Search

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.

Combinations of certain antibiotics and normal human serum at concentrations at which there was no killing by the agents when used alone were found to be bactericidal for Escherichia coli K-12 cells. This effect was observed with tetracycline, streptomycin (SM), trimethoprim, and ampicillin, but not with chloramphenicol or nalidixic acid. Synergy between SM and human serum was also observed against four of nine smooth strains of E. coli . A plasmid-bearing strain of E. coli K-12 was also killed by combinations of tetracycline or SM plus serum, even though the plasmid conferred resistance to tetracycline and SM. Evidence is presented that the synergy between antibiotics and serum is due to a complement-mediated effect on the bacterial cells that makes the cells more susceptible to the bactericidal effects of the antibiotics.