No abstract

Sixty-two isolates of

Two oxacillin disk methods were compared with a cefoxitin disk diffusion test for detection of methicillin-resistant Staphylococcus aureus (MRSA), with PCR for mecA as the reference method. When tested with 115 MRSA and 350 methicillin-susceptible S. aureus isolates, the cefoxitin disk test (specificity 100%, sensitivity 96.5%) was superior to the oxacillin disk methods (specificity 99.1%, sensitivity 90.4%). Testing with both oxacillin and cefoxitin disks would give better sensitivity (100%) than the cefoxitin test alone, but at the expense of specificity (99.1%). The cefoxitin disk test required no special test conditions and would improve the reliability of routine tests for detection of MRSA.

clinical strains of Streptococcus agalactiae, recovered from female genital specimens and from gastric fluid or ear specimens from infected newborns, were isolated at the Laboratory of Microbiology of Charles Nicolle Hospital of Tunis. They were investigated to determine the prevalence of antibiotic resistance and to characterize the mechanisms of resistance to macrolide and tetracycline. All strains were susceptible to penicillin, ampicillin and quinupristin-dalfopristin. They were resistant to chloramphenicol (3.1 %), rifampicin (19.1 %), erythromycin (40 %) and tetracycline (97.3 %); 3.1 % were highly resistant to streptomycin and 1.3 % to gentamicin. Among the erythromycin-resistant isolates, 78.7 % showed a constitutive macrolide-lincosamide-streptogramin B (MLS B ) phenotype with high-level resistance to macrolides and clindamycin (MIC 50 .256 mg ml ) and low MICs of clindamycin (MIC 50 58 mg ml "1 ) and 2.2 % showed an M phenotype with a low erythromycin-resistance level (MIC range512-32 mg ml "1 ) and low MICs of clindamycin (MIC range: 0.75-1 mg ml). All strains were susceptible to quinupristin-dalfopristin and linezolid (MIC 90 : 0.75 mg ml "1 for each). MLS B phenotypes were genotypically confirmed by the presence of the erm(B) gene and the M phenotype by the mef(A) gene. Resistance to tetracycline was mainly due to the tet(M) gene (93.1 %) encoding a ribosome protection mechanism. This determinant is commonly associated with the conjugative transposon Tn916 (P¡0.0002). tet(O) and tet(T) existed in a minority (2.2 % and 0.4 %, respectively). The efflux mechanism presented by tet(L) was less frequently present (4.5 %). No significant association was found between erm(B) and tet(M) genes.