scholarly journals Emergence of Nosocomial Pneumonia Caused by Colistin-Resistant Escherichia coli in Patients Admitted to Chest Intensive Care Unit

Antibiotics ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 226 ◽  
Author(s):  
Mohamed A. El-Mokhtar ◽  
Enas Daef ◽  
Aliae A. R. Mohamed Hussein ◽  
Maiada K. Hashem ◽  
Hebatallah M. Hassan

(1) Background: Colistin is a last-resort antibiotic used in treating multidrug-resistant Gram-negative infections. The growing emergence of colistin resistance in Escherichia coli (E. coli) represents a serious health threat, particularly to intensive care unit (ICU) patients. (2) Methods: In this work, we investigated the emergence of colistin resistance in 140 nosocomial E. coli isolated from patients with pneumonia and admitted to the chest ICU over 36 months. Virulence and resistance-related genes and E. coli pathotypes in colistin-resistant and colistin-sensitive isolates were determined. (3) Results: Colistin resistance was observed in 21/140 (15%) of the nosocomial E. coli isolates. The MIC50 of the resistant strains was 4 mg/L, while MIC90 was 16 mg/L. Colistin-resistant isolates were also co-resistant to amoxicillin, amoxicillin/clavulanic, aztreonam, ciprofloxacin, and chloramphenicol. The mechanism of colistin resistance was represented by the presence of mcr-1 in all resistant strains. Respectively, 42.9% and 36.1% of colistin-resistant and colistin-sensitive groups were extended-spectrum β-lactamase (ESBL) producers, while 23.8% and 21% were metallo β-lactamase (MBL) producers. blaTEM-type was the most frequently detected ESBL gene, while blaIMP-type was the most common MBL in both groups. Importantly, most resistant strains showed a significantly high prevalence of astA (76.2%), aggR (76.2%), and pic (52.4%) virulence-related genes. Enteroaggregative E. coli (76%) was the most frequently detected genotype among the colistin-resistant strains. (4) Conclusion: The high colistin resistance rate observed in E. coli strains isolated from patients with nosocomial pneumonia in our university hospital is worrisome. These isolates carry different drug resistance and virulence-related genes. Our results indicate the need for careful monitoring of colistin resistance in our university hospital. Furthermore, infection control policies restricting the unnecessary use of extended-spectrum cephalosporins and carbapenems are necessary.

Author(s):  
Ifeyinwa N. Nwafia ◽  
Martin E. Ohanu ◽  
Samuel O. Ebede ◽  
Uchenna C. Ozumba

Abstract Background The use of antibiotic agents in the treatment of infectious diseases has greatly contributed to the decrease in morbidity and mortality, but these great advances in treatment are being undermined by the rapidly increasing antimicrobial resistant organisms. Extended-spectrum beta-lactamases are enzymes hydrolyzing the beta lactam antibiotics, including third generation cephalosporins and monobactams but not cephamycins and carbapenems. They pose a serious global health threat and have become a challenge for health care providers. The aim of this research was to assess the prevalence of extended-spectrum beta-lactamase producing Escherichia coli in University of Nigeria Teaching Hospital Ituku-Ozalla Enugu and to detect the risk factors for acquisition of the resistant organism. To proffer advice on antibiotic stewardship in clinical practice and public health interventions, to curb the spread of the resistant organisms in the hospital. Results Out of the 200 E. coli isolates, 70 (35.00%) were confirmed positive for extended-spectrum beta-lactamase production. Fifty-three (75.7%) were from hospital acquired infections. All the isolates were resistant to ampicillin, tetracycline and chloramphenicol while 68 (97.14%) of the 70 isolates were susceptible to imipenem. BlaTEM, blaSHV and blaTEM were detected in 66 (94%) of the 70 isolates. The ESBL bla genes detected were blaCTX-M (n = 26; 37.14%), blaTEM (n = 7; 10.00%), blaSHV (n = 2; 2.86%), blaCTX-M/TEM (n = 7; 10.0%), blaCTX-M/SHV (n = 14; 20.0%) and blaCTX-M/TEM/SHV (n = 10; 14.29%). The three bla genes were not detected in 4 (5.71%) of the isolates. Recent surgery, previous antibiotic and intensive care unit admission were the associated risk factors to infections caused by extended-spectrum beta-lactamase producing E. coli. Conclusion There is a high rate of infections caused by extended-spectrum beta-lactamase producing E. coli. Recent surgery, previous antibiotic and intensive care unit admission were associated risk factors.


2021 ◽  
Vol 7 (1) ◽  
pp. 8
Author(s):  
Ni Luh Ranthi Kurniawathi ◽  
Indramawan Setyojatmiko ◽  
Ni Nyoman Sri Budayanti

Resistesi antibiotik meningkat secara global dalam beberapa tahun ini, terutama kejadian Escherichia coli (E.coli) dan Klebsiella pneumoniae (K.pneumoniae) penghasil Extended Spektrum Beta Lactamases (ESBL). Tujuan dari penelitian ini adalah untuk memberikan gambaran prevalensi keberadaan dan antibiogram isolat E.coli dan K. pneumoniae penghasil ESBL di rumah sakit tersier di Bali. Penelitian retrospektif potong lintang ini dlikaukan pada Januari 2018- Desember 2020 di Rumah Sakit Umum Pusat Sanglah, Bali. Identifikasi bakteri dan uji sensitivitas antibiotik dilakukan dengan alat otomatis Vitek®2 Compact. Hasil penelitian menunjukkan dari 2972 isolat, 1067 (63,82%) isolat adalah E. coli penghasil ESBL dan 902 isolat (69,39%) adalah K. pneumoniae penghasil ESBL. Isolat penghasil ESBL ditemukan terbanyak pada non-ICU (89,39%). Bakteri E.coli penghasil ESBL menunjukkan sensitivitas > 80% terhadap Amikacin, Ertapenem, Meropenem, Nitrofurantoin, Piperacillin-tazobactam, dan Tigecycline. Sedangkan, K. pneumoniae penghasil ESBL menunjukkan sensitivitas > 80% terhadap Amikacin, Ertapenem, Meropenem, dan Tigecycline. Penelitian ini menyoroti tingginya prevalensi E.coli dan K.pneumoniae penghasil ESBL di rumah sakit rujukan tersier di Bali. Analisis yang seksama dari antibiogram kedua spesies penghasil ESBL tersebut akan membantu menyusun kebijakan penggunaan antibiotik dan pencegahan, pengendalian penyebaran bakteri penghasil ESBL.Kata Kunci: Escherichia coli; Klebsiella pneumoniae; Extended Spectrum Beta Lactamases; ICU dan Non-ICU


2011 ◽  
Vol 56 (1) ◽  
pp. 54-58 ◽  
Author(s):  
Jesús Oteo ◽  
Emilia Cercenado ◽  
Sara Fernández-Romero ◽  
David Saéz ◽  
Belén Padilla ◽  
...  

ABSTRACTLittle information is available about pediatric infections caused by extended-spectrum-β-lactamase (ESBL)-producingEscherichia coli. We characterized an outbreak caused by a CTX-M-14-producingE. coliisolate in a neonatal intensive care unit (NICU) and studied other infections caused by ESBL-producingE. coliin non-NICU pediatric units. All children ≤4 years old who were infected or colonized by ESBL-producingE. coliisolates between January 2009 and September 2010 were included. Molecular epidemiology was studied by phylogroup analysis, pulsed-field gel electrophoresis (PFGE), and multilocus sequence typing. Antibiotic resistance genes were analyzed by PCR and sequencing. Plasmids were studied by PFGE with S1 nuclease digestion and by incompatibility group analysis using a PCR-based replicon-typing scheme. Of the ESBL-producingE. coliisolates colonizing or infecting the 30 newborns, identical PFGE results were observed for 21 (70%) isolates, which were classified as CTX-M-14-producingE. coliof ST23 phylogroup A.blaCTX-M-14awas linked to ISEcp1and was carried on an ∼80-bp IncK plasmid. A smaller ongoing outbreak due to SHV-12-producing ST131E. coliwas also identified in the same NICU. Fifteen additional infections with ESBL-producingE. coliwere identified in non-NICU pediatric units, but none was caused by the CTX-M-14-producingE. coliepidemic clone. Overall, CTX-M-14 (71.1%), CTX-M-15 (13.3%), and SHV-12 (13.3%) were the most important ESBLs causing pediatric infections in this study. Infections of newborns with CTX-M-14-producingE. coliwere caused by both clonal and nonclonal isolates.


2020 ◽  
Vol 19 (2) ◽  
pp. 447-453
Author(s):  
Abdulaziz Alqasim

Extra-intestinal pathogenic Escherichia coli (ExPEC) is commonly associated with causing urinary tract and bloodstream infections. Over the past two decades, the antimicrobial resistance of ExPEC has increasingly been reported [1]. Given that Saudi Arabia annually hosts mass religious events, such as Hajj, this review investigated several aspects of antimicrobial resistance of ExPEC in this country including the current prevalence of resistance and molecular epidemiology of ExPEC isolates. Generally, the overall prevalence of antibiotic resistance of ExPEC in Saudi Arabia is on increase. The current emergence of colistin resistance in ExPEC represents a major challenge to public health. Local molecular epidemiological studies have shown the dominance of E. coli sequence type 131 (E. coli ST131) over other major ExPEC STs. This is an important observation given that this clone has been associated with high multidrug resistance and extended-spectrum β-lactamases carriage. To reduce the burden of this resistance in the future, it would be crucial to avoid uncontrolled use of antibiotics in either clinical settings or animal food industry. Keywords: Extra-intestinal pathogenic Escherichia coli, Antimicrobial resistance, ST131, Saudi Arabia, Colistin resistance, Extended-spectrum β-lactamases


2014 ◽  
Vol 58 (8) ◽  
pp. 4814-4825 ◽  
Author(s):  
Tracy H. Hazen ◽  
LiCheng Zhao ◽  
Mallory A. Boutin ◽  
Angela Stancil ◽  
Gwen Robinson ◽  
...  

ABSTRACTThe IncA/C plasmids have been implicated for their role in the dissemination of β-lactamases, including gene variants that confer resistance to expanded-spectrum cephalosporins, which are often the treatment of last resort against multidrug-resistant, hospital-associated pathogens. AblaFOX-5gene was detected in 14Escherichia coliand 16Klebsiellaisolates that were cultured from perianal swabs of patients admitted to an intensive care unit (ICU) of the University of Maryland Medical Center (UMMC) in Baltimore, MD, over a span of 3 years. Four of the FOX-encoding isolates were obtained from subsequent samples of patients that were initially negative for an AmpC β-lactamase upon admission to the ICU, suggesting that the AmpC β-lactamase-encoding plasmid was acquired while the patient was in the ICU. The genomes of fiveE. coliisolates and sixKlebsiellaisolates containingblaFOX-5were selected for sequencing based on their plasmid profiles. An ∼167-kb IncA/C plasmid encoding the FOX-5 β-lactamase, a CARB-2 β-lactamase, additional antimicrobial resistance genes, and heavy metal resistance genes was identified. Another FOX-5-encoding IncA/C plasmid that was nearly identical except for a variable region associated with the resistance genes was also identified. To our knowledge, these plasmids represent the first FOX-5-encoding plasmids sequenced. We used comparative genomics to describe the genetic diversity of a plasmid encoding a FOX-5 β-lactamase relative to the whole-genome diversity of 11E. coliandKlebsiellaisolates that carry this plasmid. Our findings demonstrate the utility of whole-genome sequencing for tracking of plasmid and antibiotic resistance gene distribution in health care settings.


1992 ◽  
Vol 24 (1) ◽  
pp. 65-70 ◽  
Author(s):  
SØRen Loumann Nielsen ◽  
Bent Røder ◽  
Pascal Magnussen ◽  
Allan Engquist ◽  
Niels Frimodt-møller

2020 ◽  
Vol 8 (6) ◽  
pp. 893 ◽  
Author(s):  
Daniel Jaén-Luchoro ◽  
Antonio Busquets ◽  
Roger Karlsson ◽  
Francisco Salvà-Serra ◽  
Christina Åhrén ◽  
...  

Escherichia coli strain CCUG 78773 is a virulent extended-spectrum β-lactamase (ESBL)-producing ST131-O25b type strain isolated during an outbreak at a regional university hospital. The complete and closed genome sequence, comprising one chromosome (5,076,638 bp) and six plasmids (1718–161,372 bp), is presented. Characterization of the genomic features detected the presence of 59 potential antibiotic resistance factors, including three prevalent β-lactamases. Several virulence associated elements were determined, mainly related with adherence, invasion, biofilm formation and antiphagocytosis. Twenty-eight putative type II toxin-antitoxin systems were found. The plasmids were characterized, through in silico analyses, confirming the two β-lactamase-encoding plasmids to be conjugative, while the remaining plasmids were mobilizable. BLAST analysis of the plasmid sequences showed high similarity with plasmids in E. coli from around the world. Expression of many of the described virulence and AMR factors was confirmed by proteomic analyses, using bottom-up, liquid chromatography-tandem mass spectrometry (LC-MS/MS). The detailed characterization of E. coli strain CCUG 78773 provides a reference for the relevance of genetic elements, as well as the characterization of antibiotic resistance and the spread of bacteria harboring ESBL genes in the hospital environment.


2008 ◽  
Vol 52 (5) ◽  
pp. 1846-1849 ◽  
Author(s):  
Patricia J. Baudry ◽  
Kim Nichol ◽  
Melanie DeCorby ◽  
Laura Mataseje ◽  
Michael R. Mulvey ◽  
...  

ABSTRACT Resistance profiles were compared among 18 extended-spectrum-β-lactamase-producing (ESBL) and 27 acquired AmpC β-lactamase-producing Escherichia coli isolates collected from Canadian intensive care units from 2005 to 2006. ESBL-producing E. coli isolates were more likely to be gentamicin resistant (P < 0.03), fluoroquinolone resistant (P < 0.0001), and multidrug resistant (P < 0.0001) than AmpC-producing E. coli isolates.


mSphere ◽  
2020 ◽  
Vol 5 (2) ◽  
Author(s):  
Axel B. Janssen ◽  
Toby L. Bartholomew ◽  
Natalia P. Marciszewska ◽  
Marc J. M. Bonten ◽  
Rob J. L. Willems ◽  
...  

ABSTRACT Infections by multidrug-resistant Gram-negative bacteria are increasingly common, prompting the renewed interest in the use of colistin. Colistin specifically targets Gram-negative bacteria by interacting with the anionic lipid A moieties of lipopolysaccharides, leading to membrane destabilization and cell death. Here, we aimed to uncover the mechanisms of colistin resistance in nine colistin-resistant Escherichia coli strains and one Escherichia albertii strain. These were the only colistin-resistant strains of 1,140 bloodstream Escherichia isolates collected in a tertiary hospital over a 10-year period (2006 to 2015). Core-genome phylogenetic analysis showed that each patient was colonized by a unique strain, suggesting that colistin resistance was acquired independently in each strain. All colistin-resistant strains had lipid A that was modified with phosphoethanolamine. In addition, two E. coli strains had hepta-acylated lipid A species, containing an additional palmitate compared to the canonical hexa-acylated E. coli lipid A. One E. coli strain carried the mobile colistin resistance (mcr) gene mcr-1.1 on an IncX4-type plasmid. Through construction of chromosomal transgene integration mutants, we experimentally determined that mutations in basRS, encoding a two-component signal transduction system, contributed to colistin resistance in four strains. We confirmed these observations by reversing the mutations in basRS to the sequences found in reference strains, resulting in loss of colistin resistance. While the mcr genes have become a widely studied mechanism of colistin resistance in E. coli, sequence variation in basRS is another, potentially more prevalent but relatively underexplored, cause of colistin resistance in this important nosocomial pathogen. IMPORTANCE Multidrug resistance among Gram-negative bacteria has led to the use of colistin as a last-resort drug. The cationic colistin kills Gram-negative bacteria through electrostatic interaction with the anionic lipid A moiety of lipopolysaccharides. Due to increased use in clinical and agricultural settings, colistin resistance has recently started to emerge. In this study, we used a combination of whole-genome sequence analysis and experimental validation to characterize the mechanisms through which Escherichia coli strains from bloodstream infections can develop colistin resistance. We found no evidence of direct transfer of colistin-resistant isolates between patients. The lipid A of all isolates was modified by the addition of phosphoethanolamine. In four isolates, colistin resistance was experimentally verified to be caused by mutations in the basRS genes, encoding a two-component regulatory system. Our data show that chromosomal mutations are an important cause of colistin resistance among clinical E. coli isolates.


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