Resistance to macrolides by ribosomal mutation in clinical isolates of Turicella otitidis

Leyla Boumghar-Bourtchai (1) , Hubert Chardon (2) , Brigitte Malbruny (1, 3) , Senda Mezghani (1) , Roland Leclercq (1, 3) , Anne Dhalluin (1)

1 Interactions hôte et microorganismes des épithéliums
2 CHIAP - Centre Hospitalier d'Aix en Provence [Aix-en-Provence]
3 CHU Caen

The genetic basis of erythromycin resistance in , a coryneform bacteria associated with otitis, was studied in five macrolide-resistant clinical isolates. Macrolide resistance genes were searched for by polymerase chain reaction (PCR). Genes for domain V of 23S rRNA () as well as (L4 protein) and (L22 protein) genes were characterised, amplified by PCR from total genomic DNA and sequenced. In the resistant isolates, cross-resistance to macrolides and clindamycin was associated with mutations at positions 2058 and/or 2059 ( numbering). Three isolates displayed A2058 mutations, one isolate had an A2059G mutation whereas another one contained mutations at positions 2058 and 2059. Southern blot experiments revealed that had three copies of the gene. In conclusion, resistance to macrolides in is due, at least in part, to mutations in the gene.

Mots clés: 23S ribosomal RNA; Macrolides; Azalides; Antibiotic resistance

Domaines: Sciences du Vivant [q-bio]

Leyla Boumghar-Bourtchai, Hubert Chardon, Brigitte Malbruny, Senda Mezghani, Roland Leclercq, et al.. Resistance to macrolides by ribosomal mutation in clinical isolates of Turicella otitidis. International Journal of Antimicrobial Agents, 2009, 34 (3), pp.274. ⟨10.1016/j.ijantimicag.2009.03.023⟩. ⟨hal-00556343⟩