Clonal relationships, antimicrobial susceptibilities, and molecular characterization of extended-spectrum beta-lactamase-producing escherichia coli isolates from urinary tract infections and fecal samples in southeast Iran

<div><p>Abstract INTRODUCTION: Multidrug-resistant (MDR) Escherichia coli, a species that is a leading cause of urinary tract infections (UTIs) and is a major global public health concern. This study was designed to detect the differences in antibiotic resistance patterns, the production and type of extended spectrum β-lactamases (ESBLs), and the clonal relationships among E. coli isolates from UTIs and fecal samples. METHODS: Antibacterial resistance was determined by the disk diffusion method. ESBL, carbapenemase, and AmpC-producing isolates were detected phenotypically. Then, the ESBL genes were sequenced to detect the type. Enterobacterial repetitive intergenic consensus-polymerase chain reaction (ERIC-PCR) was performed on the ESBL-positive isolates. RESULTS: The most common effective antibacterial agents were colistin, imipenem, and amikacin. Among the isolates, 204 (56.6%) were MDR. Of the 163 ESBL-positive isolates, 11 (6.7%) produced AmpC, and the frequencies of beta-lactamase-positive genes were as follows: bla CTX-Mgroup1, 76%; bla TEM1, 74.8%; bla SHV12, 1.2%; and bla OXA1, 12.88%. ERIC PCR showed a diverse pattern, suggesting that clonal spread of E. coli in this area is uncommon, and that most of the infecting strains are endogenous. CONCLUSIONS: The high rates of antibacterial-resistant and MDR isolates are quite important since these strains can act as source of resistant bacteria that can be spread in the community. Controlling antibiotic use, against inappropriate use and abuse, in the community and continuous surveillance of emerging resistance traits are critical to controlling the spread of resistance.</p></div

Comparison of virulence genes and phylogenetic groups of Escherichia coli isolates from urinary tract infections and normal fecal flora

Introduction: Escherichia coli is the most common cause of urinary tract infections (UTI). The gut is a suggested to be a common pool of E. coli isolates causing UTIs. The aim of present study was determination of phylogenetic groups in UTI and normal fecal flora isolates of E. coli and to compare the presence of virulence genes between these isolates. Material and methods: A total of 100 E. coli comprising 50 nonduplicated isolates from UTI and 50 isolates from fecal flora were collected in this study. All these isolates were identification by routine biochemical tests. Virulence genes were determined by the PCR method. Phylogenetic groups were determined using PCR and multiplexes PCR method. Results: The fyuA and iucD genes were the most common virulence factors among both UTIs and fecal flora isolates. The virulence genes vat, chuA, iroN was found to be significantly dominant in the UTI isolates compared to the fecal flora isolates (P < .05). vat gene was only detected in the UTIs isolates. Most of the isolates were in the phylogroups B1 and D. However, significantly higher isolates from UTIs belonged to the phylogroup B2 and D and the fecal flora in the phylogroup B1 and clade 1. The prevalence of vat and yfcV genes was significantly higher in the phylogroupB2 and vat gene in group D. Conclusions: This study showed that the E. coli isolates from UTIs have significantly higher numbers of virulence genes compared to the fecal flora, and the phylogroups of these isolates were not the same. Study with the higher number of isolates is recommended for a better characterization of E. coli causing UTIs. © 2020 Elsevier Inc

In vitro reducing effect of cloxacillin on minimum inhibitory concentrations to imipenem, meropenem, ceftazidime, and cefepime in carbapenem-resistant pseudomonas aeruginosa isolates

Today, resistance to antibacterial agents is the most important problem facing public health. Pseudomonas aeruginosa is a common gram-negative bacterium and an important cause of nosocomial infections. Resistance to many antibiotics in strains of P. aeruginosa isolated from hospital settings such as cephalosporins and carbapenems have been recently reported. Therefore, the introduction of a new strategy to treat the infection of these organisms will be beneficial. In this study we determined the ability of cloxacillin to reduce Minimum Inhibitory Concentrations (MICs) of carbapenem-resistant P. aeruginosa to imipenem (IMI), meropenem (MEM), ceftazidime (CAZ), and cefepime (FEP). From 2015 to 2017, 61 non-duplicates of carbapenem-resistant P. aeruginosa were collected from clinical samples of hospitalized patients in Kerman, Iran. The MICs of the isolates to IMI, MEM, CAZ, and FEP with/without cloxacillin were determined by microbroth dilution method. The level of MIC of isolates to carbapenems (IMI and MEM) and cephalosporins (CAZ and FEP) ranged from 1-256 μg/mL and 4-1024 μg/mL alone and from 1-32 μg/mL and 1-512 μg/mL in combination with cloxacillin, respectively. The MIC showed a significant difference reduction after the addition of cloxacillin (P � 0.05). Our results showed in vitro potentially of cloxacillin in reduction of MIC to IMI, MEM, CAZ, and FEP in multi-drug resistant P. aeruginosa, therefore combination of these antibiotics with cloxacillin could be beneficial for treatment of infections caused by multi-drug resistant P. aeruginosa. © 2020, Yale Journal of Biology and Medicine Inc. All rights reserved

ISPpu22, a novel insertion sequence in the oprD porin gene of a carbapenem-resistant Pseudomonas aeruginosa isolate from a burn patient in Tehran, Iran

BACKGROUND AND OBJECTIVES: The oprD mutation and AmpC overproduction are the main mechanisms of intrinsic resistance to carbapenems such as imipenem and meropenem in Pseudomonas aeruginosa. MATERIALS AND METHODS: In this study, we investigated intrinsic resistance to carbapenems including mutation of oprD and AmpC overproduction in a carbapenem-resistant P. aeruginosa isolated from a burn patient by phenotypic and molecular methods. RESULTS: In our study, the carbapenem-resistant P. aeruginosa isolate was resistant to imipenem, meropenem, cefepime, gentamicin, ceftriaxone, carbenicillin, aztreonam and ciprofloxacin but was susceptible to ceftazidime and polymyxin B. The minimum inhibitory concentrations (MICs) against imipenem, meropenem and ceftazidime were 64 μg/ml, 16 μg/ml and 2μg/ml, respectively. The isolate was ESBLs and AmpC overproducer. No carbapenemase activity was detected by Modified Hodge test (MHT). This isolate was carrying only bla OXA-10 . PCR amplification and sequencing of oprD performed on isolate resulted in PCR product of 2647bp. Sequence analysis of the 2647bp product revealed insertion of a sequence of 1232 bp at position 8 in coding region of oprD. CONCLUSION: According to the results of this study, oprD mutation and AmpC overproduction can cause the main mechanism of resistance of P. aeruginosa to carbapenems