BackgroundColistin resistance is mainly driven by alterations in the Gram-negative outer membrane lipopolysaccharides and is caused, in most cases, by mutations in mgrB gene. However, the recent emergence of plasmid-encoded colistin resistance among Enterobacteriaceae strains represents a serious threat to global public health. In this paper we have investigated the rates of colistin resistance and the underlying mechanisms in 450 Klebsiella pneumoniae and Escherichia coli isolates obtained from cancer patients in Egypt.MethodsColistin susceptibility and minimum inhibitory concentrations were determined according to the European Committee on Antimicrobial Susceptibility Testing, by broth microdilution, and by E-test. The mcr-1, mcr-2 and mgrB genes were detected by PCR and then sequenced. Clonal diversity in colistin-resistant K. pneumoniae was evaluated by multilocus sequence typing.ResultsForty (8.8%) colistin-resistant isolates, including 22 K. pneumoniae and 18 E. coli, were isolated over 18 months. Of these, 50% were carbapenem-resistant, out of which nine were blaOXA-48 and seven blaNDM-1 positive. The mechanisms of colistin resistance could be revealed only in three of the 40 resistant strains, being represented by mcr-1 in one blaNDM-1-positive E. coli strain and in one K. pneumoniae ST11 and by mgrB mutations, detected in one K. pneumoniae isolate. None of the studied isolates harbored mcr-2.ConclusionsOur results demonstrate a high frequency of colistin resistance in enterobacterial strains isolated from cancer patients, but a low prevalence of the most well known resistance mechanisms.

The main objective of this work was to characterize carbapenemases, extended-spectrum β-lactamases (ESBLs), and plasmid-mediated quinolone resistance (PMQR) among carbapenem-insensitive Klebsiella pneumoniae and Escherichia coli clinical isolates which were isolated from three hospitals in Riyadh. Thirty-one carbapenem-insensitive isolates (21 K. pneumoniae and 10 E. coli) were recovered from March 2014 to May 2014. Susceptibility testing and phenotypic detection tests were used to characterize the classes of β-lactamases. PCR assays were performed for the detection of the genes encoding ESBL (bla, blabla, and bla), carbapenemase (blablabla, bla, bla, and bla), and PMQR (qnrA, qnrB, qnrS, aac(6)-Ib-cr, qepA, oqxA, and oqxB) genes. All carbapenem-insensitive isolates were carbapenemase producers, with 41.9% and 58.1% being class B carbapenemases class D OXA-48, respectively. While the prevalence of ESBL producers was 80.6%. The following resistance genes were detected; OXA-48-like (58.1%), NDM-type (41.9%), CTX-M-1-like (77.4%), CTX-M-9-like (9.6%), TEM-1 (74.2%), OXA-1 (54.8%), SHV-1 (4.4%), qnrS (58.1%), qnrB (3.2%), and aac(6)-Ib-cr (51.6%). The predominant carbapenemases in the isolates that had carbapenem MIC≤4μg/ml and MIC≥12μg/ml were bla and bla respectively. CTX-M-1-like and qnrS were the dominant ESBL and PMQR genes, respectively. This is the first report in which qnrS was described in the isolates from Saudi Arabia.

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Biosynthesis methods employing microorganisms have emerged as an eco-friendly, clean, and viable alternative to chemical and physical processes. The present study reports the synthesis of copper oxide nanoparticles (CuONPs) using cell-free culture supernatant of marine Streptomyces sp. MHM38. For the optimized production of CuONPs, the influence of some parameters, such as the concentration of copper sulfate (CuSO4), reaction time, filtrate to substrate ratio, and pH, was studied. 5 mM of CuSO4 was optimal for nanoparticle (NP) production. Well-defined CuONP formation occurred after 60 min of incubation when an equal volume of filtrate (cell-free supernatant) to substrate (CuSO4 solution) was added. UV-visible spectroscopy analysis of CuONPs exhibited a peak at 550 nm, which corresponds to the surface plasmon resonance of CuONPs. Most of the particles were spherical and were 1.72–13.49 nm when measured using a transmission electron microscope. The antimicrobial activity of CuONPs was determined using a well diffusion method against Enterococcus faecalis ATCC 29212, Salmonella typhimurium ATCC 14028, Pseudomonas aeruginosa ATCC 9027, Escherichia coli ATCC 8939, fungi (Rhizoctonia solani, Fusarium solani, and Aspergillus niger), and yeast (Candida albicans ATCC 10237). The highest antimicrobial activities were recorded against Candida albicans ATCC 10237, whereas Salmonella typhimurium ATCC 14028 and Escherichia coli ATCC 8939 showed the less activity. The biochemical findings of the CuONP groups were significant ( p < 0.05 ) with diminished levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), total and direct bilirubin, urea, and creatinine compared with the paracetamol group. Nonenzymatic and enzymatic antioxidants of the CuONP groups were significantly elevated ( p < 0.05 ) in SOD and GSH levels, and exceptionally low nitric oxide (NO) and malondialdehyde (MAD) levels were found for the paracetamol group. The histopathological examination of the CuONP groups assured the impact of improving CuONPs against paracetamol-induced liver damage.

Acinetobacter baumannii has become a major challenge to clinicians worldwide due to its high epidemic potential and acquisition of antimicrobial resistance. This work aimed at investigating antimicrobial resistance determinants and their context in four extensively drug-resistant (XDR) NDM-producing A. baumannii clinical isolates collected between July and October 2020 from Kasr Al-Ainy Hospital, Cairo, Egypt. A total of 20 A. baumannii were collected and screened for acquired carbapenemases (blaNDM, blaVIM and blaIMP) using PCR. Four NDM producer A. baumannii isolates were identified and selected for whole-genome sequencing, in silico multilocus sequence typing, and resistome analysis. Antimicrobial susceptibility profiles were determined using disk diffusion and broth microdilution tests. All blaNDM-positive A. baumannii isolates were XDR. Three isolates belonged to high-risk international clones (IC), namely, IC2 corresponding to ST570Pas/1701Oxf (M20) and IC9 corresponding to ST85Pas/ST1089Oxf (M02 and M11). For the first time, we report blaNDM-1 gene on the chromosome of an A. baumannii strain that belongs to sequence type ST164Pas/ST1418Oxf. Together with AphA6, blaNDM-1 was bracketed by two copies of ISAba14 in ST85Pas isolates possibly facilitating co-transfer of amikacin and carbapenem resistance. A novel blaADC allele (blaADC-257) with an upstream ISAba1 element was identified in M19 (ST/CC164Pas and ST1418Oxf/CC234Oxf). blaADC genes harbored by M02 and M11 were uniquely interrupted by IS1008. Tn2006-associated blaOXA-23 was carried by M20. blaOXA-94 genes were preceded by ISAba1 element in M02 and M11. AbGRI3 was carried by M20 hosting the resistance genes aph(3`)-Ia, aac(6`)-Ib`, catB8, ant(3``)-Ia, sul1, armA, msr(E), and mph(E). Nonsynonymous mutations were identified in the quinolone resistance determining regions (gyrA and parC) of all isolates. Resistance to colistin in M19 was accompanied by missense mutations in lpxACD and pmrABC genes. The current study provided an insight into the genomic background of XDR phenotype in A. baumannii recovered from patients in Egypt. WGS revealed strong association between resistance genes and diverse mobile genetic elements with novel insertion sites and genetic organizations.