scholarly journals Acfr-Like Gene from Clostridium difficile Confers Multiple Antibiotic Resistance by the Same Mechanism as thecfrGene

2015 ◽  
Vol 59 (9) ◽  
pp. 5841-5843 ◽  
Author(s):  
Lykke H. Hansen ◽  
Birte Vester

ABSTRACTThe Cfr RNA methyltransferase causes multiple resistances to peptidyl transferase inhibitors by methylation of A2503 23S rRNA. Manycfr-like gene sequences in the databases code for unknown functions. This study confirms that a Cfr-like protein from aPeptoclostridium difficile(formerlyClostridium difficile) strain does function as a Cfr protein. The enzyme is expressed inEscherichia coliand shows elevated MICs for five classes of antibiotics. A primer extension stop indicates a modification at A2503 in 23S rRNA.

2012 ◽  
Vol 56 (7) ◽  
pp. 3563-3567 ◽  
Author(s):  
Lykke H. Hansen ◽  
Mercè H. Planellas ◽  
Katherine S. Long ◽  
Birte Vester

ABSTRACTThecfrgene encodes the Cfr methyltransferase that methylates a single adenine in the peptidyl transferase region of bacterial ribosomes. The methylation provides resistance to several classes of antibiotics that include drugs of clinical and veterinary importance. This paper describes a first step toward elucidating natural residences of the worrisomecfrgene and functionally similar genes. Threecfr-like genes from the orderBacillaleswere identified from BLAST searches and cloned into plasmids under the control of an inducible promoter. Expression of the genes was induced inEscherichia coli, and MICs for selected antibiotics indicate that thecfr-like genes confer resistance to PhLOPSa (phenicol, lincosamide, oxazolidinone, pleuromutilin, and streptogramin A) antibiotics in the same way as thecfrgene. In addition, modification at A2503 on 23S rRNA was confirmed by primer extension. Finally, expression of the Cfr-like proteins was verified by SDS gel electrophoresis of whole-cell extracts. The work shows thatcfr-like genes exist in the environment and thatBacillalesare natural residences ofcfr-like genes.


2011 ◽  
Vol 55 (5) ◽  
pp. 2438-2441 ◽  
Author(s):  
Zeynep Baharoglu ◽  
Didier Mazel

ABSTRACTAntibiotic resistance development has been linked to the bacterial SOS stress response. InEscherichia coli, fluoroquinolones are known to induce SOS, whereas other antibiotics, such as aminoglycosides, tetracycline, and chloramphenicol, do not. Here we address whether various antibiotics induce SOS inVibrio cholerae. Reporter green fluorescent protein (GFP) fusions were used to measure the response of SOS-regulated promoters to subinhibitory concentrations of antibiotics. We show that unlike the situation withE. coli, all these antibiotics induce SOS inV. cholerae.


2012 ◽  
Vol 57 (1) ◽  
pp. 189-195 ◽  
Author(s):  
Migla Miskinyte ◽  
Isabel Gordo

ABSTRACTMutations causing antibiotic resistance usually incur a fitness cost in the absence of antibiotics. The magnitude of such costs is known to vary with the environment. Little is known about the fitness effects of antibiotic resistance mutations when bacteria confront the host's immune system. Here, we study the fitness effects of mutations in therpoB,rpsL, andgyrAgenes, which confer resistance to rifampin, streptomycin, and nalidixic acid, respectively. These antibiotics are frequently used in the treatment of bacterial infections. We measured two important fitness traits—growth rate and survival ability—of 12Escherichia coliK-12 strains, each carrying a single resistance mutation, in the presence of macrophages. Strikingly, we found that 67% of the mutants survived better than the susceptible bacteria in the intracellular niche of the phagocytic cells. In particular, allE. colistreptomycin-resistant mutants exhibited an intracellular advantage. On the other hand, 42% of the mutants incurred a high fitness cost when the bacteria were allowed to divide outside of macrophages. This study shows that single nonsynonymous changes affecting fundamental processes in the cell can contribute to prolonged survival ofE. coliin the context of an infection.


1997 ◽  
Vol 41 (12) ◽  
pp. 2699-2704 ◽  
Author(s):  
D G White ◽  
K Maneewannakul ◽  
E von Hofe ◽  
M Zillman ◽  
W Eisenberg ◽  
...  

The multiple antibiotic resistance operon (marORAB) in Escherichia coli controls intrinsic susceptibility and resistance to multiple, structurally different antibiotics and other noxious agents. A plasmid construct with marA cloned in the antisense direction reduced LacZ expression from a constitutively expressed marA::lacZ translational fusion and inhibited the induced expression of LacZ in cells bearing the wild-type repressed fusion. The marA antisense construction also decreased the multiple antibiotic resistance of a Mar mutant. Two antisense phosphorothioate oligonucleotides, one targeted to marO and the other targeted to marA of the mar operon, introduced by heat shock or electroporation reduced LacZ expression in the strain having the marA::lacZ fusion. One antisense oligonucleotide, tested against a Mar mutant of E. coli ML308-225, increased the bactericidal activity of norfloxacin. These studies demonstrate the efficacy of exogenously delivered antisense oligonucleotides targeted to the marRAB operon in inhibiting expression of this chromosomal regulatory locus.


2019 ◽  
Vol 31 (3) ◽  
pp. 159-164
Author(s):  
Yaqdhan Alnomani ◽  
Abdolmajid Ghasemian ◽  
Mojtaba Memariani ◽  
Majid Eslami ◽  
Abdolreza Sabokrouh ◽  
...  

2017 ◽  
Vol 61 (4) ◽  
Author(s):  
Pan Sun ◽  
Zhenwang Bi ◽  
Maud Nilsson ◽  
Beiwen Zheng ◽  
Björn Berglund ◽  
...  

ABSTRACT We report on the coexistence of mcr-1 and bla CTX-M in multidrug-resistant, extended-spectrum β-lactamase-producing Escherichia coli belonging to the sequence type 10 complex isolated from well water in rural China. Raoultella ornithinolytica with bla KPC-2 was also detected in well water from the same area. This study shows that genes coding for resistance to last-resort antibiotics are present in wells in rural China, indicating a potential source of antibiotic resistance.


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