Bacterial resistance to antimicrobial agents generally involves drug inactivation, target site modification, impermeability, or efflux mechanisms. Macrolide antibiotic resistance in Staphylococcus aureus and coagulase-negative staphylococci (CNS) may be due to an active efflux mechanism encoded by msrA (conferring resistance to macrolides and type B streptogramins only) (16, 17) or may be due to ribosomal target modification, affecting macrolides, lincosamides, and type B streptogramins (MLS B resistance). erm genes encode enzymes that confer inducible or constitutive resistance to MLS agents via methylation of the 23S rRNA, reducing binding by MLS agents to the ribosome (15). Resistance is induced by the binding of a macrolide to upstream translational attenuator sequences, leading to changes in mRNA secondary structure, exposure of the ribosomal binding site, and translation of the erm methylase. Alterations in these 5Ј upstream sequences, including deletions, duplications, and other mutations, lead to constitutive expression of the methylase gene and constitutive MLS B resistance (1,15,24). Strains with inducible MLS B resistance (MLS B i) strains demonstrate in vitro resistance to 14-and 15-member macrolides (e.g., erythromycin), while appearing susceptible to 16-member macrolides, lincosamides, and type B streptogramins; strains with constitutive MLS B resistance (MLS B c strains) show in vitro resistance to all of these agents (15).MLS antibiotics are commonly used in treatment of staphylococcal infections. Clindamycin is a frequent choice for some staphylococcal infections, particularly skin and soft-tissue infections, and as an alternative in the penicillin-allergic patient. Inducible MLS B resistance is not recognized by using standard susceptibility test methods, including standard broth-based or agar dilution susceptibility tests. Failure to identify inducible MLS B resistance may lead to clinical failure of clindamycin therapy (3). Conversely, labeling all erythromycin-resistant staphylococci as clindamycin resistant prevents the use of clindamycin in infections caused by truly clindamycin-susceptible staphylococcal isolates.Low levels of erythromycin are the most effective inducer of inducible MLS B resistance (23). To detect MLS B i strains, there are special disk approximation tests that incorporate erythromycin induction of clindamycin resistance (23). These tests involve the placement of an erythromycin disk in close proximity to a disk containing clindamycin or lincomycin. As the erythromycin diffuses through the agar, resistance to the lincosamide is induced, resulting in a flattening or blunting of the lincosamide zone of inhibition adjacent to the erythromycin disk, giving a D shape to the zone (D-zone effect). Jenssen and colleagues suggested that closer spacing than in a standard disk dispenser was necessary to discern inducible resistance, with optimal spacing of 10 to 15 mm (6); 20-mm spacing of disks and a higher concentration of erythromycin (30 g) have also been suggested (18).

The susceptibilities of 142 Acinetobacter baumannii-calcoaceticus complex isolates (95 from wounded U.S. soldiers deployed overseas) to 13 antimicrobial agents were determined by broth microdilution. The most active antimicrobial agents (>95% of isolates susceptible) were colistin, polymyxin B, and minocycline.

This study has shown that inducible clindamycin resistance in staphylococci can be detected by disk testing on sheep blood agar inoculum purity plates used with the bioMerieux VITEK 2. Tests of 150 erythromycinresistant isolates correlated with standard D-zone tests on Mueller-Hinton agar and with PCR for erm(A

Increasing penicillin resistance and the initial recognition of resistance to extended-spectrum cephalosporins among Streptococcus pneumoniae isolates have placed greater emphasis on accurate methods for susceptibility testing of clinical isolates. This study has evaluated the use of the E test (AB Biodisk NA, Piscataway, N.J.) for the detection of penicillin and cefotaxime resistance among 147 pneumococcal clinical isolates in three geographically separate laboratories. These included 42 penicillin-resistant (MIC, .2 tLg/ml) and 14 cefotaxime-resistant (defined here as an MIC of .2 tig/ml) isolates. E test strips were applied to the surface of Mueller-Hinton sheep blood agar plates and incubated at 35°C in 5% CO2 for 20 to 24 h. E test MICs were compared with MICs determined with lysed horse blood-supplemented Muelier-Hinton broth in a microdilution format as recommended by the National Committee for Clinical Laboratory Standards. Penicillin MICs agreed within one log2 dilution for 136 of 147 (92.5%) isolates, and cefotaxime MICs agreed within one log2 dilution for 142 of 147 (96.6%) isolates. No very major or major interpretive errors occurred with either penicillin or cefotaxime E test MIC results. There were 9.5 and 5.4% minor interpretive category errors with penicillin and cefotaxime E test MICs, respectively. These data indicate that the E test represents a convenient and reliable method for the detection of penicillin or cephalosporin resistance in pneumococci.

We report a case of bacteremia due to Abiotrophia species in a patient with neutropenic fever and cancer who was receiving levofloxacin prophylaxis, followed by empirical therapy with cefepime; the organism was resistant to both antibiotics. We provide susceptibility data on 20 additional bloodstream isolates of Abiotrophia species.