Mutations in 23S rRNA Account for Intrinsic Resistance to Macrolides in Mycoplasma hominis and Mycoplasma fermentans and for Acquired Resistance to Macrolides in M. hominis
23S ribosomal RNA
Mycoplasma hominis
DOI:
10.1128/aac.46.10.3142-3150.2002
Publication Date:
2002-09-16T15:23:02Z
AUTHORS (9)
ABSTRACT
ABSTRACT The mechanisms of intrinsic resistance Mycoplasma hominis to 14- and 15-membered macrolides were investigated in comparison with those M. pneumoniae , which is naturally susceptible macrolides. Radiolabeled erythromycin was not accumulated by PG21, but addition an ABC transporter inhibitor increased the level uptake more than two times, suggesting existence active efflux process. affinity [ 14 C]erythromycin ribosomes isolated from dramatically reduced relative that pneumoniae. nucleotide sequences 23S rRNA both ribosomal operons rrnA rrnB proteins L4 L22 obtained. Compared sequence harbored a G2057A transition its sequence, as did fermentans another mycoplasma resistant. An additional C2610U change also found . Moreover, clinical isolates acquired 16-membered examined for mutations domain II V L22. reference strain one isolate A2059G C2611U rrn operons, while other mutated only at position 2059, on same operon. No mutation protein sequences. Overall, present study exhaustive characterization first description resistant macrolide, lincosamide, streptogramin antibiotics harboring 2611 rRNA.
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