Shortridge V D, Flamm R K, Ramer N, Beyer J, Tanaka S K
Abbott Laboratories, Abbot Park, Illinois, USA.
Diagn Microbiol Infect Dis. 1996 Oct;26(2):73-8. doi: 10.1016/s0732-8893(96)00183-6.
The mechanism of macrolide resistance was examined in 73 clinical isolates of Streptococcus pneumoniae. Two distinct resistance phenotypes were observed: high-level macrolides-lincosamides-streptogramin B (MLS) resistance and low-level macrolide resistance with lincosamide susceptibility. High-level MLS resistance was associated with the presence of ermAM. Strains with the low-level resistant phenotype (novel) were negative for ermA, ermC, ermAM, ereA, ereB and msrA by polymerase chain reaction (PCR) amplification with gene-specific primers. Ribosomes isolated from novel strains bound the same amount of [14C]-erythromycin as ribosomes from sensitive strains. These novel strains also did not inactivate the macrolide. The novel mechanism was found in 41% of the erythromycin resistant S. pneumoniae examined.
对73株肺炎链球菌临床分离株的大环内酯类耐药机制进行了研究。观察到两种不同的耐药表型:高水平大环内酯-林可酰胺-链阳菌素B(MLS)耐药和低水平大环内酯耐药伴林可酰胺敏感。高水平MLS耐药与ermAM的存在有关。通过使用基因特异性引物的聚合酶链反应(PCR)扩增,低水平耐药表型(新发现的)菌株的ermA、ermC、ermAM、ereA、ereB和msrA均为阴性。从新发现的菌株中分离出的核糖体与敏感菌株的核糖体结合的[14C] - 红霉素量相同。这些新发现的菌株也不会使大环内酯失活。在所检测的红霉素耐药肺炎链球菌中,41%发现了这种新机制。