AI Article Synopsis

  • Rifampicin effectively inhibits the transfer of R-factors in bacteria, showing consistent results regardless of the specific host strain or R-factor type.
  • The primary impact of rifampicin occurs during the early stages of conjugation, where it appears to lead to a reduction in R+ conjugants, likely due to the promotion of spontaneous R- variants rather than direct effects on R+ cells.
  • Short exposure to rifampicin increases the sensitivity of E. coli strains to other antibiotics like chloramphenicol and tetracycline, indicating a potential interaction, while combinations of rifampicin with other antibiotics show a synergistic effect, though the mechanisms behind these observations are still unclear.

Article Abstract

The studies on the effect of a number of antibiotics on transfer of R-factors with the use of a kinetic conjugation system showed that rifampicin inhibited the transfer of various R-factors independent of the microbial host strain and R-factor type (the inhibition coefficient of I infinity equals 7.5-16.8). The early conjugation stages preceding the transfer of R-factor DNA were most sensitive to the antibiotic effect. Decreased number of R+ conjugants observed on the donor strain growth in the presence of rifampicin were due rather to selection of spontaneous R- variants with the antibiotic found in our experiments than to its direct effect on the donor competence of R+ cells. It was also found that exposure of E. coli strains to rifampicin for 30 minutes increased their sensitivity to chloramphenicol and tetracycline, this being more pronounced in the cells which not long ago acquired the R-factor. The mechanism of the phenomenon is not clear yet. It was shown to be not associated with the cell permeability impairement under the effect of rifampicin. It was noted that rifampicin combination with neomycin chloramphenicol, tetracycline or streptomycin had a synergistic effect on the strains of E. coli.

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