[Mechanism of bacterial resistance to tetracyclines and the importance of structural elements of tetracycline molecule for induction of resistance].

The resistance of Staphylococcus aureus P-282 and E. coli E-107 to chlorotetracycline is based on the acquired ability of energy-dependent "counteraction" with regard to penetration of the antibiotic in to the cells. Thus, inhibitors of energy processes stimulate chlorotetracycline absorption by resistant strains and increase their sensitivity to the antibiotic. The studied bacterial hospital strains absorb chlorotetracycline by means of oxalacetic acid transport system similar to resistant strains obtained in the laboratory. The transport system of chlorotetracycline is stereospecific and is involved in absorption of analogues of the antibiotic with the intact phenoldiketone or diphenol structure of the molecule. These analogues, like the natural antibiotic, induce an increase in the resistance to the antibiotic. No changes in the nature of the antibiotic transport system occur during induction. The increased resistance caused by induction is due entirely to a decrease in absorption of the antibiotic by the cells.