Erm(X)-mediated resistance to macrolides, lincosamides and streptogramins in Actinobaculum schaalii.

OBJECTIVES

Actinobaculum schaalii is a Gram-positive bacillus increasingly reported as a causative agent of urinary tract infections as well as invasive infections, mainly in the elderly and patients with underlying urological conditions. Since little is known about the molecular basis of antimicrobial resistance in A. schaalii, the aim of this study was to investigate resistance to macrolides, lincosamides and streptogramins (MLS) in this emerging pathogen.

METHODS

A total of 32 A. schaalii clinical isolates from France and Switzerland were studied. MICs of erythromycin, spiramycin, lincomycin, clindamycin and quinupristin/dalfopristin were determined by the agar dilution method. Resistance genes erm(A), erm(B), erm(C), erm(F), erm(G), erm(X), msr(A) and mef(A) were screened by PCR. The genetic environment was determined by random cloning and PCR mapping.

RESULTS

Out of 32 isolates tested, 21 were highly resistant to erythromycin, spiramycin, lincomycin and clindamycin (MICs >256 mg/L), whereas 11 exhibited low MICs (MICs < 0.12 mg/L). On the other hand, quinupristin/dalfopristin remained active against all the isolates. An inducible MLSB resistance phenotype was noted in all cases. The erm(X) gene was detected among all resistant strains, whereas none was detected in susceptible strains. Analysis of genetic support and environment revealed that erm(X) was probably part of the chromosome of A. schaalii.

CONCLUSIONS

This study is the first molecular characterization of MLS resistance in A. schaalii. In all cases, it was due to the presence of erm(X), a methylase gene previously identified in other clinically relevant Gram-positive bacilli.