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Green Metal-Based Nanoparticles Synthesized Using Medicinal Plants and Plant Phytochemicals against Multidrug-Resistant Staphylococcus aureus
Published in Richard L. K. Glover, Daniel Nyanganyura, Rofhiwa Bridget Mulaudzi, Maluta Steven Mufamadi, Green Synthesis in Nanomedicine and Human Health, 2021
Abeer Ahmed Qaed Ahmed, Lin Xiao, Tracey Jill Morton McKay, Guang Yang
Some of the fundamental phenotypical characteristics of VISA include increased thickness of the cell wall as a result of differentially regulated stimulatory pathways and cell wall biosynthesis (Daum et al., 1992; Moreira et al., 1997; Hanaki et al., 1998; Boyle-Vavra et al., 2001). This reduces peptidoglycan cross-linking, affecting cell wall turnover enzymes by decreasing their autolytic activity (Vaudaux et al., 2001; Boyle-Vavra et al., 2003; Howden et al., 2006,). There is also a change in the protein profile of the surface, compromising the agr function and changing growth characteristics (Pfeltz et al., 2000; Sakoulas et al., 2002; McCallum et al., 2006). Several methods have been used to explore the VISA phenotype molecular genetic basis. Multiple genes, as well as mutations thereof, appear to be responsible for vancomycin intermediate phenotype (Pfeltz et al., 2000; Boyle-Vavra et al., 2001; Muthaiyan et al., 2004; Scherl et al., 2006; Mwangi et al., 2007). Multiple studies show that VISA could have originated from a multistep process. Most probably numerous pathways are involved with intermediatory vancomycin resistance (Howden et al., 2010). A complete reconstitution of VISA from vancomycin-susceptible S. aureus (strain N315ΔIP) concluded that all six mutated genes are needed to develop the VISA phenotype (Katayama et al., 2016). These genes are involved in maintaining cell physiology. Therefore, VISA phenotype is achieved via multiple genetic incidents leading to extreme alteration in cell physiology.
Vancomycin-Resistant Enterococci
Published in Firza Alexander Gronthoud, Practical Clinical Microbiology and Infectious Diseases, 2020
Enterococci are part of the commensal gut flora. The clinically relevant enterococci which may cause infections are Enterococcus faecium and Enterococcus faecalis (see Chapter 2.1 for how commensal flora may cause disease). Commensal Enterococcus faecium and E. faecalis are sensitive to glycopeptides. Since the 1980s, vancomycin resistance is increasingly found in hospital-acquired infections caused by E. faecium and E. faecalis. They are referred to as vancomycin-resistant enterococci (VRE). Because the predominant VREs are also resistant to teicoplanin, another term used is glycopeptide-resistant enterococci. Although enterococci are low-virulent organisms, VRE infections have been associated with complicated treatment courses and increased mortality. Although this may in part be attributable to underlying medical conditions of patients who are at risk of VRE infections, it is worthwhile to consider the following.
Enterococcus: An Important Opportunistic Pathogen—Basic and Clinical Aspects
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Karen Flores-Moreno, Claudia Mayoral-Teran, Yolanda Lopez-Vidal
Besides performing these, more biochemical tests are necessary to identify the species. There are different methodologies to identify microorganisms; some identification is performed using equipment or kits. Equipment like VITEK 2 or MALDI-TOF can carry out automated tests, while semiautomated equipment as MicroScan are still in use but have been lately substituted by automated systems. Additionally, there are molecular identification methods in which metabolic genes as ddl, sodA, 16S rRNA, or cpn660 are amplified and sequenced to identify the species. Some research groups have used catheters with genes efaA and ace. As for antimicrobial resistances, they can be performed following methods like agar dilution and disk diffusion. Systems like VITEK or equipment such as MicroScan can be used to identify antimicrobial susceptibility.60 Amplification of resistance genes and identification of the vancomycin resistance genotype are an alternative to the use of automated equipment. The selection of the methodology depends on the laboratory where the tests are to be performed.
Increasing trend in enterococcal bacteraemia and vancomycin resistance in a tertiary care hospital in Croatia, 2017–2021
Published in Infectious Diseases, 2023
Zrinka Todorić, Ivana Majdandžić, Tea Keretić Kregar, Zoran Herljević, Mario Ćorić, Joško Lešin, Tomislav Kuliš, Ivana Mareković
Vancomycin resistance proportion of all enterococcal isolates was 16.4% (71/432). Vancomycin resistance proportion in E. faecium isolates was 36.4% (64/176) and in E. faecalis isolates 2.7% (7/256) (p < .0001). The overall proportion of vancomycin-resistant enterococcal isolates increased from 12,7% (n = 8/63) in 2017 to 25.7% (n = 29/113) in 2021, statistically significant increasing trend (p = .0455). The proportion of vancomycin-resistant E. faecium increased from 26,9% (n =7/26) in 2017 to 58.5% (n = 24/41) in 2021, statistically significant increasing trend (p = .0169). Seven E. faecalis isolates were vancomycin-resistant over the 5-year study period and the trend was not statistically significant (p = .1049) (Table 3).
Fecal carriage of vanB antibiotic resistance gene affects adipose tissue function under vancomycin use
Published in Gut Microbes, 2022
Lars M. M. Vliex, Giang N. Le, Marina Fassarella, Dorien Reijnders, Gijs H. Goossens, Erwin G. Zoetendal, John Penders, Ellen E. Blaak
We quantified common ARGs conferring resistance against vancomycin and β-lactam antibiotics, as well as the opportunistic pathogens Clostridioides difficile and Escherichia coli. The vanB vancomycin resistance gene and the TEM and SHV gene-families, conferring resistance against amoxicillin, were the most prevalent ARGs (Table 1). At baseline, vanB was present in 60% of our population (33/55). CTX-M genes, encoding extended-spectrum β-lactamases (ESBL), and CMY genes, encoding AmpC-type beta-lactamases, were only sparsely detected. E. coli was detected in almost every sample, while C. difficile was only detected sporadically. The four most prevalent ARGs (vanB, TEM, SHV) and OPs (E. coli) were further investigated to determine how their presence would change after antibiotic use and follow-up.
A synthetic consortium of 100 gut commensals modulates the composition and function in a colon model of the microbiome of elderly subjects
Published in Gut Microbes, 2021
Marta Perez, Alexandra Ntemiri, Huizi Tan, Hugh M. B. Harris, Henrik M. Roager, Céline Ribière, Paul W. O’Toole
We sequenced the MCC100 genomes and screened them for the presence of genes involved in antibiotic resistance, virulence and bacteriocin production. We annotated 278 sequences belonging to 88 different antibiotic resistance genes across 64 of the MCC100 strains, which are predicted to encode resistance to 13 drug classes (Supplementary Table S6a). The number of genes ranged from 1 to 49 per strain. While most of the genomes harbored one or two predicted antibiotic resistance genes, the three Escherichia/Shigella genomes harbored more than half of the annotated sequences (141) encoding the majority of multidrug transport genes identified here, and all the fosfomycin, peptide antibiotics, and sulfonamide resistance proteins. Tetracycline resistance genes were present in 40 strains of Bacteroidetes and Firmicutes, being the most widespread resistance function. Mupirocin and rifampycin resistance genes were exclusively found in Actinobacteria. Gene prediction and phenotypic resistance were correlated for 18 out of 35 benzylpenicillin and 6 out of 13 clindamycin resistant strains (Supplementary Table S6a). No genetic basis was identified for the vancomycin and chloramphenicol resistant strains. In contrast, three strains contained vancomycin resistance genes in their genomes even though they were susceptible; and the genomes of three enterococcal and three enterobacterial strains susceptible to gentamicin and streptomycin harbored aminoglycosides resistance genes.