Although carbapenems have not been approved for animal use, carbapenem-resistant Escherichia coli (CREC) strains are increasingly being detected in food-producing animals, posing a significant public health risk. However, the epidemiological characteristics of CREC isolates in yellow-feather broiler farms remain unclear. We comprehensively investigated the genetic features of carbapenem-resistance genes among E. coli isolates recovered from a yellow-feather broiler farm in Guangdong province, China. Among the 172 isolates, 88 (51.2%) were recovered from chicken feces (88.5%, 54/61), the farm environment (51.1%, 24/47), and specimens of dead chickens (15.6%, 41/64). All CREC isolates were positive for the blaNDM-5 gene and negative for other carbapenem-resistance genes. Among 40 randomly selected isolates subjected to whole-genome sequencing, 10 belonged to distinct sequence types (STs), with ST167 (n = 12) being the most prevalent across different sources, suggesting that the dissemination of blaNDM-5 was mainly due to horizontal and clonal transmission. Plasmid analysis indicated that IncX3, IncHI2, and IncR-X1-X3 hybrid plasmids were responsible for the rapid transmission of the blaNDM-5 gene, and the genetic surrounding of blaNDM-5 contained a common mobile element of the genetic fragment designated \"IS5-△ISAba125-blaNDM-5-bleMBL-trpF-dsbC\". These findings demonstrate a critical role of multiple plasmid replicons in the dissemination of blaNDM-5 and carbapenem resistance.

This 4-month-long prospective observational study investigated the epidemiological characteristics, genetic composition, transmission pattern, and infection control of carbapenem-resistant Escherichia coli (CREC) colonization in patients at an intensive care unit (ICU) in China. Phenotypic confirmation testing was performed on nonduplicated isolates from patients and their environments. Whole-genome sequencing was performed for all E. coli isolates, followed by multilocus sequence typing (MLST), and antimicrobial resistance genes and single nucleotide polymorphisms (SNPs) were screened. The colonization rates of CREC were 7.29% from the patient specimens and 0.39% from the environmental specimens. Among the 214 E. coli isolates tested, 16 were carbapenem resistant, with the blaNDM-5 gene identified as the dominant carbapenemase-encoding gene. Among the low-homology sporadic strains isolated in this study, the main sequence type (ST) of carbapenem-sensitive Escherichia coli (CSEC) was ST1193, whereas the majority of CREC isolates belonged to ST1656, followed by ST131. CREC isolates were more sensitive to disinfectants than were the carbapenem-resistant Klebsiella pneumoniae (CRKP) isolates obtained in the same period, which may explain the lower separation rate. Therefore, effective interventions and active screening are beneficial to the prevention and control of CREC. IMPORTANCE CREC represents a public health threat worldwide, and its colonization precedes or occurs simultaneously with infection; once the colonization rate increases, the infection rate rises sharply. In our hospital, the colonization rate of CREC remained low, and almost all of the CREC isolates detected were ICU acquired. Contamination of the surrounding environment by CREC carrier patients shows a very limited spatiotemporal distribution. As the dominant ST of the CSEC isolates found, ST1193 CREC might be considered a strain of notable concern with potential to cause a future outbreak. ST1656 and ST131 also deserve attention, as they comprised the majority of the CREC isolates found, while blaNDM-5 gene screening should play an important role in medication guidance as the main carbapenem resistance gene identified. The disinfectant chlorhexidine, which is used commonly in the hospital, is effective for CREC rather than CRKP, possibly explaining the lower positivity rate for CREC than for CRKP.

UNASSIGNED: Carriage of carbapenem-resistant Enterobacteriaceae (CRE) in humans may contribute to the dissemination of CRE and impact on communities and healthcare facilities. Carbapenem-resistant Escherichia coli (CREC) is one of the major type of CRE in the human gut. Here, we describe a cross-sectional study to investigate the prevalence of CREC, and in particular the mcr-1 carrying CREC, in health volunteers in China.
UNASSIGNED: During September to December 2016, 3859 non-duplicated stool specimens were collected from healthy volunteers who received regular physical examinees in healthcare centers located in 19 provinces across China. Enrichment culture supplemented meropenem was used to isolate CREC. Carbapenemase producing determinants and the mcr-1 gene were determined by PCR amplification and sequencing. Isolates were further analyzed by antibiotic susceptibility test, genotyping, and whole genome analysis.
UNASSIGNED: A total of 92 non-duplicated CREC were isolated from 3859 stool specimens, among which 43 CREC are carbapenemase positive. In addition, the co-existence of bla NDM and mcr-1 was found in 14 CREC, which also showed resistance to the majority of all antimicrobial agents analyzed. The genetic background of these CREC isolates are highly diversified based on molecular typing. Furthermore, whole genome sequence indicated that NDM-5 is the predominant determinant conferring carbapenem resistance in CREC, and that NDM-5 carrying plasmids (IncX3) are very similar.
UNASSIGNED: The incidence of CREC carriage in healthy people in China was small; however, the co-existence of CREC with mcr-1 is disconcerting. Therefore, pre-screening prior to admission and monitoring of patients on high-dependency wards is highly recommended to control and prevent the dissemination of CRE in hospitals.
UNASSIGNED: The high prevalence of CREC in the healthy people should not be underestimated, as it may increase the risk of infection. This knowledge could have impact on the pre-screening and monitoring of CRE before patient administration.

The emergence and spread of Carbapenem-resistant Escherichia coli (CREC) is becoming a serious problem in Chinese hospitals, however, the data on this is scarce. Therefore, we investigate the risk factors for healthcare-associated CREC infection and study the incidence, antibiotic resistance and medical costs of CREC infections in our hospital.
We conducted a retrospective, matched case-control-control, parallel study in a tertiary teaching hospital. Patients admitted between January 2012 and December 2015 were included in this study. For patients with healthcare-associated CREC infection, two matched subject groups were created; one group with healthcare-associated CSEC infection and the other group without infection.
Multivariate conditional logistic regression analysis demonstrated that prior hospital stay (<6 months) (OR:3.96; 95%CI:1.26-12.42), tracheostomy (OR:2.24; 95%CI: 1.14-4.38), central venous catheter insertion (OR: 8.15; 95%CI: 2.31-28.72), carbapenem exposure (OR: 12.02; 95%CI: 1.52-95.4), urinary system disease (OR: 16.69; 95%CI: 3.01-89.76), low hemoglobin (OR: 2.83; 95%CI: 1.46-5.50), and high blood glucose are associated (OR: 7.01; 95%CI: 1.89-26.02) with CREC infection. Total costs (p = 0.00), medical examination costs (p = 0.00), medical test costs (p = 0.00), total drug costs (p = 0.00) and ant-infective drug costs (p = 0.00) for the CREC group were significantly higher than those for the no infection group. Medical examination costs (p = 0.03), total drug costs (p = 0.03), and anti-infective drug costs (p = 0.01) for the CREC group were significantly higher than for the CSEC group. Mortality in CREC group was significantly higher than the CSEC group (p = 0.01) and no infection group (p = 0.01).
Many factors were discovered for acquisition of healthcare-associated CREC infection. CREC isolates were resistant to most antibiotics, and had some association with high financial burden and increased mortality.

Alongside the well-established carbon catabolite repression by glucose and other sugars, acetate causes repression in Aspergillus nidulans. Mutations in creA, encoding the transcriptional repressor involved in glucose repression, also affect acetate repression, but mutations in creB or creC, encoding components of a deubiquitination system, do not. To understand the effects of acetate, we used a mutational screen that was similar to screens that uncovered mutations in creA, creB, and creC, except that glucose was replaced by acetate to identify mutations that were affected for repression by acetate but not by glucose. We uncovered mutations in acdX, homologous to the yeast SAGA component gene SPT8, which in growth tests showed derepression for acetate repression but not for glucose repression. We also made mutations in sptC, homologous to the yeast SAGA component gene SPT3, which showed a similar phenotype. We found that acetate repression is complex, and analysis of facA mutations (lacking acetyl CoA synthetase) indicates that acetate metabolism is required for repression of some systems (proline metabolism) but not for others (acetamide metabolism). Although plate tests indicated that acdX- and sptC-null mutations led to derepressed alcohol dehydrogenase activity, reverse-transcription quantitative real-time polymerase chain reaction showed no derepression of alcA or aldA but rather elevated induced levels. Our results indicate that acetate repression is due to repression via CreA together with metabolic changes rather than due to an independent regulatory control mechanism.