Piendl W, Böck A
Antimicrob Agents Chemother. 1982 Aug;22(2):231-6. doi: 10.1128/AAC.22.2.231.
The mechanism of resistance of the gentamicin-producing organism Micromonospora purpurea was analyzed. Determination of minimal inhibitory concentrations revealed high resistance to the 4,6-substituted deoxystreptamine aminoglycosides amikacin, gentamicin, kanamycin, netilmicin, sisomicin, and tobramycin and also to lividomycin A and hygromycin B, but susceptibility to streptomycin, dihydrostreptomycin, paromomycin, and neomycin during all phases of the growth cycle. The nonproducing, closely related Micromonospora melanosporea was susceptible to these compounds. In agreement with results from previous studies (R. Benveniste and J. Davies, Proc. Natl. Acad. Sci. U.S.A. 70:2276-2280, 1973), extracts from M. purpurea showed no activity of enzymes specifically modifying gentamicin. 70S ribosomes from M. purpurea but not from M. melanosporea were resistant to inhibition by gentamicin, kanamycin, tobramycin, and lividomycin in a polyuridylic acid-dependent polyphenylalanine synthesis system and susceptible to those compounds which were inhibitory in vivo. The former antibiotics were also unable to induce misreading. Subunit exchange experiments between M. purpurea and M. melanosporea showed that the main site for inhibition and induction of misreading is the 30S subunit (up to gentamicin concentrations of 10 micrograms/ml).
对产生庆大霉素的紫色小单孢菌的耐药机制进行了分析。最低抑菌浓度的测定表明，该菌对4,6-取代脱氧链霉胺氨基糖苷类抗生素阿米卡星、庆大霉素、卡那霉素、奈替米星、西索米星和妥布霉素以及对利维霉素A和潮霉素B具有高耐药性，但在生长周期的所有阶段对链霉素、双氢链霉素、巴龙霉素和新霉素敏感。不产生抗生素的近缘菌黑色小单孢菌对这些化合物敏感。与先前研究结果一致（R. 本维尼斯特和J. 戴维斯，《美国国家科学院院刊》70:2276 - 2280，1973），紫色小单孢菌的提取物未显示出特异性修饰庆大霉素的酶活性。在多聚尿苷酸依赖性多聚苯丙氨酸合成系统中，紫色小单孢菌的70S核糖体对庆大霉素、卡那霉素、妥布霉素和利维霉素的抑制具有抗性，而黑色小单孢菌的70S核糖体对这些化合物敏感，且这些化合物在体内具有抑制作用。前一种抗生素也不能诱导错读。紫色小单孢菌和黑色小单孢菌之间的亚基交换实验表明，抑制和诱导错读的主要位点是30S亚基（在庆大霉素浓度高达10微克/毫升时）。
