McDougal L K, Tenover F C, Lee L N, Rasheed J K, Patterson J E, Jorgensen J H, LeBlanc D J
Hospital Infections Program, Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA.
Antimicrob Agents Chemother. 1998 Sep;42(9):2312-8. doi: 10.1128/AAC.42.9.2312.
A series of macrolide-lincosamide-streptogramin B (MLS)-resistant pneumococcal isolates of a variety of serotypes was examined and was found to contain Tn917-like elements by DNA-DNA hybridization. Like Tn1545, Tn917 also encodes an ermAM gene but does not mediate resistance to other antimicrobial agents. Furthermore, nucleotide sequence analyses of the DNAs flanking three of the Tn917-like elements revealed that they were inserted into orf9 of a Tn916-like element in a composite transposon-like structure (Tn3872). Other MLS-resistant strains appeared to contain Tn1545-like elements that had suffered a deletion of sequences including the aphA-3 sequences responsible for kanamycin resistance. Thus, the MLS resistance phenotype in pneumococci appears to be mediated by the ermAM present on a much wider variety of genetic elements than was previously appreciated.
对一系列多种血清型的耐大环内酯-林可酰胺-链阳菌素B(MLS)肺炎球菌分离株进行了检测,通过DNA-DNA杂交发现它们含有Tn917样元件。与Tn1545一样,Tn917也编码ermAM基因,但不介导对其他抗菌剂的耐药性。此外,对三个Tn917样元件侧翼DNA的核苷酸序列分析表明,它们以复合转座子样结构(Tn3872)插入到Tn916样元件的orf9中。其他耐MLS菌株似乎含有Tn1545样元件,这些元件发生了序列缺失,包括负责卡那霉素耐药性的aphA-3序列。因此,肺炎球菌中的MLS耐药表型似乎是由ermAM介导的,而ermAM存在于比以前认识到的更为多样的遗传元件上。