates were higher than clinical isolates. The abaI, csuE, and ompA genes were detected in all isolates with biofilm formation and the bap and bla_PER-1genes were positive in 14.2% and 13.3% of A. baumannii isolates, respectively. The sequence of genes were submitted in NCBI. Based on our results, the Congo red agar method was significantly better than the Microtiter plate technique for phenotypic evaluation of biofilm formation in the A. baumannii. Our study indicates that abaI, csuE, and ompA genes were detected in all isolates unlike the bap and bla_PER-1genes. Keywords: Nosocomial Infections; Biofilm Formation; Iran; Acinetobacter baumannii

Background: This study was aimed to characterize the genetic diversity and expression of three putative resistance-nodulation-cell division (RND)-type efflux systems and their contribution to multidrug efflux in clinical isolates ofAcinetobacter baumannii.Methods: Antimicrobial susceptibility testing of 95A. baumanniiisolates was determined by Kirby-Bauer disk diffusion for 18 antibiotics and minimum inhibitory concentration (MIC) of colistin was determined by the broth microdilution method. Moreover, the MIC of five classes of antibiotics was assessed using E-test strips in the presence and absence of phenylalanine-arginine beta-naphthylamide (PAβN). Regulatory genes of the RND efflux pumps (adeRS,adeL,adeNandbaeSR) were subjected to sequencing. The relative expression ofadeB,adeGandadeJgenes was determined by quantitative real-time PCR (qRT-PCR).Results: Overall, the majority of isolates (94%) were extensively drug-resistant (XDR). In the phenotypic assay, efflux pump activity was observed in 40% of the isolates against multiple antibiotics mainly tigecycline. However, we found no efflux activity against imipenem. Several amino acid substitutions were detected in the products of regulatory genes; except in AdeN. Of note, G186V mutation in AdeS was found to be associated with overexpression of its efflux pump. No insertion sequences were detected.Conclusions: Our findings outlined the role of RND efflux pumps in resistance ofA. baumanniito multiple antibiotics particularly tigecycline, and pointed out the importance of a variety of single mutations in the corresponding regulatory systems. Further studies are required to decipher the precise role of RND efflux pumps in multidrug-resistant clinical isolates ofA. baumannii.

The present study was aimed to investigate molecular diversity of Echinococcus granulosus isolates collected from human clinical samples using two mitochondrial genes cox1 and nad1 in Iran. Forty seven human hydatid cysts were collected through surgery from two hospitals in Tehran during 2010-2012. To determine the fertility of protoscoleces, the cyst fluids were subjected to morphological microscopic examinations. Protoscoleces were removed from each cyst and their total genomic DNAs were extracted. PCR was performed to amplify fragments of 450 and 400 base pair (bp) for cox1 and nad1 genes, respectively. Genotype diversity and sequence variation of the strains were studied by bioinformatics software and in comparison with those mtDNA sequences already deposited in GenBank. Sixteen, (53.3%), 13 (43.3%), and 1 (3.3%) samples were related to lung, liver, and spleen, respectively. The remained 17 unfertile samples were excluded from the study. From the 29 isolates, 86.7% (n=26) and 10% (n=3) were related to G1, and G3 genotypes, respectively. The sole isolate with G6 genotype was obtained from lung sample. Analysis of concatenated sequences of cox1+nad1 indicated the presence of 11 haplotypes among our strains that were related to genotypes G1 (n=9), G3 (n=1) and G6 (n=1). In consistent to other reports from Iran, genotypes G1, G3, and G6 were observed in our human isolates. The rate of G3 genotype was however higher than other studies implying that human can be considered as a new appropriate host for G3 genotype. Further studies with more sample size from different geographic areas of Iran are needed for E. granulosus mapping.