Plasmid-mediated resistance to vancomycin and teicoplanin in Enterococcus faecium.
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Anti-Bacterial Agents↗
Biomedical subjects
J Duval
Publications and source records attributed to J Duval.
5 alpha-DHT metabolism in monolayer cultures of distinct pituitary cell populations.
5 alpha-Dihydrotestosterone (DHT) metabolism into 5 alpha-androstane-3 alpha, 17 beta-diol (alpha-diol) and 5 alpha-androstane-3 beta, 17 beta-diol (beta-diol) was studied in monolayer cultures of distinct cell populations from prepubertal male rats pituitaries. Cells were characterized through immunocytochemistry with the various antihormone antisera. Centrifugal elutriation was used to prepare a gonadotrope-enriched population "G" and a gonadotrope-depleted population "L", containing most lactotropes and somatotropes. Using centrifugation on Percoll gradient, two sub-populations, P1 and P2, were prepared by further fractionation of the "L" population. Cells were incubated for 48 h with [3H]DHT (1 microM, sp. act. 0.9 Ci/mmol) and metabolites extracted from the whole cell and medium. DHT was metabolized to about the same extent (30-40%) in all cell fractions. Compared with unfractionated population, the conversion of DHT into alpha-diol increased significantly in the P1 fraction, consisting of lactotropes, somatotropes and highly depleted in gonadotropes. This increase was lower in the somatotrope-enriched P2 fraction in which the amount of lactotropes was similar to P1 but that of gonadotropes slightly higher. In contrast, the conversion of DHT into alpha-diol decreased significantly in the "G" population compared with total or "L" fractions, whereas androstanedione formation, low in every population, increased significantly. The increase in alpha-diol formation could be related either to the decrease of gonadotropes or to a role of non-immunoreactive cells. As the beta-diol formation was constant in all cell types, the beta-diol/alpha-diol amount increased significantly in gonadotropes. Then, beta-diol and DHT could be both active steroids in gonadotrope regulation inasmuch as specific binding sites were identified for these two steroids. It can be concluded that DHT action at the pituitary level is subject to complex control mechanisms involving a specific balance of its metabolites in each particular cell type.
Animals↗
The gonadotrope polypeptide (GP 87) released from pituitary cells under luteinizing hormone-releasing hormone stimulation is a secretogranin II form.
Cultured gonadotrope cells from 14 day old female rat pituitaries have been shown to release a highly acidic protein when incubated with LHRH: the gonadotrope polypeptide (GP 87). Moreover, a new tyrosine-sulfated acidic protein, secretogranin II (Sg II), clearly distinct from the chromogranin species, was described in the secretory granule matrix of endocrine cells secreting peptide hormones by the regulated pathway. Recently, the release of Sg II from female rat pituitary stimulated by LHRH was demonstrated in vitro. Several physicochemical (Mr; pI) and biological (cellular localization in the pituitary; LHRH-stimulated release) properties are common to Sg II and GP 87. To verify if these 2 polypeptides are similar or distinct components, other physicochemical characteristics (heat-stability, sulfation, phosphorylation) were compared using isotope incorporation followed by either 1- or 2-dimensional polyacrylamide gel electrophoresis and autoradiography. Furthermore, the similarity of GP 87 to Sg II was studied by immunoblotting on nitrocellulose sheets following electrophoresis of intracellular and secreted proteins. Antisera raised against bovine Sg II (extracted from whole pituitaries) and against rat GP 87 (released into the medium of cultured pituitary cells stimulated by LHRH) were used. The overall data presented here suggest that GP 87 is the Sg II form contained in, and released by, gonadotrope cells.
Animals↗
Peptides co-released with luteinizing hormone by perifused pituitary cell aggregates.
The proteins co-released with gonadotropins were analyzed using perifusion of pituitary cell aggregates from 14-day-old female rats, after a pre-labeling period with [35S]methionine. Radioimmunoassays of hormones and electrophoretic analysis were performed on each 4 min effluent. Gonadotropin-releasing hormone (GnRH) pulses increased significantly (P less than 0.01) the release of several proteins (Mr range from 140,000 to 28,000). The main stimulation appeared for -1, a 87 kDa species, previously characterized as gonadotrope polypeptide 87 (GP87) in monolayer cultures and identified as a secretogranin II (SgII) form; -2, a second species of 80 kDa designated as B2. Secretory patterns of radiolabeled GP87 and B2 paralleled the luteinizing hormone (LH) ones. The release of these species was -1, GnRH dose dependent; -2, monophasic for short pulses but complex when the duration of GnRH pulses increased to 16 min, suggesting different pools of GP87 and B2 as for LH; -3, induced by thyrotropin-releasing hormone (TRH). A slight output was also elicited by corticotropin-releasing factor (CRF) and growth hormone-releasing hormone (GHRH), but this release was partly impaired in the presence of a potent anti-GnRH ([Ac-D-(2)-NAL1,pF-D-Phe2,D-Trp3,D-Arg6]-LAF) suggesting a non-specific effect of these two factors. GP87/SgII thus appeared mainly associated with the release of hormonal glycoproteins. In conclusion, perifusion of pituitary cell aggregates allows a precise minute-to-minute kinetic analysis of the various proteins co-released with hormones. The similar timing in output of LH, GP87 and B2 suggests that these three proteins co-exist in the same secretory granules inside gonadotropes.
Animals↗
[In vitro activity of roxithromycin against hospital bacteria and the concordance curve].
This study was set up to establish the regression curve for roxithromycin 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 roxithromycin. 373 bacterial strains were studied in three university hospital. Roxithromycin was active against erythromycin sensitive Staphylococcus aureus and coagulase negative Staphylococci at concentrations of 0.06 to 4 micrograms/ml (mode 0.5). Erythromycin resistant strains were also resistant to roxithromycin. Enterococci could be divided into two populations, one resistant (MIC greater than 128 micrograms/ml) and the other with MIC of 0.5 to 32 (mode 1-2). This was also the case for Streptococci and Pneumococci with MIC lower for susceptible strains (mode 0.06-0.12). Roxithromycin was active on Haemophilus at concentrations of 0.12 to 32 micrograms/ml; MIC for beta-lactamase producing strains were comparable to those of strains not producing. MIC for Gonococci were low (less than 0.008 to 0.12), except for three strains. They were higher for Meningococci (0.03 to 32) with a majority of strains inhibited by 0.5 to 4 micrograms/ml. MIC were 4 for Clostridium perfringens; Bacteroides fragilis strains were inhibited by 0.5 to 2 micrograms/ml. The correlation coefficient for regression curve was 0.79; for critical concentrations less than or equal to 1 and greater than 4 micrograms/ml, critical diameters are greater than or equal to 22 and less than 17 mm.
Anti-Bacterial Agents↗
[In vitro antibacterial activity of a new macrolide: miokamycin. Comparison with erythromycin and josamycin].
Minimal inhibitory concentrations (MIC) of miokamycin (M) were evaluated by agar dilution, comparatively with erythromycin (E) and josamycin (J) for 81 bacterial strains chosen as a function of susceptibility and resistance to Macrolides-Lincosamides-Streptogramins group (MLS). On Gram positive cocci, mode MIC of E, J, and M for strains sensitive to MLS were respectively (micrograms/ml): Staphylococci: 0.25; 1; 2-Streptococci and Pneumococci: 0.016; 0.03-0.12; 0.06-0.25-Enterococci: 0.5; 0.5-1; 1-2. Activity of the three antibiotics was similar against Staphylococci resistant to lincomycin and streptogramin A, those resistant to streptogramins A and B, on Staphylococci and Streptococci only resistant to lincosamides by inactivation. M, as J, was active on coagulase negative (Staphylococci resistant to E by inactivation and on MLBB inducible Staphylococci; on these strains, M is a resistance non-inducible macrolide. Activity of E, J and M was reduced on MLSB inducible Streptococci. The three antibiotics were inactive on Staphylococci Streptococci and Enterococci MLSB resistant constitutive. On Haemophilus, E (2-8 micrograms/ml) was more active than J (2-16) and M (8-32). Thus, M, as J, was shown to be among macrolide antibiotics of resistance non-inducing type on MLSB inducible resistant Staphylococci; its activity was slightly inferior to that of J, but very similar to that of spiramycin, other macrolide of this group.
Bacteria↗
[Activity of 9 beta-lactam antibiotics combined with clavulanic acid or sulbactam against the strains of broad-spectrum beta-lactamase (CTX-1) producing Enterobacteriaceae isolated at the Henri Mondor Hospital].
Minimal inhibitory concentrations (MICs) of seven cephalosporins: cefotaxime (CTX), ceftriaxone (CRO), ceftazidime (CAZ), latamoxef (MOX), cefoxitin (FOX), cefotetan (CTT) and CM 40876 (CM), of aztreonam (ATM) and imipenem (IPM) were evaluated by agar dilution with and without 5 mg/l of clavulanic acid (AC) or sulbactam (SB) for 28 strains isolated in 1986 (15 K. pneumoniae, 3. K. oxytoca, 4 E. coli, 4 E. cloacae, 1 E. aerogenes and 1 C. freundii). Comparatively to MICs of sensitive strains and to those of cured variants, MICs of these strains were very increased for CTX, CRO, ATM (mode MIC: 1 mg/l), and CAZ (2); weakly increased for MOX and CTT (0.25), and identical for IMP (0.12-0.25), CM (0.06) and FOX (2-4), except for Enterobacter and Citrobacter (64). Association with AC or SB did not modify MICs of FOX, CM and IMP. For the other antibiotics, MICs were reduced by addition of AC: Klebsiella: 5 log2 for CTX and CRO, 4 for CAZ and ATM, 2 for MOX and CTT; E. coli: 4 log2 for CTX and ATM, 3 for CRO and CAZ, 1 for MOX and CTT; Enterobacter and Citrobacter 2 log2 for CTX, CRO, CAZ and ATM, 1 for MOX and CTT. With SB, decrease of MICs was two to for fold lesser than with AC. AC, and less efficiently SB, restored activity of CTX, CRO, CAZ and ATM on CTX-1 producing Enterobacteriaceae, particularly Klebsiella and E. coli. It was the same for MOX and CTT, weakly affected by this resistance. AC and SB had not effect on FOX, CM and IPM which remained active on these strains.
Anti-Bacterial Agents↗
[Sensitivity to clavulanic acid of Escherichia coli isolated at the Henri Mondor hospital in 1986 according to phenotypes of beta-lactam antibiotic resistance].
Susceptibility to Augmentin (AUG) was studied as a function of resistance phenotypes toward amoxicillin (AMX), carbenicillin (CAR), cephalothin (CFT) and cefotaxime (CTX) for 1817 strains of Escherichia coli isolated at Henri-Mondor hospital during 1986. For strains susceptible to the 4 beta-lactams (phenotype SSSS: 66%), the median zone diameter observed with AUG was 26.4 mm. It was slightly inferior (22.1) for acquired - penicillinase producing strains (phenotype RRSS: 21.5%), but zone diameters were greater than or equal to 21 mm for over than 75% of these strains. Strains of phenotype RRIS (6%), probably high penicillinase-producers, were generally intermediate to AUG (median zone diameter: 17.8), showing partial inhibition of enzyme by clavulanic acid. Cephalosporinase hyperproducers mutants (phenotype RSRS: 4%) and strains with a RRRS phenotype (2.5%), probably penicillinase and cephalosporinase producers, were resistant to AUG (median zone diameters: 15.6 and 12.6 mm). Among rarely observed phenotypes, some were readily integrated to major phenotypes: RSIS, ISRS and ISIS to phenotype RSRS; RIRS to phenotype RRRS; IISS to phenotype RRSS; apparently "aberrants" phenotypes (ISSS, RSSS, SSIS, SSRS) required interpretation of results as a function of observed zone diameters and at time a verification of tests. This study confirms the in vitro activity of AUG on penicillinase producing E. coli; in addition simultaneous reading of zone diameters observed with AMX, CAR, CFT and CTX, permitted to infer the probable mechanism of resistance to beta-lactams and therefore to correct possible discrepancies observed in antibiogram results.
Amoxicillin↗
[In vitro antibacterial activity of apalcillin on aerobic bacteria and the regression curve].
Minimal inhibitory concentrations (MICs) of apalcillin (APL) were evaluated by agar dilution on 1,201 bacterial strains isolated simultaneously in four university hospitals; agar diffusion tests (disks APL: 75 micrograms) were performed on these strains to establish relationship between MIC and zone diameters. For Enterobacteriaceae naturally non beta-lactamase-producing (E. coli and P. mirabilis), mode MIC was 0.5 microgram/ml; some acquired penicillinase-producing strains were only inhibited by concentrations greater than or equal to 16. Chromosomal penicillinase producing Klebsiella were inhibited by 2 to 8 micrograms/ml but APL was inactive on acquired penicillinase-producing strains. For chromosomal cephalosporinase-producing species (Enterobacter, Citrobacter, Serratia, indole + Proteus and Providencia) two populations of strains were observed: one sensitive and the second resistant to carboxypenicillins: on the first population, mode MIC of APL was 1 to 4 micrograms/ml; on the second MIC were generally greater than or equal to 64 micrograms/ml. P. aeruginosa strains sensitive to carboxypenicillins were inhibited by 1 and 2 micrograms/ml; this activity was diminished on strains resistant to these antibiotics (MIC APL 8-32). MIC of Acinetobacter varied to 0.25 to greater than 128 with a majority of strains inhibited by 4 to 64 micrograms/ml. APL was active against non penicillinase producing Staphylococci; mode MIC was 2 micrograms/ml for Enterococci. Correlation coefficient of regression curve was 0.87. For critical concentrations less than or equal to 8 and greater than 64 micrograms/ml, critical diameters could be greater than or equal to 19 and less than 12 mm.
Acinetobacter↗
[In vitro antibacterial activity of piperacillin/quinolone combinations].
Combinations of piperacillin (PIP) with 3 systemic fluoroquinolones: pefloxacin (PEF), ofloxacin (OFL) and ciprofloxacin (CIP) were evaluated by checkerboard technique (bacteriostatic activity) and by time-killing curve technique (bactericidal activity as a function of time) for 4 bacterial strains with following MICs (micrograms/ml): 1 E. coli (PIP: 1, PEF: 0.12, OFL: 0.06, CIP: 0.016); 1 S. marcescens (0.25, 0.06, 0.06, 0.016); 2 P. aeruginosa (2, 1, 0.5, 0.12 and 4, 2, 2, 0.25). Bacteriostatic activity of the 3 combinations showed only different or additive effects (index FIC: 0.62 to 1.5). If the bactericidal activity was defined as a less than or equal to 3 log 10 decrease in CFU/ml in 3-6 h and less than or equal to 4 log 10 in 6-24 h, PIP was not bactericidal at MIC x 8 for all strains; nevertheless, combinations of PIP 2 + PEF 0.25, OFL 0.12 or CIP 0.016 on E. coli and PIP 1 + PEF 0.25, OFL 0.25 or CIP 0.06 on S. marcescens showed bactericidal activity, superior to each antibiotic singly. For P. aeruginosa a less than or equal to 4 log 10 decrease in 6-24 h was observed only in combination with PIP 16 + PEF 1, OFL 1 or CIP 0.25 and PIP 32 + PEF 4, OFL 4 or CIP 0.5. Combinations of PIP with quinolones showed synergistic effects: bactericidal activity was more rapid and prolonged with such combinations at concentrations near MICs and obtained with usual therapeutic doses.
Anti-Bacterial Agents↗
Transferable enzymatic resistance to third-generation cephalosporins during nosocomial outbreak of multiresistant Klebsiella pneumoniae.
Klebsiella pneumoniae strains that were resistant to third-generation cephalosporins and amikacin were recovered from 62 of 395 patients (15.7%) during 1986. 25 isolates (40%) caused urinary tract infections. The outbreak involved three intensive care units (54 isolates), and spread from one unit to another and then to four wards (8 isolates). K pneumoniae of various serotypes and strains of different Enterobacteriaceae demonstrating the same antibiotic resistance pattern were isolated, which suggests dissemination of an R-factor. The isolates had low-level resistance to third-generation cephalosporins (mode minimum inhibitory concentration of cefotaxime, 2 mg/l) but remained sensitive to cephamycins. Cefotaxime was effective in cases of uncomplicated urinary tract infection, but failed in major infections at other sites. 1-5 mg/l of the beta-lactamase inhibitors clavulanic acid or sulbactam restored normal activity to cefotaxime against the multiresistant strains. Resistance to third-generation cephalosporins was mediated by a new broad-spectrum enzyme of isoelectric point 6.3. Resistance to beta-lactams and aminoglycosides was transferable to Escherichia coli. The emergence of transferable enzymatic resistance to newer beta-lactams in K pneumoniae strains indicates a major risk of spread of such resistance to otherwise sensitive strains.
Amikacin↗
Determination of binding parameters of macrolides, lincosamides, and streptogramins to Legionella pneumophila.
Parameters of [3H]erythromycin binding to Legionella pneumophila were determined in vitro using both an equilibrium and a kinetic method. Different L. pneumophila serogroups, 1-3, and a virulent strain serogroup, 1, were tested. All strains of bacteria exhibited the same binding pattern, with a dissociation constant of 0.15 microM. Other macrolides, streptogramin B-types, and lincosamides competitively displaced bound erythromycin suggesting that these compounds share common binding sites on the bacteria. Minimum inhibitory concentration (MIC) values for macrolides, streptogramin B-types, and lincosamides were determined with buffered charcoal yeast extract (BCYE) medium. A good correlation (r = 0.994) was found between the corresponding inhibition constants of these antibiotics and their MIC. It was also noted that for lincosamides the microbiological inactivity was associated with a very low bacterium affinity. Thus, it is concluded that binding parameters of these antibiotics reflect their efficacy against L. pneumophila in vitro and may serve as a useful adjunct in developing new compounds.
Anti-Bacterial Agents↗
Binding parameters and microbiological activity of macrolides, lincosamides and streptogramins against Staphylococcus aureus.
Parameters of erythromycin binding to Staphylococcus aureus were measured in-vitro using an equilibrium method with [3H]erythromycin. The dissociation constant of the complex, erythromycin-S. aureus sensitive strain, was KD = 0.11 microM. The maximal binding, representing the density of binding sites was 14,847 molecules/cell. No binding was detectable on the constitutive resistant strain. Macrolides, streptogramins and lincosamides displaced bound [3H]erythromycin by a competitive process indicating that these compounds share common binding sites on the bacteria, i.e. 50 S ribosomal subunits. A good correlation (r = 0.99) was demonstrated between the corresponding inhibition constants (Ki) and the minimal inhibitory concentration. It is proposed that knowledge of the binding parameters provides a good indication of bacterial susceptibility and may serve as a useful adjunct in developing new compounds.
Anti-Bacterial Agents↗
Phenotypic expression and genetic heterogeneity of lincosamide inactivation in Staphylococcus spp.
We examined the resistance phenotype and the genetic basis of lincosamide modification in 25 clinical isolates of Staphylococcus spp. inactivating lincomycin and clindamycin. The strains were resistant to high levels of lincomycin but remained susceptible to clindamycin. However, MBCs and inoculum effects showed that the activity of clindamycin was impaired. The distribution in these strains of nucleotide sequences related to linA and linA', the genes encoding lincosamide nucleotidylation in Staphylococcus haemolyticus BM4610 and S. aureus BM4611, respectively, was studied by dot blot hybridization. The genes responsible for lincosamide inactivation in Staphylococcus spp. were found to constitute a family of related sequences which are not species specific.
Anti-Bacterial Agents↗
[Natural substances regulating fertility. Effect of plant extracts in the Ivory Coast pharmacopoeia on the release of LH by hypophyseal cells in culture].
The in vitro action of hydro-alcoholic extracts of plants from Ivory Coast pharmacopoeia was analyzed on cultured rat pituitary cells. Cells were treated for 24 hours with various doses of extracts and then stimulated for 4 hours with 10(-8) M LHRH. Extracts from Afrormosia laxiflora, Cola nitida, Pterocarpus erinaceus and Tetrapleura tetraptera inhibit the LHRH-induced release of LH. On the contrary, extract from Combretodendron africanum stimulates the basal release of LH and this increase is added to the LHRH-induced release. Therefore, the natural substances contained in these plants may in vitro exert a regulation of the gonadotropin release.
Animals↗
[Antibacterial activity of enoxacin in vitro and in urine].
Minimal inhibitory concentrations (MIC) of enoxacin (ENO) were evaluated by agar dilution, in comparison with MIC of nalidixic acid (NAL), pipemidic acid (PIP), oxolinic acid (OXO), pefloxacin (PEF), norfloxacin (NOR), ofloxacin (OFL) and ciprofloxacin (CIP), for eleven Enterobacteriaceae reference strains chosen as a function of sensitivity and level of resistance to NAL. In the four strains susceptible to NAL, MIC of ENO (0.06 to 0.25 micrograms/ml) were similar to those for PEF and NOR, 2 to 4 times inferior to those for OXO, 16 to those for PIP and 32 to those for NAL; this ratio of activity was also seen in the majority of strains resistant to NAL. Measurement of MIC of ENO for 397 recent clinical isolates confirmed efficacy of this substance against Enterobacteriaceae and showed its activity against Pseudomonas aeruginosa (mode MIC: 0.5-1 micrograms/ml), and Gram positive cocci, essentially Staphylococcus aureus (mode MIC: 0.5-1). Antibacterial activity in the urine was measured by the Heilman test in 5 male adults after two doses of 200 mg of ENO administered at 12 hours intervals, two doses of 400 mg of ENO and, in comparison two of 400 mg of PIP administered under the same conditions. Maximal inhibitory dilutions obtained with ENO reached (mean for 5 subjects): 1/64 to 1/128 after 200 mg and 1/128 to 1/512 after 400 mg for a sensitive Providencia strain (MIC ENO: 0.25); 1/32 to 1/128 and 1/64 to 1/256 for an E. coli strain of low level of resistance to NAL (MIC ENO: 2); activity was very low on a Serratia strain highly resistant to NAL (MIC ENO: 16).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[In vitro antibacterial activity of 2 new quinolones: A 56619 (difloxacin) and A 56620. Comparison with pefloxacin, ofloxacin and ciprofloxacin].
Minimal inhibitory concentration (MIC) of two new quinolones, A 56619 (difloxacin) and A 56620 were evaluated by agar dilution for 511 bacterial strains, in comparison with pefloxacin (PEF), ofloxacin (OFL) and ciprofloxacin (CIP). For Enterobacteriaceae, A 56620 (MIC 50 and 90 p. 100: 0,12 and 2 micrograms/ml) was less active than CIP (0,03 and 1) and more active than OFL (0,12 and 4) whereas A 56619 (1 and 16) appeared slightly inferior to PEF (0,25 and 8); the same range of activity was observed for Pseudomonas aeruginosa: CIP: 0,12-0,5; A 56620: 0,5-2; OFL and PEF: 1-4; A 56619: 1-8. For the majority of Acinetobacter (mode MIC: 0,5-1), Haemophilus (0,008-0,016), Meningococci (less than or equal to 0,008), Gonococci (0,06 à 0,25) and Legionella (0,12), activity of the two new compounds appeared very similar to those of the three other quinolones. A 56619 and A 56620 had a good activity (mode MIC: 0,25-0,5 micrograms/ml), similar to those of the three other quinolones, on Staphylococci sensitive strains whereas they were inactive on resistant strains. For Streptococci, A 56620 is about two times superior to A 56619; its activity is similar to that of PEF for Enterococci (mode MIC: 4) and to that of CIP on Streptococci A and Pneumococci (mode MIC: 0,5-1). For anaerobes, the two compounds had about the same activity similar to that of OFL and CIP (C. perfringens: 0,25-0,5 and B. fragilis: 4 micrograms/ml).
Anti-Bacterial Agents↗
[In vitro effect of piperacillin on aerobic bacteria. Variations according to the phenotypes of resistance to beta-lactam antibiotics].
In a first study the MICs of piperacillin (PIP), mezlocillin (MEZ), azlocillin (AZL), carbenicillin (CARB) and ticarcillin (TIC) against 563 strains of aerobic bacteria were compared. The MIC50 of PIP against E. coli and P. mirabilis was 0.5 to 1 mg/l, that is equal to those of MEZ and TIC but 2 or 3 times lower than those of AZL and CAR. The MIC50 of PIP and MEZ against Klebsiella, a species that is naturally resistant to TIC and CAR, was 4 mg/l. Enterobacter, Serratia and Citrobacter showed two populations of strains: the first was sensitive to the five penicillins tested (MIC50 of PIP: 1 to 2 mg/l); the second was resistant to all of them. PIP and AZL were more active (MIC50 8 mg/l) against Ps. aeruginosa than MEZ, TIC and CAR. All five penicillins had limited activity against Acinetobacter (MIC50 less than 16 mg/l). PIP, MEZ and AZL were more active than TIC and CAR against enterococci. In a second study, the activity of PIP was evaluated by standard sensitivity tests on 4993 strains of enterobacteria, Ps. aeruginosa and Acinetobacter classified according to their phenotype of resistance to beta-lactam antibiotics. PIP was regularly active against enterobacteria and Ps. aeruginosa strains devoid of acquired resistance. The activity of PIP was significantly reduced against enterobacteria strains with a phenotype suggesting induced penicillinase production. However, the inhibition zone diameters, although reduced, remained within what is now considered the sensitivity range (notably with E. coli and Proteus spp), which raises the problem of in vitro tests interpretation. PIP was active against E. coli strains with a "cephalosporinase" phenotype, but inactive against cefotaxime resistant strains of: Enterobacter, Citrobacter and Serratia. The activity of PIP on CAR-resistant Ps. aeruginosa strains was significantly reduced, but the inhibition zone diameter in one quarter of them was still within limits of sensitivity.
Azlocillin↗