Response mechanisms of different antibiotic-resistant bacteria with different resistance action targets to the stress from photocatalytic oxidation
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Surmmary The SOS DNA repair system is induced in bacteria treated with 4-quinolones. However, whether the response exacerbates or repairs the damage caused by these drugs is still unclear. The recA13 and the recB21 mutations impair recombination repair and render bacteria unable to induce the SOS response when treated with nalidixic acid or other agents that affect DNA synthesis. However, UV treatment induces the SOS response in recB21 mutants but not in recA13 mutants. Both these mutants are hypersensitive to nalidixic acid and, therefore, either recombination repair or SOS repair would appear to repair DNA damage caused by the drug. However, since the lexA3 mutation (which also renders bacteria incapable of inducing the SOS response without affecting recombination repair) had no effect on the susceptibility of bacteria to nalidixic acid, the SOS response neither contributes to nor repairs DNA damage caused by the drug. Consequently, it would seem that the hypersensitivity of the recA13 and recB21 mutants to nalidixic acid is due to their deficiency in recombination repair. This view was confirmed by testing a recA430 mutant that is recombination-repair proficient but SOS repair-deficient and finding it to be no more sensitive to nalidixic acid than its parent. Thus it would appear that, although induced by nalidixic acid treatment, the SOS DNA repair system does not play any role in bacterial responses to the damage caused by the drug. In contrast, the recombination repair system does repair damage caused by nalidixic acid.
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The studies on the effect of nalidixic acid (negram) on the synthesis of DNA and determination of its minimal inhibitory concentrations revealed a regular decrease in the sensitivity levels to negram of the tetracycline resistant mutants selected on media with tetracycline. Heterogene ty of the tetracycline resistant mutants to EDTA showed that one of the causes of insensitivity of the mutants to negram was a change in the surface structures of the microbial cell.
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The uptakes of 3 H-tetracycline by 12 tetracycline-sensitive and 24 tetracycline-resistant Escherichia coli hospital cultures were found to be 270 and 75 nmoles of tetracycline per milliliter of cell water per 20 min, respectively. This confirms reports by other investigators who, by using only one or two cultures, suggested a relationship between tetracycline uptake and tetracycline resistance. However, minimum inhibitory concentrations of tetracycline for the cultures bore no relation to the tetracycline uptake values, suggesting that loss of tetracycline uptake may not be the primary cause of resistance. In addition there were three resistant cultures with uptake values greater than 140 and two sensitive cultures with uptakes lower than 180, raising the question of how these tetracycline-resistant cultures could grow with tetracycline at concentrations nearly as high as those found to inhibit growth of sensitive organisms. Of the tetracycline-resistant cultures, 15 were able to transfer tetracycline resistance to a recipient organism and 9 were not. Two of the cultures transferred TC-resistance to a recipient with no modification-restriction system ( E. coli C) but did not transfer resistance to a recipient with a known modification-restriction system ( E. coli K-12).
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Fluoroquinolones, antibiotics that cause DNA damage by inhibiting DNA topoisomerases, are clinically important, but their mechanism of action is not yet fully understood. In particular, the dynamical response of bacterial cells to fluoroquinolone exposure has hardly been investigated, although the SOS response, triggered by DNA damage, is often thought to play a key role. Here, we investigated the growth inhibition of the bacterium
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RecBCD
Repressor lexA
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The response of Escherichia coli to nalidixic acid was investigated by continuous turbidimetric monitoring of cultures exposed to the drug. Two distinct types of turbidimetric response were detected when dense populations of E. coli were exposed to nalidixic acid in a static system, but this difference was not found in low-inoculum experiments, nor in experiments in which initially dense inocula of E. coli were exposed to the drug in conditions similar to those encountered in the treatment of bacterial cystitis. Stable resistance to nalidixic acid was readily induced in cultures of E. coli. Such resistance emerged by a step-wise process and cultures could easily be converted to resistance to at least 64 μg nalidixic acid per millilitre by sequential transfer. Resistance to drug levels greater than 64 μg/ml was more difficult to induce and such variants were unstably resistant to the higher drug levels. 'Wild' nalidixic-acid-resistant E. coli were correspondingly found to be partially susceptible to concentrations of nalidixic acid exceeding 64 μg/ml. Nalidixic acid resistance was even easier to induce in an in vitro model of the treatment of bacterial cystitis than in the static system, in that a single cycle of exposure to a 'dose' of the drug allowed the emergence of a population exhibiting a relatively high level of resistance. It is suggested that the therapeutic efficiency of nalidixic acid resides in a highly effective initial onslaught, and that, if infection is not controlled at this stage, the emergence of resistance is likely to be a cause of therapeutic failure.
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Minocycline (7-dimethylamino-6-demethyl-6-deoxytetracycline) is a new semisynthetic tetracycline with potent activity against tetracycline-susceptible bacterial pathogens and unique activity against tetracycline-resistant staphylococci. Studies to determine the basis for this unique activity showed that, whereas tetracycline-resistant staphylococci took up less 3 H-tetracycline than the susceptible cells, both the tetracycline-resistant and -susceptible cells accumulated equivalent amounts of 14 C-minocycline. In contrast, tetracycline-resistant Escherichia coli cells were relatively resistant to minocycline and accumulated less of both drugs than did the susceptible organisms. It is proposed that minocycline is effective against tetracycline-resistant staphylococci because of its ability to penetrate the cells sufficiently to reach inhibiting concentrations at sensitive reaction sites.
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Penicillin binding proteins
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