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Carbapenem-resistant (CRE) is a major concern leading to morbidity and mortality in the world. CRE often is becoming a cause of therapeutic failure in both hospital and community-acquired infections. This study aimed to investigate the resistance mechanisms of CRE by phenotypic and molecular methods. Sixty CRE (50 , 6 , and 4 spp.) were isolated from October 2018 to June 2019. Antimicrobial susceptibility testing was carried out using phenotypic methods. The carbapenem resistance mechanisms including efflux pump hyperexpression, AmpC overproduction, carbapenemase genes, and deficiency in and were determined by phenotypic and molecular methods, respectively. Sixty CRE (50 , 6 , and 4 spp.) were isolated from October 2018 to June 2019. Amikacin was found to be the most effective drug against CRE isolates. All isolates were resistant to imipenem and meropenem by the micro-broth dilution. AmpC overproduction was observed in all spp. and three isolates. No efflux pump activity was found. Carba NP test and Modified Hodge Test could find carbapenemase in 59 (98%) isolates and 57 (95%) isolates, respectively. The most common carbapenemase gene was (72.8%) followed by (50.8%), (18.6%), (11.8%), and (6.7%). The and genes were not detected in 10 and 7 isolates, respectively. The amikacin is considered as a very efficient antibiotic for the treatment of CRE isolates in our region. Carbapenemase production and overproduction of AmpC are the main carbapenem resistance mechanisms in CRE isolates. Finally, Carba NP test is a rapid and reliable test for early detection of carbapenemase-producing isolates.

There has been excessive rate of use of antibiotics to fight Pseudomonas aeruginosa (P. aeruginosa) infections worldwide, which has consequently caused the increased resistance to multiple antibiotics in this pathogen. Due to the widespread resistance and the current poor effect of antibiotics consumed to treat P. aeruginosa infections, finding some novel alternative therapeutic methods are necessary for the treatment of infections. The P. aeruginosa biofilms can cause severe infections leading to the increased antibiotic resistance and mortality rate among the patients. In this regard, there are no approaches that can efficiently manage these infections; therefore, novel and effective antimicrobial and antibiofilm agents are needed to control and treat these bacterial infections. Quorum sensing inhibitors (QSIs) or quorum quenchings (QQs) are now considered as potential therapeutic alternatives and/or adjuvants to the current failing antibiotics, which can control the virulence traits of the pathogens, so as a result, the host immune system can quickly eliminate bacteria. Thus, the aims of this review article were presenting a brief explanation of the research reports on the natural and synthetic QSIs of P. aeruginosa, and the assessment of the current understanding on the QS mechanisms and various QQ strategies in P. aeruginosa. Keywords: Pseudomonas aeruginosa, quorum quenchings, quorum sensing, nanoparticle, natural compounds, synthetic compounds

Carbapenemase-resistant Klebsiella pneumoniae (CRKP) is a genuine burden for physicians and researchers. We aimed at carbapenemase resistance and its relation with capsular serotyping in K. pneumoniae and studied some clinical determinants, which may influence the clinical infections. Initially, 61 K. pneumoniae isolates obtained from various clinical specimens were confirmed at the molecular level and then antimicrobial susceptibility test was performed followed by capsular serotyping performed by multiplex PCR. All isolates were subjected to the detection of carbapenemase genes including blaKPC, blaNDM-1, blaOXA-48, blaVIM, and blaIMP. Clinical and demographic data of all patients were reviewed including age, gender, underlying diseases, and the treatment obtained. Multidrug-resistance was a predominant feature in 77% K. pneumoniae strains. Presence of extended-spectrum beta-lactamase was detected phenotypically in 59% K. pneumoniae strains. Carbapenem resistance was noticed phenotypically in 24.6% isolates. blaOXA-48 and blaNDM-1 were the most frequent carbapenemase genes. blaNDM-1 positive isolates correlated with gentamicin, amikacin, imipenem, and meropenem resistance (p<0.05). The nosocomial isolates mostly harbored blaOXA-48 gene (p<0.02). Amongst all the K. pneumoniae isolates, 59% isolates could be typed and serotype K54 had the highest prevalence followed by K20 and K5. Correlation between the carbapenemase genes, serotype and type of infection showed that blaOXA-48 positive strains had a significant association with K20 serotype and urinary tract infections (p=0.2) while, K20 serotype and blaKPC positive strains were significantly associated with wound infections (K20, p=0.3 and blaKPC, and p=0.4). Mucoid phenotype was not found related to presence of specific carbapenemase genes or serotypes except serotype K20 (p<0.001). Patients with monotherapy had treatment failure in comparison to the combination therapy for blaKPC-associated infections. In conclusion, the present investigation exhibited the significant association between K20 serotype with blaOXA-48. The predominance of K54 reveals the possibility of endemicity in our hospital setting. K. pneumoniae isolated from wound specimens significantly harbors K20 serotype and blaKPC gene. Comprehensive clinical information and the distribution of antibiotic resistance genes, and serotypes may play important roles in the treatment process.

Background Neutropenia is the most important cause of life-threatening invasive fungal infections (IFIs). Here, we studied the frequency and antifungal susceptibility profiles of Candida species that colonized or caused infections among neutropenic patients with solid or hematological malignancies. Methods A total of 362 clinical samples were collected from 138 patients. After initial isolation using a mix of mycological methods, isolates were screened using chromogenic culture media. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was applied for molecular identification. Positive or suspected cases were confirmed using the reference method of sequencing. Antifungal susceptibility testing for voriconazole and caspofungin was carried out using the microbroth dilution method. An in-silico assay was applied for phylogenetic analysis. Results Thirty-four Candida strains were isolated. C. albicans (47.06%) and C. glabrata (29.41%) were the most frequent strains. Antifungal treatment reduced the chance of Candida colonization by almost 76% in neutropenic patients (OR: 1.759; 95% CI: 1.349 to 2.390; p value: 0.000). An unusual and non-resistant strain, C. lambica , was reported from the bloodstream of a 56-year-old man with hematologic malignancy (HM). Eight isolates were non-susceptible, and one isolate was resistant to voriconazole. Also, four isolates were non-susceptible to caspofungin. Conclusion We can conclude that there is a cause-and-effect relationship between neutropenia, HM background, and Candida species separated from neutropenic patients, which can lead to possible infections. Further and repetitive studies are recommended using different molecular methods for better prediction and management of fungal infections in neutropenic patients.

Different clones of community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) are dominating geographically. One of the significant, hypervirulent, CA-MRSA and a significant health concern clones is USA3000, found worldwide regionally with varying frequencies. The clone harbors several mobile genetic elements (MGEs) including, arginine catabolic mobile element (ACME) and copper and mercury resistance genes (COMER), accomplished by horizontal gene transfer from S. epidermidis. Evidence suggests that ACME and COMER have a more prominent role in enhancing biofilm capacity and ultimately persistent infections. This review highlights the comprehensive view on ACME and COMER structure, their distribution, and the mechanism of action along with pathogenetic features of USA3000 encompassing their role in biofilm formation, adhesion, quorum sensing, resistance to antibiotics, chemotaxis, and nutrient uptake. We also provided an insight into the role of ACME and COMER genes in the survival of bacterium. Our results shed light on the emergence of two independent clones possessing ACME (North American) and COMER (South American) elements which later disseminated to other regions. ACME and COMER both are adjacent to staphylococcal cassette chromosome mec type IV (SCCmec IV). The acquisition of mecA, followed by COMER or ACME has been shown as a significant factor in the rise and fall of MRSA strains and their complex ability to adapt to hostile environments. The presence of ACME increases fitness, thereby allowing bacteria to colonize the skin and mucous membrane while COMER contributes to genetic stability by knocking over the copper-mediated killing in macrophages. Evidence suggests that ACME and COMER have a more prominent role in enhancing biofilm capacity and ultimately persistent infections. Interestingly, ACME strains have been shown to possess the ability to counteract skin acidity, thereby allowing increased skin colonization. A profound understanding of MGEs in S. aureus plays an important role in the prevention of epidemic clones.

, one of the clinical superbugs, causes diverse infections because of its variable capsular antigens. This study focused on and aimed to assess any correlation between capsular serotype, capsule-associated virulence genes, and evaluate its resistance to conventional antibiotics in order to gain insight into any regional differences. A total of 61 collected from various clinical specimens were confirmed genotypically. Clinical and demographic data for all patients were reviewed. All isolates were subjected to antimicrobial susceptibility tests. Capsular serotyping and capsule-associated virulence genes were studied using the molecular method. All typeable isolates were typed into K5, K20, and K54 serotypes, and among them, K54 was observed to be predominant. The most common capsule-associated virulence genes comprised (93.4%), (91.8%), and (88.5%), while (29.5%) and (21.3%) were noted at much lower prevalence rates. The gene was significantly associated with K54 positive isolates ( = 0.001), while was associated with K20 positive isolates ( = 0.01). Serotype K54 had a high frequency in isolates collected from patients with pulmonary diseases, while serotype K20 was associated with burn patients. Carbapenems and levofloxacin were the best therapeutic options for the treatment of infections with serotypes K20 and K54.

Accumulating evidence indicates that specific strains of mucosa-associated Escherichia coli (E. coli) can influence the development of colorectal carcinoma. This study aimed to investigate the prevalence and characterization of mucosa-associated E. coli obtained from the colorectal cancer (CRC) patients and control group. At two referral university-affiliated hospitals in northwest Iran, 100 patients, 50 with CRC and 50 without, were studied over the course of a year. Fresh biopsy specimens were used to identify mucosa-associated E. coli isolates after dithiothreitol mucolysis. To classify the E. coli strains, ten colonies per sample were typed using enterobacterial repetitive intergenic consensus-based PCR (ERIC-PCR). The strains were classified into phylogroups using the quadruplex PCR method. The PCR method was used to examine for the presence of cyclomodulin, bfp, stx1, stx2, and eae-encoding genes. The strains were tested for biofilm formation using the microtiter plate assay. CRC patients had more mucosa-associated E. coli than the control group (p<0.05). Enteropathogenic Escherichia coli (EPEC) was also found in 23% of CRC strains and 7.1% of control strains (p<0.05). Phylogroup A was predominant in control group specimens, while E. coli isolates from CRC patients belonged most frequently to phylogroups D and B2. Furthermore, the frequency of cyclomodulin-encoding genes in the CRC patients was significantly higher than the control group. Around 36.9% of E. coli strains from CRC samples were able to form biofilms, compared to 16.6% E. coli strains from the control group (p<0.05). Noticeably, cyclomodulin-positive strains were more likely to form biofilm in comparison to cyclomodulin-negative strains (p<0.05). In conclusion, mucosa-associated E. coli especially cyclomodulin-positive isolates from B2 and D phylogroups possessing biofilm-producing capacity colonize the gut mucosa of CRC patients.

Cell density-based intercellular signaling mechanism is known as Quorum sensing (QS); it serves a significant role in regulating the pathogenic factors. The objective of the present study was to assess the influence of chitosan-zinc oxide nanocomposite (CH-ZnO nanocomposite), alone and in combination with gentamicin, on the sensitivity to hydrogen peroxide (H2O2), the production of pathogenic factors and QS-regulated genes of Pseudomonas aeruginosa. The efficacy of the minimum inhibitory concentration (MIC) and 1/4 MIC of the CH-ZnO nanocomposite, alone and in combination with gentamicin, on the sensitivity to H2O2, pyocyanin secretion, swarming and twitching motilities was evaluated. In addition, the expression of some QS-regulated genes including rhlI, rhlR, lasI and lasR genes was measured by Real-time quantitative PCR (RT-qPCR) following exposure to the nanocomposite. The results demonstrated that at MIC concentrations, the gentamicin-loaded CH-ZnO nanocomposite significantly inhibited QS-regulated phenotypes such as pyocyanin secretion (82.4%), swarming (76%) and twitching (73.6%) motilities; further it increased the inhibition growth zone (134.5%), as well as, at 1/4 MIC concentration decreased the expression of lasI (72%), lasR (78%), rhlI (76%) and rhlR (82%) genes; as compared to untreated P. aeruginosa PAO1 (P < 0.05). Our results also demonstrated that the CH-ZnO nanocomposite combined with gentamicin could be a potential innovative candidate, which could be broadly applied in the treatment of P. aeruginosa infections.

Background: The success of Staphylococcus aureus is as an important human pathogen is probably due to possession of various virulence determinants. Attachment and biofilm formation is considered the main step in any infection. The present study aimed to determine the presence of S. aureus surface (sas) genes and their association with biofilm formation and antibiotic resistance. Methods: S. aureus isolates collected were analyzed for biofilm formation using polystyrene microtitre plates. All S. aureus isolates were also examined for the determination of sas genes by PCR assays and antibiotic susceptibility assay by disk diffusion method. Results: Biofilm formation assay revealed that 29 S.aureus isolates were weak biofilm producers, 57 had moderate biofilm production, while only five isolates showed strong biofilm formation. The biofilm production was not revealed among nine isolates. The frequency of sas genes were 95 (88%), 94 (87%), 94 (87%), 92 (85.2%), 98 (90.7%), 93 (86.1%), 97 (89.8%), 87 (80.6%), and 85 (78.7%) for sasF, sasA, sasC, sasE, sasG, sasH, sasI, sasJ, and sasK genes, respectively. Conclusion: High incidence of biofilm production was noticed in S.aureus strains positive for sas genes indicating the precise role of them as virulence-associated genes. Moreover, phenotypically weak or moderate biofilm formation can be well managed by antibiotic therapeutics and allow timely elimination of planktonic cells prior biofilm production.