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Bacteria causing human infections can develop antibiotic resistance due to various factors. Temperature affects bacterial growth and gene transfer; however, studies exploring the association between the changes in local temperature and antibiotic resistance are limited. Here, we investigated the effects of local temperatures on the distribution of antibiotic resistance and transmission of carbapenemase-producing Enterobacterales using the data on Klebsiella pneumoniae from sentinel hospitals in eight regions included in the Korea Global Antimicrobial Resistance Surveillance System between 2017 and 2021. The resistance rates to most antibiotics, including carbapenems, varied significantly according to local temperature (p < 0.047), except for aminoglycosides. Conjugation experiments at various temperatures for strains encoding the carbapenemase gene on a plasmid revealed significant variation in the optimal conjugation temperatures for plasmids carrying blaKPC and blaNDM genes. The optimal conjugation temperatures demonstrating the highest stability for blaKPC- and blaNDM-carrying plasmids were 25 °C (p = 0.030) and 30 °C (p = 0.007), respectively. The stability of blaKPC-IncF was higher at 25 °C than that at 30 °C (p = 0.032) or 37 °C (p = 0.047), while blaKPC-IncX3 exhibited the lowest stability at 37 °C (p = 0.047). blaNDM-IncX3 was more stable at 30 °C than at 37 °C (p = 0.049). These findings suggest that the optimal temperature for carbapenemase gene transmission varied between 25 °C and 30 °C, indicating that warmer seasons promote the transfer of more antibiotic resistance-related genes and highlighting the importance of local temperature in the spread and transmission of plasmids carrying carbapenemases. [ABSTRACT FROM AUTHOR]

The emergence of third-generation cephalosporin resistance in Escherichia coli is increasing at an alarming rate in many countries. Thus, the aim of this study was to analyze co-infecting bla CTX-M-producing pathogenic E. coli isolates linked to three school outbreaks. Among 66 E. coli isolates, 44 were identified as ETEC O25, an ETEC isolate serotype was O2, and the other 21 were confirmed as EAEC O44. Interestingly, six patients were co-infected with EAEC O44 and ETEC O25. For these isolates, molecular analysis [antibiotic susceptibility testing, identification of the β-lactamase gene, multilocus sequence typing (MLST), and pulsed-field gel electrophoresis (PFGE)] was performed for further characterization. In addition, the transmission capacity of bla CTX-M genes was examined by conjugation experiments. Whole-genome sequencing (WGS) was performed on representative EAEC O44 and ETEC O25 isolates associated with co-infection and single-infection. All isolates were resistant to cefotaxime and ceftriaxone. All EAEC isolates carried the bla CTX-M-14 gene and all ETEC isolates the bla CTX-M-15 gene, as detected by multiplex PCR and sequencing analysis. Sequence type and PFGE results indicated three different patterns depending on the O serotype. WGS results of representative isolates revealed that the ETEC O25 strains harbored bla CTX-M-15 located on IncK plasmids associated with the Δ bla TEM- bla CTX-M-15- orf477 transposon. The representative EAEC O44 isolates carried bla CTX-M-14 on the chromosome, which was surrounded by the IS Ecp1 - bla CTX-M-14- IS903 transposon. To the best of our knowledge, this is the first report of co-infection with chromosomally located bla CTX-M-14 and plasmid-encoding bla CTX-M-15 in pathogenic E. coli. Our findings indicate that resistance genes in clinical isolates can spread through concurrent combinations of chromosomes and plasmids. [ABSTRACT FROM AUTHOR]

L-phenylalanine (Phe), one of the aromatic amino acids, and its hydrated clusters were generated in supersonic expansion and investigated by resonant two-photon ionization. Excitation spectra of Phe and Phe-(H[sub 2]O)[sub 1] were obtained near their S[sub 0]-S[sub 1] origins. We found that, by comparing the experimental results with the density functional theory and ab initio calculations, the water in Phe-(H[sub 2]O)[sub 1] tends to form a cyclic hydrogen bond at the carboxyl group while inducing little change in the corresponding monomer structure. No sign of water making bridged hydrogen bonds with both polar groups was found. In order to form the cyclic hydrogen bond, hydration takes place only with the conformers whose carboxyl hydrogen is free, i.e., not occupied in the intramolecular hydrogen bonding with the amino nitrogen in the monomer. [ABSTRACT FROM AUTHOR]

Objectives: To investigate the risk factors of patients with Klebsiella pneumoniae (KP) bloodstream infection (BSI) with a focus on antimicrobial resistance and virulence factors.Methods: All KP BSI patients (n = 579) from six general hospitals during a 1 year period were included in this study. The risk factors of hosts and causative KP isolates were assessed to determine associations with the 30 day mortality of KP BSI patients by multivariate Cox hazards modelling.Results: The 30 day mortality rate of KP BSI patients was 16.9% (98/579). Among the host-associated factors, increased SOFA score and leucopenia status exhibited strong associations with increased 30 day mortality. Among the pathogenic factors, carriage of the pks gene cluster (adjusted HR 1.80; 95% CI 1.16-2.79) was a risk factor, especially when accompanied by MDR. In this regard, KP isolates of the wzi50 capsular type (n = 22) frequently harboured pks (63.6%, 14/22) and ybtA (68.2%, n = 15) and mostly exhibited MDR (63.6%, n = 14), resulting in increased 30 day mortality. In contrast, hypermucoviscous KP isolates showed an inverse association with 30 day mortality (adjusted HR 0.55; 95% CI 0.33-0.90).Conclusions: Despite the reported virulence of hypermucoviscous KP strains, they were associated with good prognoses in KP BSI patients. Importantly, carriage of the pks gene cluster, which is responsible for the synthesis of colibactin, was a relevant marker of early mortality. [ABSTRACT FROM AUTHOR]

Objectives: High rates of carbapenem resistance in the human pathogen Acinetobacter baumannii threaten public health and need to be scrutinized.Methods: A total of 356 A. baumannii and 50 non-baumannii Acinetobacter spp. (NBA) strains collected in 2013 throughout South Korea were studied. The type of blaOXA-23 transposon was determined by PCR mapping and molecular epidemiology was assessed by MLST. Twelve representative strains and two comparative A. baumannii were entirely sequenced by single-molecule real-time sequencing.Results: The carbapenem resistance rate was 88% in A. baumannii, mainly due to blaOXA-23, with five exceptional cases associated with ISAba1-blaOXA-51-like. The blaOXA-23 gene in A. baumannii was carried either by Tn2006 (44%) or Tn2009 (54%), with a few exceptions carried by Tn2008 (1.6%). Of the NBA strains, 14% were resistant to carbapenems, two with blaOXA-58 and five with blaOXA-23 associated with Tn2006. The Tn2006-possessing strains belonged to various STs, whereas Tn2008- and Tn2009-possessing strains were limited to ST208 and ST191, respectively. The three transposons were often multiplied in the chromosome, and the gene copy number and the carbapenem MICs presented linear relationships either very strongly for Tn2008 or moderately for Tn2006 and Tn2009.Conclusions: The dissemination of Tn2006 was facilitated by its capability for intercellular transfer and that of Tn2009 was attributable to successful dissemination of the ST191 bacterial host carrying the transposon. Tn2008 was infrequent because of its insufficient ability to undergo intercellular transfer and the scarce bacterial host A. baumannii ST208. Gene amplification is an adaptive mechanism for bacteria that encounter antimicrobial drugs. [ABSTRACT FROM AUTHOR]