Murein and lipopolysaccharide biosynthesis in synchronized cells of Escherichia coli K 12 and the effect of penicillin G, mecillinam and nalidixic acid

1982 ◽  
Vol 132 (3) ◽  
pp. 245-250 ◽  
Author(s):  
Peter Essig ◽  
Hans Herbert Martin ◽  
Jobst Gmeiner
Keyword(s):  
Escherichia Coli ◽  
Nalidixic Acid ◽  
Penicillin G ◽  
Synchronized Cells ◽  
Lipopolysaccharide Biosynthesis ◽  
K 12

scholarly journals Adaptation of Esherichia coli to Antiobiotic Cycling via Single Nucleotide Polymorphisms

2017 ◽  
Vol 14 (1) ◽  
Author(s):  
Samuel Hager ◽  
Ellen Jensen ◽  
Timothy Johnson ◽  
David Mitchell
Keyword(s):  
Escherichia Coli ◽  
Minimum Inhibitory Concentration ◽  
Nalidixic Acid ◽  
Inhibitory Concentration ◽  
Acid Resistance ◽  
Penicillin G ◽  
Single Nucleotide ◽  
E Coli ◽  
Esherichia Coli ◽  
Nalidixic Acid Resistance

Bacteria are quick to adapt and evolve, especially under the effects of selective pressures from chemical antibiotics. In addition, bacteria may develop resistance to antibiotics from multiple classes simultaneously, making their eradication from the human body particularly challenging. This study aims to demonstrate that bacterial multiple-drug resistance can be developed and retained in a laboratory setting. Escherichia coli B was grown in tryptic soy broth in the presence of a small, increasing concentration of streptomycin. This exposure resulted in a strain of E. coli, which had an increased minimum inhibitory concentration (MIC) towards streptomycin, or “resistance.” This resistant strain was then grown in like manner in nalidixic acid and then penicillin G. The result was a strain that became resistant to streptomycin and nalidixic acid, and increasingly resistant to nalidixic acid after penicillin G exposure. Additionally, the bacteria retained resistance to streptomycin and nalidixic acid even after exposure to those chemicals ceased. Genome sequencing and comparison to E. coli B reference strain REL606 revealed the emergence of point mutations with each exposure to an antibiotic. Of particular interest is a mutation associated with the appearance of nalidixic acid resistance. Base pair 4,553,488 was changed from adenine to guanine, resulting in a change from aspartate to glycine in the protein helicase. Previous studies have not indicated mutations to this locus as nalidixic acid resistance conferring. Thus, this mutation may be a novel mutation conferring E. coli B nalidixic acid resistance. Since the region of the mutated helicase is functionally undefined, a mechanism is not apparent. Further research needs to be done to confirm this hypothesis and illuminate a mechanism. KEYWORDS: Bacteria; Escherichia coli; Evolution; Antibiotic Resistance; Nalidixic Acid; Streptomycin; Point Mutation; Single-nucleotide Polymorphism; Helicase; Minimum Inhibitory Concentration

Spread of Marker Bacteria from the Hides of Cattle in a Simulated Livestock Market and at an Abattoir

2004 ◽  
Vol 67 (11) ◽  
pp. 2397-2402 ◽  
Author(s):  
V. J. COLLIS ◽  
C.-A. REID ◽  
M. L. HUTCHISON ◽  
M. H. DAVIES ◽  
K. P. A. WHEELER ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Pseudomonas Fluorescens ◽  
Nalidixic Acid ◽  
Microbial Contamination ◽  
Market Process ◽  
Market Environment ◽  
E Coli ◽  
Environmental Surfaces ◽  
K 12 ◽  
Two Stages

The spread of microbial contamination on the hides of beef was investigated at two stages in the meat chain: (i) in a simulated livestock market (“the market”) using 33 animals, and (ii) in the unloading-to-skinning area of a commercial abattoir using 18 animals. At both stages, harmless bacterial markers (nalidixic acid–resistant Escherichia coli K-12; rifampicin- and nalidixic acid–resistant Pseudomonas fluorescens; and a tetracycline-resistant E. coli) were inoculated on the hides of a small number of selected animals, and their transfer to other animals and the environment was examined. At the market, the initial prevalence of animals positive for the hide markers (9.1% in each phase) introduced in the presale pen, sale ring, and postsale pen changed to 39.4, 15.1, and 54.5%, respectively, by the end of the market process. In addition, widespread contamination of the market environment with the hide markers was observed. At the abattoir, the initial prevalence of animals positive for the hide marker (11.1%) inoculated at unloading increased to 100% (hide before skinning) and 88.8% (skinned carcass). In addition, another marker inoculated on environmental surfaces in lairage pens, races, and stunning box was detected on 83.3% (hide before skinning) and 88.8% (skinned carcass). These results, although obtained with a relatively small number of animals, demonstrate that both the livestock market process and the unloading-to-skinning process at abattoirs can facilitate the extensive spread of microbial contamination on hides not just within, but also between, batches of animals.

scholarly journals Mechanisms of Fluoroquinolone Resistance in Escherichia coli Isolates from Food-Producing Animals

2011 ◽  
Vol 77 (20) ◽  
pp. 7113-7120 ◽  
Author(s):  
Maria Karczmarczyk ◽  
Marta Martins ◽  
Teresa Quinn ◽  
Nola Leonard ◽  
Séamus Fanning
Keyword(s):  
Escherichia Coli ◽  
Nalidixic Acid ◽  
Target Genes ◽  
Efflux Pump ◽  
Multidrug Resistant ◽  
Fluoroquinolone Resistance ◽  
Efflux Pump Inhibitor ◽  
Content Type ◽  
Field Isolates ◽  
K 12

ABSTRACTEleven multidrug-resistantEscherichia coliisolates (comprising 6 porcine and 5 bovine field isolates) displaying fluoroquinolone (FQ) resistance were selected from a collection obtained from the University Veterinary Hospital (Dublin, Ireland). MICs of nalidixic acid and ciprofloxacin were determined by Etest. All showed MICs of nalidixic acid of >256 μg/ml and MICs of ciprofloxacin ranging from 4 to >32 μg/ml. DNA sequencing was used to identify mutations within the quinolone resistance-determining regions of target genes, and quantitative real-time PCR (qRT-PCR) was used to evaluate the expression of the major porin, OmpF, and component genes of the AcrAB-TolC efflux pump and its associated regulatory loci. Decreased MIC values to nalidixic acid and/or ciprofloxacin were observed in the presence of the efflux pump inhibitor phenylalanine-arginine-β-naphthylamide (PAβN) in some but not all isolates. Several mutations were identified in genes coding for quinolone target enzymes (3 to 5 mutations per strain). All isolates harbored GyrA amino acid substitutions at positions 83 and 87. Novel GyrA (Asp87 → Ala), ParC (Ser80 → Trp), and ParE (Glu460 → Val) substitutions were observed. The efflux activity of these isolates was evaluated using a semiautomated ethidium bromide (EB) uptake assay. Compared to wild-typeE. coliK-12 AG100, isolates accumulated less EB, and in the presence of PAβN the accumulation of EB increased. Upregulation of theacrBgene, encoding the pump component of the AcrAB-TolC efflux pump, was observed in 5 of 11 isolates, while 10 isolates showed decreased expression of OmpF. This study identified multiple mechanisms that likely contribute to resistance to quinolone-based drugs in the field isolates studied.

scholarly journals Role of the rapA Gene in Controlling Antibiotic Resistance of Escherichia coli Biofilms

2007 ◽  
Vol 51 (10) ◽  
pp. 3650-3658 ◽  
Author(s):  
S. V. Lynch ◽  
L. Dixon ◽  
M. R. Benoit ◽  
E. L. Brodie ◽  
M. Keyhan ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
High Throughput Screening ◽  
Screening Method ◽  
Resistance Mechanisms ◽  
Planktonic Cell ◽  
Penicillin G ◽  
Wild Type ◽  
E Coli ◽  
K 12 ◽  
Dual Mechanism

ABSTRACT By using a high-throughput screening method, a mutant of a uropathogenic Escherichia coli strain affected in the rapA gene was isolated. The mutant formed normal-architecture biofilms but showed decreased penicillin G resistance, although the mutation did not affect planktonic cell resistance. Transcriptome analysis showed that 22 genes were down-regulated in the mutant biofilm. One of these genes was yhcQ, which encodes a putative multidrug resistance pump. Mutants with mutations in this gene also formed biofilms with decreased resistance, although the effect was less pronounced than that of the rapA mutation. Thus, an additional mechanism(s) controlled by a rapA-regulated gene(s) was involved in wild-type biofilm resistance. The search for this mechanism was guided by the fact that another down-regulated gene in rapA biofilms, yeeZ, is suspected to be involved in extra cell wall-related functions. A comparison of the biofilm matrix of the wild-type and rapA strains revealed decreased polysaccharide quantities and coverage in the mutant biofilms. Furthermore, the (fluorescent) functional penicillin G homologue Bocillin FL penetrated the mutant biofilms more readily. The results strongly suggest a dual mechanism for the wild-type biofilm penicillin G resistance, retarded penetration, and effective efflux. The results of studies with an E. coli K-12 strain pointed to the same conclusion. Since efflux and penetration can be general resistance mechanisms, tests were conducted with other antibiotics. The rapA biofilm was also more sensitive to norfloxacin, chloramphenicol, and gentamicin.

L-Serine deaminase activity is induced by exposure of Escherichia coli K-12 to DNA-damaging agents

1982 ◽  
Vol 152 (2) ◽  
pp. 702-705
Author(s):  
E B Newman ◽  
D Ahmad ◽  
C Walker
Keyword(s):  
Escherichia Coli ◽  
High Temperature ◽  
Nalidixic Acid ◽  
Mitomycin C ◽  
Uv Irradiation ◽  
Elevated Level ◽  
Sos System ◽  
Dna Damaging Agents ◽  
K 12 ◽  
Serine Deaminase

The synthesis of L-serine deaminase in Escherichia coli K-12 was induced after exposure of cells to a variety of DNA-damaging agents, including UV irradiation, nalidixic acid, and mitomycin C. Synthesis was also induced during growth at high temperature. A mutant constitutive for SOS functions showed an elevated level of L-serine deaminase activity. The response to DNA-damaging agents thus may be mediated via the SOS system.

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