Objective: Multi and extensively drug-resistant (MDR and XDR), Pseudomonas aeruginosa (P. aeruginosa) and Acinetobacter baumannii (A. baumannii) are two main causative agents of nosocomial infections leading to increased morbidity and mortality. We aim to study the prevalence of MDR and XDR-A. baumannii and P. aeruginosa phenotypes in clinical specimens. We conducted this for 1 year (2017-2018) and isolated bacteria from the clinical samples. Then, XDR and MDR strains were determined by susceptibility testing (disc diffusion). Results: Out of 3248 clinical samples, A. baumannii and P. aeruginosa strains were detected in 309(9.51%) of them. Susceptibility testing indicated that (16.50%) and (15.53%) of the P. aeruginosa and (74.75%) and (73.13%) of the A. baumannii isolates were screened as the MDR and XDR strains. The frequency of MDR isolates was higher in wound samples 222 (71.8%). This rate in behavioral intensive care unit (BICU) and restoration ward, were 187 (60.5%) and 63 (20.4%). The frequency of XDR isolates in BICU 187 (59.54%), restoration 58(18.77%), and burns 30 (9.70%) were assessed as well. Considering high isolation rates of MDR and XDR of mentioned strains, it is necessary to apply prevention criteria for eradication of the mentioned bacteria from hospital wards.

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In this study, mechanisms of carbapenem resistance in carbapenem-resistant but cephalosporin-susceptible (Car-R/Ceph-S) Pseudomonas aeruginosa were investigated. A total of 243 P. aeruginosa isolates were studied. The disk diffusion and agar dilution methods were used for determination of antibiotic susceptibility patterns. AmpC and efflux pump overproductions were detected by phenotypic methods. The presence of carbapenemase-encoding genes was detected by polymerase chain reaction (PCR). The expression of OprD, MexAB-OprM, and MexXY-OprM efflux pumps was assessed by real-time PCR. According to disk diffusion method, altogether 116 P. aeruginosa isolates (47.7%) were carbapenem-resistant and among them, 23 isolates (19.8%) were cephalosporin-susceptible. Carbapenemase producer was not detected. Overexpression of AmpC was detected in one (4.3%) isolate that was ceftazidime-susceptible but cefepime-resistant. Overexpression of MexAB-OprM and MexXY-OprM efflux pumps was detected in 12 (60.9%) and 16 (68.8%) of isolates, respectively. A total of 16 (68.8%) isolates showed decreased expression of OprD. The Car-R/Ceph-S P. aeruginosa did not develop by carbapenemase production. The resistance to carbapenem was mediated in our clinical isolates by decreased expression of OprD and overexpression of MexAB-OprM and MexXY-OprM efflux systems or the combination of these mechanisms.

Background Klebsiella pneumoniae is a common cause of nosocomial infections. Antibiotic resistance and ability to form biofilm, as two key virulence factors of K. pneumoniae, are involved in the persistence of infections. The purpose of this study was to investigate the correlation between antimicrobial resistance and biofilm formation capability among K. pneumoniae strains isolated from hospitalized patients in Iran. Methods Over a 10-month period, a total of 100 non-duplicate K. pneumoniae strains were collected. Antibiotic susceptibility was determined by Kirby–Bauer disk diffusion method according to CLSI. Biofilm production was assessed by tissue culture plate method. Finally, polymerase chain reaction was conducted to detect four families of carbapenemase: blaIMP, blaVIM, blaNDM, blaOXA−48; biofilm formation associated genes: treC, wza, luxS; and K. pneumoniae confirming gene: rpoB. Results Most of the isolates were resistant to trimethoprim-sulfamethoxazole (52 %), cefotaxime (51 %), cefepime (43 %), and ceftriaxone (43 %). Among all the 100 isolates, 67 were multidrug-resistant (MDR), and 11 were extensively drug-resistant (XDR). The prevalence of the blaVIM, blaIMP, blaNDM, and blaOXA−48 genes were 7 , 11 , 5 , and 28 %, respectively. The results of biofilm formation in the tissue culture plate assay indicated that 75 (75 %) strains could produce biofilm and only 25 (25 %) isolates were not able to form biofilm. Among these isolates, 25 % formed fully established biofilms, 19 % were categorized as moderately biofilm-producing, 31 % formed weak biofilms, and 25 % were non-biofilm-producers. The antimicrobial resistance among biofilm former strains was found to be significantly higher than that of non-biofilm former strains (p < 0.05). Molecular distribution of biofilm formation genes revealed that 98 , 96 , and 34 % of the isolates carried luxS, treC, and wza genes, respectively. Conclusions The rise of antibiotic resistance among biofilm-producer strains demonstrates a serious concern about limited treatment options in the hospital settings. All of the data suggest that fundamental actions and introduction of novel strategies for controlling of K. pneumoniae biofilm-related infections is essential.