The in vitro activities of the new agents linezolid, quinupristin-dalfopristin, moxifloxacin, and trovafloxacin were determined and compared with those of penicillin, clindamycin, and four macrolides against 53 erythromycin-resistant Streptococcus pneumoniae, 117 S. pyogenes (64 erythromycin-susceptible and 53 -resistant), and 101 S. agalactiae (53 erythromycin-susceptible and 48 -resistant) isolates. Differentiation of macrolide resistance phenotypes was performed by the double-disk method. The genetic basis for macrolide resistance in 52 strains was also determined. The M phenotype was found in 84.9, 6.3, and 1.9% of S. pyogenes, S. agalactiae, and S. pneumoniae isolates, respectively. These strains were susceptible to miocamycin and clindamycin. Strains with the inducible phenotype accounted for 27.1% of S. agalactiae isolates and 9.4% each of S. pyogenes and S. pneumoniae isolates. All erythromycin-resistant isolates were also resistant to the 14-and 15-membered macrolides tested. Strains with all three phenotypes were susceptible to <2 g of linezolid per ml. Quinupristin-dalfopristin exhibited good in vitro activity against all strains, irrespective of their resistance to erythromycin (MICs at which 90% of the isolates tested were inhibited [MIC 90 s], 0.2 to 1 g/ml). Against the erythromycin-resistant S. pyogenes and S. agalactiae strains, moxifloxacin and trovafloxacin were the most active agents (MIC 90 s, 0

Mechanisms for tetracycline and macrolide resistance in 54 isolates of erythromycin-resistant Streptococcus agalactiae were analyzed by PCR. The erm(B), erm(A), and mef(A) genes, either alone or in combination, were detected in all the erythromycin-resistant isolates. The tet(M) and tet(O) genes were responsible for tetracycline resistance. Random amplification of polymorphic DNA indicated different clonal origins of the isolates.

The activity of linezolid was determined against 225 recently isolated methicillin-resistant Staphylococcus aureus (MRSA) and 20 methicillin-resistant coagulase-negative staphylococci (CoNS) with decreased levels of susceptibility to teicoplanin. Linezolid activity was compared with other new agents (quinupristin-dalfopristin, trovafloxacin, moxifloxacin, levofloxacin and telithromycin) and six other antimicrobials (erythromycin, clindamycin, gentamicin, vancomycin, teicoplanin and rifampicin). The in vitro activity of linezolid was similar to that of vancomycin. Linezolid inhibited all MRSA strains at between 0.1 and 2 mg/L and all CoNS strains tested at between 0.2 and 0.5 mg/L. These results suggest that linezolid would be useful for the treatment of infections involving these organisms.

We describe a patient who developed a pigmented plaque on the anterior aspect of his right knee clinically mimicking angiokeratoma circumscriptum or malignant melanoma. Histopathological examination demonstrated a multinodular hemosiderotic dermatofibroma in which the cellular tumor islands were separated by areas of hyalinized collagen. Multinucleated giant tumor cells were found in the lumen of a medium-size vein underlying the tumor. The differential diagnosis of angiomatoid malignant fibrous histiocytoma, a tumor with clinical and morphologic similarities, is discussed.

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