Identification of a Novel bla NDM Variant, bla NDM-33, in an Escherichia coli Isolate from Hospital Wastewater in China

Our study described a novel NDM-33 variant from an E. coli strain isolated from hospital sewage, where it was associated with human disease and antibiotic exposure. Importantly, hospital sewage was increasingly considered to be related to CRE hosts.

Complete Genome Sequence of Escherichia Phage 590B, Active against an Extensively Drug-Resistant Uropathogenic Escherichia coli Isolate

Escherichia phage 590B, which was isolated from community sewage water in Chandigarh, India, exhibited lytic activity against an extensively drug-resistant uropathogenic Escherichia coli isolate. The genome of the phage is linear, double-stranded, and 44.39 kb long. Phage 590B is a member of the Siphoviridae family and is closest to phage vB_EcoS_XY2, which was isolated in China.

The Effect of Mercury Exposure to Escherichia Coli Bacteria Resistant to Mercury and Escerichia Coli Esbl in Vitro

Background: The level of pollution in Indonesia is still very high, consist of water pollution, air pollution and soil pollution. Mercury is one of the heavy metals that pollutes the waters of the sea, while Escherichia coli is exposed to mercury will try to defend itself by doing mercury detoxification so that it can live in an environment that contains mercury. Escherichia coli that tries to defend itself from mercury exposure in the environment will experience a change in its genes into mercury resistant Escherichia coli. In plasmids or transposons, it might also stimulate the formation of resistance genes for some antibiotics, include producing the ESBL enzyme, so that it can convert non ESBL Escherichia coli into ESBL Escherichia coli. Objective: This study aims to prove that the repeated exposure of mercury will change non ESBL-mercury sensitive Escherichia coli into ESBL- mercury resistant Escherichia coli. Method: This was an experimental study with 27 non-ESBL Escherichia coli isolates as identified from Phoenix. Non-ESBL Escherichia coli clinical isolates were tested by giving exposure to HgCl2 with concentrations of 0.02 ppm, 0.10 ppm, 0.20 ppm for 1-14 days until mercury resistant Escherichia coli was formed, and then ESBL screening was tested by giving Cefotaxime exposure to them. Results: On the first day of mercury exposure, there were 9 isolates of 0.02 ppm HgCl2 resistant Escherichia coli, 9 isolates of 0.10 ppm HgCl2 resistant Escherichia coli, 9 isolates of 0.20 ppm HgCl2 resistant Escherichia coli. Furthermore, this Escherichia coli isolate was exposed to Cefotaxim as ESBL screening. The final results of post-exposure HgCl2 0.02 ppm was obtained 3 (33.3%) isolates were still sensitive to Cefotaxime and 6 (66.7%) isolates that were resistant to Cefotaxime. The final results of post-exposure HgCl2 0.10 ppm was obtained all 9 (100%) isolates that were resistant to Cefotaxime. The final results of post-exposure HgCl2 0.20 ppm obtained 2 (22.2%) isolates were still sensitive to Cefotaxime and 7 (77.8%) isolate were resistant to Cefotaxime. Conclusion: Escherichia coli in urine had the phenotive change into mercury resistant Escherichia coli. Mercury exposure of 0.02 ppm, 0.10 ppm, 0.20 ppm for 1 day in vitro on isolates of non ESBL-mercury resistant Escherichia coli caused changes in 22 isolates of Escherichia coli in urine

The Intestinal Carriage of Plasmid-Mediated Colistin-Resistant Enterobacteriaceae in Tertiary Care Settings

Background: In order to estimate the prevalence of plasmid borne colistin resistance and to characterize in detail the mcr-positive isolates, we carried out a sentinel testing survey on the intestinal carriage of plasmid-mediated colistin-resistant Enterobacteriaceae in hospitalized patients. Methods: Between June 2018 and September 2019, 1922 faecal samples from hospitalised patients were analysed by selective culture in presence of colistin (3.5 mg/L), and in parallel by direct detection of the mcr-1 to mcr-8 genes by qPCR. The mcr-positive isolates were characterised by whole-genome sequencing. Results: The prevalence of the mcr-1 gene was 0.21% (n = 4/1922); the mcr-2 to 8 genes were not detected. The mcr-1 gene was found to be localised in the IncX4 (n = 3) and IncHI2 (n = 1) plasmid type. One Escherichia coli isolate was susceptible to colistin due to the inactivation of the mcr-1 gene through the insertion of the IS2 element; however, the colistin resistance was inducible by culture in low concentrations of colistin. One human mcr-1 positive E. coli isolate was related genetically to the mcr-1 E. coli isolate derived from turkey meat of Czech origin. Conclusions: mcr-mediated colistin resistance currently poses little threat to patients hospitalised in Czech healthcare settings. The presence of the mcr-1 gene in the human population has a possible link to domestically produced, retail meat.

Emergence of the New KPC-49 Variant Conferring an ESBL Phenotype with Resistance to Ceftazidime-Avibactam in the ST131-H30R1 Escherichia coli High-Risk Clone

We report the emergence of an isolate belonging to the sequence type (ST)131-Escherichia coli high-risk clone with ceftazidime-avibactam resistance recovered from a patient with bacteremia in 2019. Antimicrobial susceptibility was determined and whole genome sequencing (Illumina-NovaSeq6000) and cloning experiments were performed to investigate its resistance phenotype. A KPC-3-producing E. coli isolate susceptible to ceftazidime-avibactam (MIC = 0.5/4 mg/L) and with non-wild type MIC of meropenem (8 mg/L) was detected in a blood culture performed at hospital admission. Following 10-days of standard ceftazidime-avibactam dose treatment, a second KPC-producing E. coli isolate with a phenotype resembling an extended-spectrum β-lactamase (ESBL) producer (meropenem 0.5 mg/L, piperacillin-tazobactam 16/8 mg/L) but resistant to ceftazidime-avibactam (16/4 mg/L) was recovered. Both E. coli isolates belonged to ST131, serotype O25:H4 and sublineage H30R1. Genomics analysis showed a core genome of 5,203,887 base pair with an evolutionary distance of 6 single nucleotide polymorphisms. A high content of resistance and virulence genes was detected in both isolates. The novel KPC-49 variant, an Arg-163-Ser mutant of blaKPC-3, was detected in the isolate with resistance to ceftazidime-avibactam. Cloning experiments revealed that blaKPC-49 gene increases ceftazidime-avibactam MIC and decreases carbapenem MICs when using a porin deficient Klebsiella pneumoniae strain as a host. Both blaKPC-3 and blaKPC-49 genes were located on the transposon Tn4401a as a part of an IncF [F1:A2:B20] plasmid. The emergence of novel blaKPC genes conferring decreased susceptibility to ceftazidime-avibactam and resembling ESBL production in the epidemic ST131-H30R1-E. coli high-risk clone presents a new challenge in clinical practice.