[In vitro antibacterial activity of a new fluoroquinolone, sparfloxacin, against nosocomial bacteria, and concordance curve]. / Activité anti-bactérienne in vitro d'une nouvelle fluoroquinolone, la sparfloxacine sur les bactéries hospitalières et courbe de concordance.

Minimal inhibitory concentrations (MICs) of sparfloxacin (SFX) were determined by agar dilution for 3,164 bacterial strains isolated in 10 university hospitals; in addition, antibiograms by agar diffusion were performed with 5 micrograms disks. Activity of SFX against nalidixic acid (NAL) susceptible (S) Enterobacteriaceae was close to that of other fluoroquinolones (FQ) (MIC 50 and 90: 0.06-0.5 microgram/ml); like for other FQ, this activity was reduced against NAL intermediate and resistant (R) Enterobacteriaceae (2-16). MICs of SFX against P. aeruginosa were between 0.12 and 16 (1-32). SFX had also a good activity against NAL-S A. baumannii (CMI < or = 0.25) but this activity is reduced against NAL-R Acinetobacter (16). SFX was highly active against Haemophilus (0.016-0.06) gonococci (0.008), meningococci (0.008) and B. catarrhalis (0.008-0.03). SFX showed activity superior to the currently available FQ against methicillin susceptible staphylococci (0.06); the resistant strains [8] are usually methicillin resistant. SFX is more effective against enterococci (0.5), streptococci (0.25-0.5) and particularly pneumococci (0.25-0.5) including penicillin-resistant strains. The coefficient correlation of the regression curve is 0.876; for MIC breakpoints of 1 and 2 micrograms/ml, zone diameter breakpoints should be 20 and 16 mm.

[In vitro antibacterial activity of cefpirome: a new cephalosporin; results of a multicenter study]. / Activité antibactérienne in vitro d'une nouvelle céphalosporine, le cefpirome: résultats d'une étude multicentrique.

The in vitro activity of cefpirome, a new injectable cephalosporin was studied against 1,082 clinical isolates in a multicentre study. Minimum inhibitory concentrations were determined using an agar dilution method. Cefpirome was active against Enterobacteriaceae. On naturally non-producing beta-lactamase species, cefpirome was active on most of the strains with MICs < or = 0.5 mg/l, including strains producing an acquired penicillinase: E. coli 0.03-0.06, P. mirabilis 0.06-0.12, Salmonella spp. 0.06-0.06, Shigella spp. 0.016-0.03. MICs of K. pneumoniae (0.06-4) ranged from 0.016 to 32:MICs were high against expanded-spectrum betalactamase producers strains. Against species producing cephalosporinase, cefpirome was also active on most of the strains with MICs < or = 0.5: E. cloacae 0.06-2, Citrobacter spp. 0.03-1, S. marcescens 0.06-0.5, P. indol + 0.06-0.25, P. stuartii 0.12-0.5. Cefpirome was less active on Pseudomonas aeruginosa, (8-32) and on A. baumanii (16-32). MICs of cefpirome were low against Haemophilus spp. betalactamase producing or not (0.01-0.03) and M. catarrhalis (0.6-4). Activity of cefpirome on methicillin-sensitive staphylococci, was higher than other third generation cephalosporins (0.25-2) comparable to that of cephalotin and cefamandol. Methicillin-resistant strains should be considered as resistant. Pneumococci (0.01-0.03), except for penicillin-R strains, and streptococci A, B, C, G (0.01-0.06) were very susceptible. Enterococci were of low sensitivity or resistant. Among anaerobes, C. perfringens appeared often susceptible, and Bacteroides spp. resistant.

[In vitro antibacterial activity of a new fluoroquinolone, fleroxacin, against hospital bacteria and regression curve]. / Activité antibactérienne in vitro d'une nouvelle fluoroquinolone, la fléroxacine, sur les bactéries hospitalières et courbe de concordance.

Minimal inhibitory concentrations (MICs) of fleroxacin (FLE) were determined by agar dilution for 1261 bacterial strains isolated in 1992 in 4 university hospitals; in addition, antibiograms by agar diffusion were performed with 5 micrograms disks. Activity of FLE against nalidixic acid (NAL) susceptible (S) Enterobacteriaceae was close to that of other fluoroquinolones (FQ) (MIC 50 and 90: 0.12-0.25 micrograms/ml); like for other FQ, this activity was reduced against NAL intermediate and resistant (R) Enterobacteriaceae (4-32). MICs of FLE against P. aeruginosa were between 1 and 128 (8-128). FLE had also a good activity against NAL-S A. baumannii (0.12-0.5) but this activity is reduced against NAL-R Acinetobacter (64-128). FLE was highly active against Haemophilus (0.06-0.12), Gonococci (0.03-0.25), Meningococci (0.016-0.03) and B. catarrhalis (0.12-0.25). FLE showed activity close to the currently available FQ against methicillin susceptible Staphylococci (0.25-1); the resistant strains (32- > 128) are usually methicillin resistant. FLE is less effective against Enterococci (4-128), Streptococci (8-16) and Pneumococci (4-8). The coefficient correlation of the regression curve is 0.93; for MIC breakpoints of 1 and 4 micrograms/ml, zone diameter breakpoints should be 20 and 15 mm.

Enhanced conjugative transfer of plasmid DNA from Escherichia coli to Staphylococcus aureus and Listeria monocytogenes.

Transfer of mobilizable shuttle cloning vectors by conjugation from Escherichia coli to Staphylococcus aureus occurred at a very low frequency (10(-9) transconjugants per donor colony-forming unit after the mating period). It was observed that subinhibitory concentrations of penicillins (oxacillin or penicillin G) in the mating medium resulted in increased transfer frequency by conjugation of the shuttle vector pAT18 from E. coli SM10 to S. aureus 80CR5 Str (54-fold) and to Listeria monocytogenes LO17RF (45-fold). These results were interpreted as indicating that the cell wall of Gram-positive bacteria constitutes an important barrier for conjugative transfer of genetic information delivered from E. coli. It was also demonstrated that presence of a restriction system(s) in S. aureus recipients represented a major barrier to introduction of foreign DNA.

Resistance of enterococci to aminoglycosides and glycopeptides.

High-level resistance to aminoglycosides in enterococci often is mediated by aminoglycoside-modifying enzymes, and the corresponding genes generally are located on self-transferable plasmids. These enzymes are similar to those in staphylococci but differ from the modifying enzymes of gram-negative bacteria. Three classes of enzymes are distinguished, depending upon the reaction catalyzed. All but amikacin and netilmicin confer high-level resistance to the antibiotics that are modified in vitro. However, the synergistic activity of these last two antibiotics in combination with beta-lactam agents can be suppressed, as has always been found in relation to high-level resistance to the aminoglycosides. Acquisition of glycopeptide resistance by enterococci recently was reported. Strains of two phenotypes have been distinguished: those that are resistant to high levels of vancomycin and teicoplanin and those that are inducibly resistant to low levels of vancomycin and susceptible to teicoplanin. In strains of Enterococcus faecium highly resistant to glycopeptides, we have characterized plasmids ranging from 34 to 40 kilobases that are often self-transferable to other gram-positive organisms. The resistance gene vanA has been cloned, and its nucleotide sequence has been determined. Hybridization experiments showed that this resistance determinant is present in all of our enterococcal strains that are highly resistant to glycopeptides. The vanA gene is part of a cluster of plasmid genes responsible for synthesis of peptidoglycan precursors containing a depsipeptide instead of the usual D-alanyl-D-alanine terminus. Reduced affinity of glycopeptides to these precursors confers resistance to the antibiotics.

Mechanisms and implications of glycopeptide resistance in enterococci.

Glycopeptide resistance is recent in enterococci and its expression is inducible by glycopeptides. Two phenotypes can be distinguished: (a) resistance to high levels of vancomycin and teicoplanin, and (b) resistance to low levels of vancomycin only. There is no cross-resistance between glycopeptides, glycolipodepsipeptides (ramoplanin), and lipopeptides (daptomycin). The determinants conferring low-level resistance are nontransferable and presumably chromosomal. High-level resistance is plasmid-mediated and the plasmids range from 34 to 40 kb, are self-transferable, and encode various resistance combinations. All plasmids share the same glycopeptide resistance determinant, which is distinct from that conferring low-level resistance. Induction of resistance is associated with induction of about a 40 kDa protein. We have determined the sequence of the vanA gene encoding one such resistance protein designated VANA. Amino acid sequence similarity was detected between VANA and D-Ala: D-Ala ligases from Enterobacteriaceae. Complementation analysis in Escherichia coli indicated that VANA possesses D-Ala: D-Ala ligase activity and is therefore related to enzymes that catalyze synthesis of glycopeptide target, i.e., terminal D-Ala-D-Ala of peptidoglycan precursors. The contribution of VANA to synthesis of peptidoglycan in the presence of glycopeptides is unknown: VANA could bind to D-Ala-D-Ala, preventing the binding of the drugs; could modify the target of the drug; and could be a ligase with novel specificity.

[In vitro antibacterial activity of a new oral cephalosporin, ceftibuten. Results of a multicenter study]. / Activité antibactérienne in vitro d'une nouvelle céphalosporine orale, le ceftibutène. Résultats d'une étude multicentrique.

Minimal inhibitory concentration (MIC) of ceftibuten (CBT) were evaluated by agar dilution for 1,416 bacterial strains isolated in 5 hospitals. For Enterobacteriaceae, MIC 50 and 90% were respectively (micrograms/ml): (I) Naturally non beta-lactamase producing species: E. coli 0.12-0.5, Shigella 0.06-0.12 and Salmonella 0.03-0.12, P. mirabilis 0.16-0.03. (II) Chromosomal penicillinase producing species: K. pneumoniae 0.03-0.5 and K. oxytoca 0.03-0.06. (III) Chromosomal cephalosporin producing species: E. cloacae and C. freundii 1- greater than 128: S. marcescens 0.25-2; indole + Proteus 0.06-0.12. Activity of CBT was not modified on plasmid mediated penicillinase producing strains; however, CBT was inactive on cephalosporinase hyperproducing strains, and its activity was variably reduced on broad spectrum beta-lactamases producing strains. CBT was inactive on P. aeruginosa (MIC greater than or equal to 32) and on A. baumannii (8- greater than 128). Haemophilus and Gonococci, regardless on beta-lactamase production status, were very susceptible to CBT (MIC 50 and 90%: 0.06-0.5 and 0.016-0.06); it is the same situation for Meningococci; B. catarrhalis was generally inhibited by 0.03 to 2 (strains susceptible to penicillin G) and 0.12 to 16 (strains resistant to penicillin G). CBT was inactive on Staphylococci. Enterococci and Streptococci B were generally resistant; Streptococci A, C, G were inhibited by low concentrations: 0.06 to 1 (MIC 50 and 90%: 0.25-0.5), whereas MIC for other Streptococci 0.12 to 128 (MIC 50 and 90%: 8-128) and for Pneumococci were 0.25 to 16 (4-8). These antibacterial properties particularly against Enterobacteriaceae placed CBT in excellent position among oral cephalosporins.

[In vitro antibacterial activity of a new fluoroquinolone, temafloxacin, against hospital isolates. Results of a multicenter study]. / Activité antibactérienne in vitro d'une nouvelle fluoroquinolone, la témafloxacine, sur les bactéries hospitalières. Résultats d'une étude multicentrique.

Minimal inhibitory concentrations (MICs) of temafloxacin (TMF) was determined by agar dilution for 2,510 bacterial strains isolated in 1989 in 9 university hospitals. Activity of TMF against nalidixic acid (NAL) susceptible (S) Enterobacteriaceae was close to that of other fluoroquinolones (FQ) (mode MIC: 0.06 micrograms/l); like for other FQ, this activity was reduced against NAL intermediate (mode 1) and resistant (R) (mode 4) Enterobacteriaceae. MICs of TMF against P. aeruginosa were between 0.12 and 128 (mode 0.5-1). TMF had also a good activity against NAL S A. baumannii (mode MIC: 0.06-0.12) but this activity is reduced against NAL R Acinetobacter (mode MIC: 16). TMF was highly active against Haemophilus mode MIC: less than or equal to 0.008), Gonococci (mode MIC: 0.008-0.032), Meningococci (mode MIC: 0.08) and B. catarrhalis (mode MIC: 0.016). TMF showed better activity to other fluoroquinolones against methicillin susceptible Staphylococci (mode MIC: 0.06); the resistant strains (mode MIC: 8) are usually methicillin resistant. Comparatively to the currently available FQ, TMF is so more effective against Enterococci (mode MIC: 1), Streptococci (mode MIC: 0.5-1) and Pneumococci (mode MIC: 0.5). Finally, for the anaerobic bacteria, TMF is more active against C. perfringens (mode MIC: 0.5) than against B. fragilis (mode MIC: 2).

[In vitro antibacterial activity of piperacillin-tazobactam combination on hospital isolates and regression curve]. / Activité antibactérienne de l'association pipéracilline + tazobactam sur les bactéries hospitalières et courbe de concordance.

Minimal inhibitory concentrations (MICs) of piperacillin (P) in combination with 4 micrograms/ml of tazobactam (T) were evaluated by agar dilution for 1,245 strains isolated in 4 hospitals. In addition antibiograms by agar diffusion were performed with disks loaded of 75 micrograms of P + 10 micrograms of T. For naturally non beta-lactamase producing Enterobacteriaceae (E), MIC 50 and 90% of P + T were (microgram/ml): E. coli 1-2; P. mirabilis: 0.5-1; activity was practically identical on plasmid mediated penicillinase (Pase) producing strains. Strains of K. pneumoniae only resistant (R) to amino- and carboxypenicillins (C) had MICs less than or equal to 4 (mode MIC 2); MICs of strains R to cephalothin and/or cefotaxime were 2 to 16 (mode MIC 4). For chromosomal cephalosporinase (Case) producing species, MICs of P + T were less than or equal to 8, including for acquired Pase producing strains, but were greater than or equal to 16 for Case hyperproducing strains. Strains of P. aeruginosa susceptible (S) to C were inhibited by 1 to 16 (with MIC 4) and strains R to C by 8 to greater than 128. MICs were generally 2 to 32 for A. baumannii S to C at 0.12 to greater than 128 for strains R to C. Haemophilus, S or R to ampicillin, were inhibited by 0.008 to 2 (MIC 50 and 90: 0.016-0.12). S. aureus S to methicillin (M), Pase producing on not, were inhibited by 0.5 to 2 (mode MIC 1) and strains R to M by 8 to greater than 128. Activity of P + T for coagulase-Staphylococci was similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Gene homogeneity for aminoglycoside-modifying enzymes in gram-positive cocci.

Aminoglycoside-resistant strains of Staphylococcus and Enterococcus, approximately 500 of each, were screened by dot blot hybridization for the presence of genes encoding aminoglycoside-modifying enzymes. The MICs of various aminoglycosides for the strains were determined, and the enzyme contents of the cells were inferred from the resistance phenotypes. The agreements (in percent) of the hybridization results with the deduced enzyme contents for Staphylococcus and Enterococcus species were, respectively, 80 and 87.6 for ANT(6) (aminoglycoside nucleotidyltransferase), 99.8 and 100 for both APH(3') (aminoglycoside phosphotransferase) and APH(2")-AAC(6') (aminoglycoside acetyltransferase), and 100 and 100 for ANT(4'). The weak correlation obtained with the probe for ANT(6) was due to the fact that gram-positive cocci can also be streptomycin resistant by synthesis of APH(3") or ANT(3")(9) and by ribosomal mutation. The remaining probes appeared to be specific: they hybridized with all the resistant clinical isolates but not with the susceptible strains. These results indicate that, except for streptomycin, nucleic acid hybridization is a valid approach for the detection and characterization of aminoglycoside resistance in gram-positive cocci.

[In vitro antibacterial activity of RU 51746 (sodium salt of cefpodoxime). Results of a multicenter study]. / Activité antibactérienne in vitro du RU 51746 (sel de sodium du cefpodoxime). Résultats d'une étude multicentrique.

Cefpodoxime proxetil, a new oral cephalosporin, is the prodrug ester of cefpodoxime. Minimal inhibitory concentrations (MIC) of RU 51746 (sodium salt of cefpodoxime: CPD) were evaluated by agar dilution for 1 696 bacterial strains isolated in 5 hospitals. For Enterobacteriaceae, MIC 50 and 90% were respectively (micrograms/ml): (1) naturally non bêtalactamase producing species: E. coli, Shigella and Salmonella 0.25-0.5; P. mirabilis 0.06-0.12. (II) chromosomal penicillinase producing species: Klebsiella 0.12-1. (III) chromosomal cephalosporinase producing species: E. cloacae and C. freundii 2-greater than 128; S. marcescens 2-64; indole + Proteus 0.25-64; P. stuartii 0.25-16. Activity of CPD was not modified on plasmid mediated penicillinase producing strains, but CPD was inactive on cephalosporinase hyperproducing strains, and on broad spectrum bêtalactamases producing strains. CPD was inactive on P. aeruginosa (MIC greater than or equal to 64) and on A. baumannii (16-pi 128). Haemophilus, regardless on bêtalactamase production status, were very susceptible to CPD (MIC less than or equal to 0.25) and B. catarrhalis was generally inhibited by 0.12 to 1. CPD was poorly active on methicillin susceptible Staphylococci (MIC 50 and 90%: 2-4) and inactive on methicillin resistant strains. Enterococci and Listeria monocytogenes were generally resistant; Streptococci A, B, C, G and Pneumococci were inhibited by low concentration: 0.002 to 0.25 (MIC 50 and 90%: 0.016-0.032) whereas MIC for other Streptococci were 0.004 to 32 (MIC 50 and 90%: 0.25-4). These antibacterial properties placed CPD in excellent position among oral cephalosporins.

[In vitro antibacterial activity of rokitamycin, a new macrolide antibiotic. Results of a multicenter study]. / Activité antibactérienne in vitro d'un nouveau macrolide, la rokitamycine. Résultats d'une étude multicentrique.

Minimal inhibitory concentrations (MIC) of rokitamycin (R) were evaluated by agar dilution for 914 bacterial strain isolated in 4 hospitals and classed as a function of susceptibility and resistance to Macrolides-Lincosamides-Streptogramines group (MLS). MICs of R ranged from 0.06 to 1 microgram/ml (mode MIC 0.25-0.5) on Staphylococci susceptible to MLS and on MLSB inducible strains; R was inactive on MLSB constitutive strains. MICs of R ranged from 0.008 to 0.5 microgram/ml (mode MIC 0.06 to 0.25) for Streptococci and Pneumococci susceptible to erythromycin (E) and from 0.06 to greater than 128 for strains resistant to E. Enterococci susceptible to E were inhibited by 0.06 to 0.5 microgram/ml (mode MIC 0.5) and strains resistant to E by 0.25 to greater than 128. Haemophilus were inhibited by 0.5 to 0.65 microgram/ml (mode MICs of R ranged generally from 0.016 to 0.5 microgram/ml (mode MIC 0.12) for C. perfringens and from 0.016 to 1 (mode MIC 0.06) for B. fragilis. Thus, R was shown to be among macrolide antibiotics of resistance strains. Its activity was superior to that of other products of this group spiramycin, josamycin, miokamycin, particularly on Gram positive cocci. R had a good activity on Neisseria, Branhamella, anaerobes and, as others macrolides, was poorly active on Haemophilus.

[In vitro antibacterial activity of clarithromycin, a new macrolide antibiotic, and regression curve]. / Activité antibactérienne in vitro d'un nouveau macrolide, la clarithromycine, et courbe de concordance.

This study was set up to establish the regression curve for clarithromycin inhibition zone diameters (disks 15 micrograms) and MIC to create a strain distribution plot, in order to allow accurate interpretation of the disk diffusion method for testing susceptibility to clarithromycin. 430 bacterial strains were studied in three university hospital. Clarithromycin was active against erythromycin sensitive Staphylococcus aureus and coagulase negative Staphylococci at concentrations of 0.12 to 0.25 microgram/ml (mode 0.25). Erythromycin resistant strains were also resistant to clarithromycin. Enterococci could be divided into two populations, one resistant (MIC greater than 128 micrograms/ml) and the other with MIC of 0.06 to 2 (mode 0.25). This was also the case for Streptococci and Pneumococci with MIC lower for susceptible strains (mode 0.03 to 0.06). Clarithromycin was active on Haemophilus at concentrations of 4 to 64 micrograms/ml (mode 16); MICs for beta-lactamase producing strains were comparable to those of strains not producing. MICs for Neisseria were 0.12 to 16 and for B. catarrhalis 0.016 to 0.5. MIC were 0.5 and 1 (mode 1) for Clostridium perfringens; Bacteroides fragilis strains were inhibited by 0.12 to 8 micrograms/ml (mode 0.5-1). So, antibacterial activity of C was similar to that of E; it was sometimes slightly superior, particularly on Gram positive cocci. For MIC breakpoints of 1 and 4 micrograms/ml, zone size breakpoints should be 23 and 17 mm and for 2 and 8 micrograms/ml, 20 and 15 mm.

Antibacterial and plasmid curing activity of lomefloxacin in vitro.

The in vitro activity of lomefloxacin in comparison to other recently developed quinolones was evaluated by determination of MICs for 89 test strains. Organisms tested included clinical isolates of gram-positive and gram-negative bacteria susceptible or resistant to quinolones, resistant mutants of Enterobacteriaceae, Pseudomonas aeruginosa, Staphylococcus aureus and Enterococcus faecalis obtained in vitro, and the wild type strain Escherichia coli K12 with its mutants na1A, nalB, nalC and nalB. The activity of lomefloxacin was similar to that of pefloxacin against gram-positive cocci and similar to that of norfloxacin against gram-negative bacteria. There was cross-resistance to all quinolones tested in pefloxacin resistant clinical isolates and in laboratory mutants. The activity of lomefloxacin was decreased against the Escherichia coli K12 mutants nalA and nalD but not nalB, whereas the nalC mutant showed increased susceptibility. Susceptible and mutant strains (n = 115) were used to establish the least-squares lines of regression with 5-micrograms and 10-micrograms lomefloxacin disks. Tests of the in vitro plasmid curing activity of lomefloxacin compared to other agents showed no statistically significant plasmid loss after treatment with lomefloxacin.

[In vitro antibacterial activity of a new macrolide, miokamycin. Results of a multicenter study]. / Activité antibactérienne in vitro d'un nouveau macrolide, la miokamycine. Résultats d'une étude multicentrique.

Minimal inhibitory concentration (MIC) of miokamycin (M) were evaluated by agar dilution for 1,024 bacterial strains isolated in 6 hospitals and classed as a function of susceptibility and resistance to macrolides, lincosamides, streptogramins group (MLS). MIC of M ranged from 0.25 to 4 micrograms/ml (mode MIC 1-2) on Staphylococcus susceptible to MLS and on MLSB inducible strains; M was inactive on MLSB constitutive strains. MIC of M ranged from 0.016 to 4 micrograms/ml (mode MIC 0.12 to 0.5) for Streptococci and Pneumococci susceptible to erythromycin (E) and from 0.12 to greater than 128 for strains resistant to E. Enterococci susceptible to E were inhibited by 0.5 to 2 micrograms/ml (mode MIC 1) and strains resistant to E by 4 to greater than 128. Haemophilus were inhibited by 2 to 64 micrograms/ml (mode MIC 32), Neisseria by 0.12 to 4 (mode MIC 0.5-1) and B. catarrhalis by 0.12 to 8 (mode MIC 1). L. pneumophila was very susceptible to M: MIC 0.016 to 0.12 (mode MIC 0.06). MIC of M ranged generally from 0.5 to 2 micrograms/ml (mode MIC 1) for C. perfringens and from 0.03 to 2 (mode MIC 1) for B. fragilis. Thus, M was shown to be among macrolide antibiotics of resistance non-inducing type on MLSB inducible resistance strains. Its activity was similar to that of spiramycin slightly superior on Staphylococci, slightly inferior on Streptococci and Enterococci, similar on Pneumococci, very superior on Neisseria, Legionella and anaerobes. M had a good activity on Branhamella and, as others macrolides, was poorly active on Haemophilus.

Transferable vancomycin and teicoplanin resistance in Enterococcus faecium.

Enterococcus faecium BM4165 and BM4178, isolated from immunocompromised patients, one treated with vancomycin, were inducibly resistant to high levels of the glycopeptide antibiotics vancomycin and teicoplanin but susceptible to the new lipopeptide daptomycin (LY146032). Strain BM4165 was also resistant to macrolidelincosamide-streptogramin B-type (MLS) antibiotics. The genes conferring resistance to glycopeptides and to MLS antibiotics in strain BM4165 were carried on plasmids pIP819 and pIP821, respectively; pIP819 also carried genes that encoded resistance to MLS antibiotics. The two plasmids, which were distinct although related, were self-transferable to other E. faecium strains. Plasmid pIP819 could also conjugate to E. faecalis, Streptococcus sanguis, S. pyogenes, S. lactis, and Listeria monocytogenes, in which it conferred inducible glycopeptide resistance, but not to S. aureus. Glycopeptide-inactivating activity was not detected, and the biochemical mechanism of resistance remains unknown. Based on this first report of transferable resistance to glycopeptides, we anticipate dissemination of resistance to these antibiotics in gram-positive cocci and bacilli in which it can be phenotypically expressed.

[Quality control of multicenter evaluation studies of the in vitro activity of antibiotics]. / Contrôle de qualité des études multicentriques d'évaluation de l'activité in vitro des antibiotiques.

The estimation of the in vitro activity of an antibiotic, by different laboratories, requires the measurement, in standardized conditions, of the inhibition zone diameters versus a series of strains distributed to these laboratories (kits). Using the studies realized with two antibiotics, denoted by A and B, we observed an important variability between the different laboratories for a given strain and a less but still significant variability within the laboratories. Variance analysis revealed a significant interaction between strains and experimental laboratories. These results prevent the establishment of a standard diameter for a given strain but permit the quality control of the measurements and the improvement of the experimental design for future studies.

[A study by the National Reference Center for Antibiotics on inocula for antibiotic sensitivity testing]. / Etude du Centre National de Référence des Antibiotiques sur l'inoculum de l'antibiogramme.

We compared the diameters of inhibition zones obtained during antibiotic sensitivity testing using two different techniques for preparing and seeding the inoculum, i.e. photometric adjustment followed by flooding, and turbidity adjustment followed by swab streaking. There was no significant difference between the results recorded following photometry-flooding of a light inoculum (2 to 3 X 10(6) CFU/ml) and following swab seeding of a bacterial suspension with a turbidity equal to 0.5 Mac Farland unit. These results indicate that both methods tested answer the NCCLS performance standards for disc antibiotic sensitivity testing and the critical values of the S.F.M. Antibiotic Sensitivity Testing Committee.

[Effect of ceftazidime on enterobacteria and Pseudomonas producers of beta-lactamases]. / Activité de la ceftazidime sur des entérobactéries et des Pseudomonas producteurs de beta-lactamases.

The activity of cephalotin, cefoxitin, cefamandole, cefoperazone, cefotaxime, latamoxef, thienamycin, azthreonam, cefsulodine and ceftazidime against beta-lactamase producing strains of Enterobacteriaceae and Pseudomonas was compared by determination of 99% inhibitory concentrations. The isogenic strains studied differed by a single genetic event: mutation, gene amplification, acquisition of a high or low copy-number plasmid or of a transposon and were representative of the major known mechanisms of resistance toward beta-lactams. The results obtained indicate an overall excellent activity of ceftazidime, in particular against Pseudomonas.