Kawabe H, Tanaka T, Mitsuhashi S
Antimicrob Agents Chemother. 1978 Jun;13(6):1031-5. doi: 10.1128/AAC.13.6.1031.
Resistance to tetracycline (Tc), chloramphenicol (Cm), streptomycin (Sm), and sulfanilamide (Sa) was surveyed in clinical isolates of Escherichia coli and Shigella strains. Among the Sm Sa-resistant strains, the frequency of nonconjugative r (Sm Sa) plasmids was much higher than that of conjugative R plasmids encoding double resistance. The biochemical mechanism of Sm resistance mediated by the conjugative plasmids R(Tc Cm Sm Sa) and R(Cm Sm Sa) and about half the numbers of conjugative R(Tc Sm Sa) and R(Sm Sa) plasmids tested were found to be due to adenylylation of the drug. The remaining conjugative R(Tc Sm Sa) and R(Sm Sa) plasmids and all nonconjugative (Sm Sa) plasmids tested inactivated Sm by phosphorylation.
对大肠杆菌和志贺氏菌临床分离株的四环素(Tc)、氯霉素(Cm)、链霉素(Sm)和磺胺(Sa)耐药性进行了调查。在耐Sm Sa的菌株中,非接合性r(Sm Sa)质粒的频率远高于编码双重耐药性的接合性R质粒。发现由接合性质粒R(Tc Cm Sm Sa)和R(Cm Sm Sa)介导的Sm耐药性的生化机制以及大约一半经测试的接合性R(Tc Sm Sa)和R(Sm Sa)质粒是由于药物的腺苷酸化。其余经测试的接合性R(Tc Sm Sa)和R(Sm Sa)质粒以及所有非接合性(Sm Sa)质粒通过磷酸化使Sm失活。