Studies on the Drug Resistance of Staphylococci and Escherichia Coli Against Antibiotics

Otaya, Hirokazu; Okamoto, Saburo; Inoue, Emiko; Adachi, Yoshiaki; Machihara, Suguru; Yoshimura, M.

doi:10.1007/978-3-642-49267-9_10

Cited by 3 publications

(3 citation statements)

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“…Otaya and Machihara (24) found a direct correlation between MIC and the number of antibiotics to which E. coli (and Staphylococcus aureus) strains were resistant, but their studies did not discriminate TC (or other) MICs at levels over 100 ug/ml. It is possible that since multiple (three or more) resistance in the isolates examined during the period of this study were for the most part TC SM -AM, the specific antibiotic markers carried along with the TC marker may be irrelevant and a similar result could be obtained with a different pattern.…”

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confidence: 93%

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Tetracycline Resistance in Escherichia coli Isolates from Hospital Patients

Camiolo

Beck

Reynard

1975

Antimicrob Agents Chemother

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Hospital isolates of Escherichia coli resistant to tetracycline (TC) were studied to identify mechanisms which regulate TC resistance levels and ability to transfer TC resistance. Antibiotic resistance patterns, resistance levels to TC, and ability to transfer TC resistance were determined for the isolates. Similar data were obtained for the transferable plasmids after transfer to several new host strains of E. coli. Of the 110 isolates, 50% were able to transfer TC resistance by conjugation. There was a nearly linear relationship between the minimum inhibitory concentration (MIC) of TC for the hospital strains and the percentage of strains at a given MIC that could transfer TC resistance. The strains that were simultaneously resistant to tetracycline, streptomycin, and ampicillin had relatively high MICs of TC and high ability to transfer TC resistance. These results and surveys of TC-resistant E. coli by others suggest that TC resistance levels and transmissibility may be influenced by other resistance markers. The isolates which did not transfer TC resistance by conjugation were tested for the presence of TC resistance plasmids by mobilization or by transformation with deoxyribonucleic acid from the isolates. Evidence for plasmid-mediated TC resistance was found in 92 (84%) of the 110 hospital strains.

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“…In these tests 17 out of 24 isolates, which did not transfer TC resistance in either conjugation or mobilization tests, were able to donate TC resistance to a second host. It is possible that a modification of the technique may show an even higher proportion of strains bearing plasmid-mediated TC resistance.…”

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Tetracycline Resistance in Escherichia coli Isolates from Hospital Patients

Camiolo

Beck

Reynard

1975

Antimicrob Agents Chemother

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“…Sulfonamide resistance is currently a problem of considerable clinical importance, especially in urinary tract infections. Twenty-five to 80% of E. coli strains found in these infections are normally resistant to 100-1000 times the normal minimum inhibitory concentration of sulfonamide-sensitive strains (8). We will deal with 15 urinary tract strains of E. coli and the closely related Citrobacter highly resistant to sulfamethoxazole.…”

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Sulfonamide resistance mechanism in Escherichia coli: R plasmids can determine sulfonamide-resistant dihydropteroate synthases.

Wise¹,

Abou‐Donia²

1975

Proc. Natl. Acad. Sci. U.S.A.

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Several natural isolate E. coli strains highly resistant to sulfonamides and antibiotics are shown to contain a sulfonamide-resistant dihydropteroate synthase (2-amino-4-hydroxy-6hydroxymethyl-7,8-dihydropteridine-di-phosphate:4-aminobenzoate 2-amino-4-hydroxydihydropteridine-6methenyltransferase, EC 2.5.1.15) in addition to the normal sensitive enzyme. The resistant dihydropteroate synthases examined are determined by an R plasmid and are smaller and less heat stable than the normal sulfonamidesensitive enzyme. One synthase resistant to any sulfonamide tested, and to sulfanilic and arsanilic acids, was still inhibited by several non-sulfonamide analogs of p-aminobenzoate. Citrobacter and Klebsiella pneumoniae strains also show similar mechanisms of sulfonamide resistance.Sulfonamide resistance in Escherichia coli and related enteric rod bacteria has been common for many years and is normally associated with multiple resistances to various antibiotics (1-4). These resistance genes are usually carried on plasmids (5)(6)(7). Sulfonamide resistance is currently a problem of considerable clinical importance, especially in urinary tract infections. Twenty-five to 80% of E. coli strains found in these infections are normally resistant to 100-1000 times the normal minimum inhibitory concentration of sulfonamide-sensitive strains (8). We will deal with 15 urinary tract strains of E. coli and the closely related Citrobacter highly resistant to sulfamethoxazole.In this report we show that the most common sulfonamide resistance mechanism in E. coli and Citrobacter, and perhaps in Klebsiella pneumoniae, is the presence of an R-plasmid-determined sulfonamide-resistant dihydropteroate synthase (DHPS; 2-amino-4-hydroxy-6-hydroxymethyl-7,8-dihydropteridine-diphosphate:4-aminobenzoate 2-amino-4-hydroxydihydropteridine-6-methenyltransferase, EC 2.5.-1.15). This is the enzyme which forms dihydropteroate from a pyrophosphorylated, partially reduced pteridine and paminobenzoic acid (PABA) on the path to dihydrofolate (see Materials and Methods). The mechanism that we report for sulfonamide resistance is reminiscent of that recently reported for R-plasmid-determined trimethoprim resistance (9, 10).MATERIALS AND METHODS Bacterial Strains. Twelve E. coli and three Citrobacter strains, resistant to 1000 gg or more of sulfamethoxazole, were obtained mostly from the urinary tract of patients in hospitals and in private practice (see Fig. 1 coli K12 strain, J62-1 (nalidixic-acid-resistant and auxotrophic for proline, histidine, and tryptophan), was the gift of N. Datta. This strain is denoted "recipient" and was used to receive sulfa-resistant R plasmids from our wild-type strains. Wild-type strains, either sulfa-sensitive or sulfa-resistant, are denoted with "wt" before the strain number. J62-1 strains containing an R plasmid from a wild-type strain are denoted "C", for cross, followed by the strain number that was the source of the sulfa-resistant R plasmid. Thus C5166 is our K12 strain with an R factor from wt5166. Six out of th...

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