Phenotypic and genotypic evaluation of aminoglycoside resistance in Escherichia coli isolated from patients with blood stream infections in Tehran, Iran.

Background and Objectives: Escherichia coli is a significant causative agent of bloodstream infections (BSIs). Aminoglycoside antibiotics play a crucial role in treating severe infections such as sepsis and pneumonia. However, resistance to these antibiotics often occurs due to the production of aminoglycoside-modifying enzymes (AMEs). This study was conducted to assess antimicrobial susceptibility patterns against various aminoglycosides and to determine the prevalence of common AME genes in E. coli strains isolated from BSIs. Materials and Methods: Sixty-five E. coli isolates were obtained from blood samples in a referral hospital in Tehran, Iran. The susceptibility patterns of aminoglycosides were determined using disk diffusion method and AMEs genes were investigated using PCR assay. Results: Resistance to aminoglycosides was observed in 64.6% (42/65) of the isolates. The most frequent resistance rate was found for kanamycin (44.6%) and gentamicin (38.5%), followed by tobramycin (29.2%) and amikacin (4.6%). The most frequent AME gene was aac(3)-IVa, which detected in 49.2% isolates, followed by aac(6)-Ib (40%), aac(3)-IIa (32.3%), and ant(2)-Ia (30.8%), respectively. Conclusion: Athough the findings of this survey are based on specimens collected from a single hospital, our study shows that the high prevalence of aminoglycoside resistance is primarily attributed to the presence of the aac(3)-Iva, aac(6)-Ib and aac(3)-IIa genes. The low rate of resistance to amikacin makes this antibiotic a good candidate for treatment of BSIs due to E. coli.

Antimicrobial resistance pattern, virulence determinants and molecular analysis of carbapenem-resistant Klebsiella pneumoniae isolated from clinical samples in Iran.

Carbapenem-resistant Klebsiella pneumoniae (CRKP) has emerged as an important global threat in recent years. The objective of the present study was to characterize the molecular characteristics, antibiotic resistance pattern and the distribution of virulence factors in CRKP isolated from different clinical specimens. A total of 60 clinical CRKP isolates were collected from clinical samples. Based on Clinical Laboratory Standards Institute guidelines, antimicrobial susceptibility testing was assessed by the disk diffusion method. Carbapenem and aminoglycoside resistance determinants in addition to virulence genes were inspected by PCR. Molecular characteristics of CRKP isolates were analyzed by random amplified polymorphic DNA (RAPD) PCR and enterobacterial repetitive intergenic consensus (ERIC) PCR. All isolates were resistant to imipenem, meropenem, cefoxitin, levofloxacin, cefotaxime, ceftazidime and ciprofloxacin. Resistance to tetracycline, gentamicin and kanamycin were detected in 53%, 75% and 72% of isolates, respectively. The most common carbapenem resistance genes were OXA-48 (28.5%) and NDM (22%). The most common aminoglycosides resistance genes were aac6´Ib (57%) and aac(3)-IVa (28%). The most prevalent virulence genes were mrkD (82%), entB (62%) and ybts (58%). ERIC and RAPD analyses revealed 55 and 53 different patterns of CRKP isolates, respectively. We conclude that CRKP infections have been associated with different genotypes and that the carbapenemase type (OXA-48) and AME gene (aac6´-Ib) were widely distributed in CRKP isolates in our hospital. Continued compliance with existing phenotypes and genotypes, and strict enforcement of infection control guidelines, are recommended approaches for the prevention and dissemination of these strains.

Multiple-locus variable-number tandem repeat analysis for genotyping of erythromycin-resistant group B streptococci in Iran.

BACKGROUND: Group B Streptococcus (GBS or S. agalactiae) is an important pathogen causing severe invasive diseases in neonates, pregnant women, and adults with underlying medical conditions. METHODS: To investigate the incidence of resistance to macrolide, lincosamide and streptogramin type B (MLSB) antibiotics, macrolide and tetracycline resistance determinants and genetic relationships, a total of 146 clinical isolates of GBS were collected from Tehran, Iran. The genetic relationships between erythromycin-resistant strains were determined by multilocus variable tandem repeat analysis (MLVA). RESULTS: All isolates were susceptible to penicillin, vancomycin, linezolid, and quinupristin-dalfopristin, but were resistant to tetracycline (96.6%, 141/146), erythromycin (28.1%, 41/146) and clindamycin (16.4%, 24/146). Among the 41 erythromycin-resistant GBS (ERGBS), the most common antimicrobial resistance gene was tetM detected in 92.7% (38/41) of the isolates followed by ermTR and ermB found in 65.8% (27/41) and 29.3% (12/41) of isolates, respectively. Of the 41 ERGBS, 95% (39/41) exhibited the constitutive MLSB phenotype, 2.4% (1/41) displayed inducible MLSB and 2.4% (1/41) had M phenotype. The erm methylase genes were widely related to MLSB phenotype isolates, while the mefA gene was associated with M phenotype. MLVA analysis performed on the 41 ERGBS revealed that 34 MLVA types (MTs). MLVA analysis showed that infections due to ERGBS have been caused by a variety of genotypes, suggesting that ERGBS were clonally unrelated and dissemination of these isolates was not due to a clonal outbreak. CONCLUSION: Careful usage of macrolide antibiotics in therapy, continued surveillance of resistance rate and appropriate infection control measures can help to reduce spreading of resistance isolates.

Postprandial glycemia and insulin secretion following glutamine administration: A randomized controlled trial.

Objective: The objective of the present study is to investigate the effects of glutamine administration on postprandial glycemia, insulin, and C-peptide concentration in patients with type 2 diabetes. Methods: A randomized, double-blind, placebo-controlled trial was conducted on patients with type 2 diabetes so that 33 subjects were recruited in each group. The patients were randomly allocated to receive either 30 g/d glutamine or placebo (with instructions to take in half glass of ice-cold water 5 to 10 min before each main meal) for 6 weeks. Postprandial C-peptide, insulin, and glucose were measured at the baseline and at the end of the study at 30 and 90 min after consuming a meal comprising wheat-cake and reduced fat milk. Results: The repeated measures ANOVA revealed no significant difference between the groups for glucose and insulin after 6 weeks of intervention (p > 0.05). However, C-peptide was reduced in both intervention groups at all measurement points. Between-group differences remained significant by the end of the study (p = 0.02). Conclusions: Glutamine supplementation before each main meal does not represent an effective nutritional strategy to improve postprandial glycemic control or postprandial insulin secretion in type 2 diabetes patients.