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[Meropenem (from foreign publications)].
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[Meningitis caused by Pseudomonas aeruginosa. Treatment with meropenem].
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A rapid high-performance liquid chromatographic assay for cefepime, cefpirome and meropenem.
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[Meropenem in the treatment of severe gynecologic infections].
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[Multiple cerebral abscesses with spontaneous emptying into the ventricles and a good response to meropenem].
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Activity of beta-lactams (ampicillin, meropenem), gentamicin, azithromycin and moxifloxacin against intracellular Listeria monocytogenes in a 24 h THP-1 human macrophage model.
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In vitro comparative activity of meropenem with 15 other antimicrobial agents against 1798 Pseudomonas aeruginosa isolates in a French multicenter study.
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[Antimicrobial activity of carbapenems and the combined effect with aminoglycoside against recent clinical isolates of Pseudomonas aeruginosa].
The carbapenem susceptibility of 32 strains of Pseudomonas aeruginosa recently isolated in Kakogawa municipal hospital was investigated. The MIC ranges of imipenem, panipenem, and meropenem were 0.25-16 mg/L, 0.5-16 mg/L, and < 0.03-4 mg/L, respectively, and meropenem showed the highest antipseudomonal activity among the three carbapenems tested. In the analysis based on the MIC interpretive standards established by NCCLS, the resistance rates of test strains for imipenem, panipenem, and meropenem were 6.3%, 15.6%, and 0%, respectively. We also investigated the in vitro combined effect of imipenem or meropenem with amikacin against another 20 isolates of P. aeruginosa by checkerboard titration assay. Antagonism (minimum FIC index > 2) was not observed in any combinations against all strains tested. Super-additive effects (minimum FIC index < 1) in the combination of imipenem and amikacin were observed in eight (40%) strains tested. In contrast, in the combination of meropenem and amikacin, super-additive effects were observed in 14 isolates (70%). These results suggested that meropenem is superior to imipenem in combined effect with amikacin against P. aeruginosa. In conclusion, meropenem showed higher antipseudomonal activities than other carbapenems tested in both conditions, alone and in combination with amikacin. With regard to the clinical efficacy and prevention of antibiotic resistance, meropenem monotherapy or combination therapy with aminoglycoside is the most superior treatment for pseudomonal infections, and the findings in this study suggest that meropenem is still clinically very useful.
Susceptibility testing of Stenotrophomonas maltophilia to carbapenems.
The susceptibility of 20 clinical isolates of Stenotrophomonas maltophilia to the carbapenems imipenem and meropenem was investigated by various methods. S. maltophilia appeared sensitive to meropenem but resistant to imipenem by disc testing in Iso-sensitest agar. Agar dilution MICs were performed using Iso-sensitest agar and with incubation under three sets of atmospheric conditions. MICs of meropenem were considerably lower than those of imipenem; this effect was maximal after incubation in 5% CO2 when the MIC of meropenem was approximately 64 times less than that of imipenem. Induction experiments showed that both carbapenems could induce production of the L1 carbapenemase. However, disc approximation tests showed that imipenem could induced resistance to meropenem. Partially stably derepressed mutants were readily selected in vitro. We conclude that, although S. maltophilia may give large zones of inhibition to meropenem on disc testing, resistant mutants are readily selected and therefore standard sensitivity tests may be poorly predictive of clinical outcome of treatment of S. maltophilia infections with meropenem.
Activity of cefepime and carbapenems in experimental pneumonia caused by porin-deficient Klebsiella pneumoniae producing FOX-5 beta-lactamase.
The in-vivo activities of cefepime, imipenem and meropenem against the porin-deficient strain Klebsiella pneumoniae C2 and its derivative K. pneumoniae C2(pMG252) coding for the AmpC-type beta-lactamase FOX-5 were determined. Bactericidal activities were determined with the kill-curve method. A pneumonia model in guinea-pigs was developed, and Cmax, t(1/2) and DeltaT/MIC were calculated for the three agents tested. Animals were treated for 72 h with sterile saline (control group) or with cefepime, imipenem or meropenem (240 mg/kg/day, intramuscularly, three times daily). Bacterial counts in lungs (log10 CFU/g tissue) were determined by serial dilution. MICs (mg/L) of cefepime, imipenem and meropenem against K. pneumoniae C2/K. pneumoniae C2(pMG252), determined by macrodilution, were: 0.5/4, 0.5/0.5 and 0.25/0.5, respectively. Bacterial counts in the lungs of animals infected with K. pneumoniae C2 and treated with antimicrobial agents were always lower than in the control group (cefepime, 4.4 +/- 0.5; imipenem, 4.6 +/- 0.4; meropenem, 4.7 +/- 0.5; control group, 5.6 +/- 0.8; p <0.01). No significant differences were observed among the groups receiving therapy (p >0.05). Bacterial lung clearance was higher in treated animals than in control animals following infection with K. pneumoniae C2(pMG252) (cefepime, 4.5 +/- 0.4; imipenem, 4.0 +/- 0.3; meropenem, 4.6 +/- 0.4; control group, 6.1 +/- 0.6; p <0.01), with imipenem producing better clearance than either cefepime or meropenem (p <0.05). Thus, in the guinea-pig pneumonia model, cefepime, imipenem and meropenem were each effective against the porin-deficient K. pneumoniae strain C2 and its derivative expressing the plasmid-mediated AmpC type beta-lactamase FOX-5.
Structure-activity relationships of carbapenems that determine their dependence on porin protein D2 for activity against Pseudomonas aeruginosa.
A number of carbapenem derivatives were examined to determine the structure-activity relationships required for dependence on porin protein D2 for activity against Pseudomonas aeruginosa. As suggested by J. Trias and H. Nikaido (Antimicrob. Agents Chemother. 34:52-57, 1990), carbapenem derivatives, such as imipenem and meropenem, containing a sole basic group at position 2 of the molecule utilize the D2 channel for permeation through the outer membrane of pseudomonads; they are more active against D2-sufficient strains of P. aeruginosa. Our results indicated that carbapenems with a basic group at position 1 or 6 of the molecule did not depend on the D2 channel for activity; i.e. they were equally active against D2-sufficient and D2-deficient pseudomonal strains. However, addition of a basic group at position 1 or 6 of a carbapenem derivative already containing a basic group at position 2 resulted in its lack of dependency on the D2 pathway. Comparison between meropenem and its 1-guanidinoethyl derivative, BMY 45047, indicated that they differed in their dependence on D2; while meropenem required the D2 channel for uptake, BMY 45047 activity was independent of D2. Meropenem and BMY 45047 had similar affinities for the penicillin-binding proteins of P. aeruginosa. However, BMY 45047 and meropenem differed in the morphological changes that they induced in pseudomonal cells. While meropenem induced filamentation, BMY 45047 induced filaments only in BMS-181139-resistant mutants and not in imipenem-resistant mutants or in carbapenem-susceptible P. aeruginosa strains. These results suggested that in Mueller-Hinton medium the uptake of BMY 45047 through the non-D2 pathway is more rapid than that of meropenem through the D2 porin. In summary, the presence of a basic group at position 2 of a carbapenem is important for its preferential uptake by the D2 channel. However the addition of a basic group at position 1 or 6 of a carbapenem already containing a basic group at position 2 dissociates its necessity for porin protein D2 for activity.
[in vitro activity of carbapenems against Enterobacteriaceae and Pseudomonas aeruginosa hyperproducers of group 1 chromosomal beta-lactamases].
Resistance to imipenem and meropenem, reported sporadically in Enterobacteriaceae and more frequently in Pseudomonas aeruginosa, can be caused, among other mechanisms, by the combination of changes in permeability and hyperproduction of inducible chromosomal beta-lactamases. In this study, the in vitro activity of imipenem and meropenem was analysed by the agar dilution method against cefotaxime, ceftazidime, and aztreonam resistant clinical strains of Enterobacteriaceae (n = 202) and P. aeruginosa (n = 90). This phenotype is consistent with the hyperproduction of group 1 chromosomal beta-lactamases and was previously determined in stably derepressed mutants in the same species, obtained from strains with inducible beta-lactamase expression by selection with cefotaxime and ceftazidime. Likewise, the activity of imipenem and meropenem against the same number of clinical isolates susceptible to cefotaxime, ceftazidime, and aztreonam was evaluated. In general, imipenem and meropenem showed an excellent activity, which was intrinsically greater for meropenem against Enterobacteriaceae and P. aeruginosa organisms. Nevertheless, imipenem and meropenem activity was slightly affected on cefotaxime, ceftazidime, and aztreonam resistant isolates of E. cloacae (MIC90, 1 and 0.2 microgram/ml, respectively), E. aerogenes (1 and 0.2 microgram/ml), C. freundii (1 and 0.1 microgram/ml), M. morganii (1 and 0.5 microgram/ml), and S. marcescens (4 and 0.5 micrograms/ml). On the other hand, the activity of imipenem and meropenem against ceftazidime and aztreonam resistant isolates of P. aeruginosa was more significantly affected, with MIC90 values of 64 and 16 micrograms/ml, respectively.
[Anti-anaerobic activity of carbapenems].
The critical concentrations of sensitivity and resistance for meropenem versus anaerobic bacterias were analyzed. It is demonstrated the meropenem is a powerful inhibitor of the microorganisms of the Bacteroides groups (MIC90 < 1 mg/l), Prevotella > Porphyromonas, Fusobacterium, Veillonella, Clostridium perfringens is inhibited at a MIC < 0.06 mg/l. The MIC of meropenem versus C. difficile is 2 mg/l. They are also highly susceptible to the Propionibacterium, Peptostreptococcus and Peptococcus type microorganisms. Meropenem is comparable to imipenem and is more active than piperacillin, metronidazole and clindamycin. The mechanism of action and acquisition of resistance versus meropenem is evaluated and discussed. The percentage of highly resistant strains (MIC > 256 mg/l) isolated in the Hospital Gregorio Marañón in Madrid (Spain) is low (1.2%). The influence of pH on the in vitro activity of the carbapenémicos is also analyzed providing experimental data suggesting that meropenem maintains its bactericide activity more effectively in low pH conditions (5.6). Finally, the authors analyze the literature and the evidence reported regarding the use of meropenem in clinical practice, as a treatment of intraabdominal infections with a clinical response of 91%-100% and bacteriologic efficacy of 84%-95%.
Resistance profile of Bacteroides fragilis isolated in Brazil. Do they shelter the cfiA gene?
The epidemiology of antimicrobial resistance of clinical isolates and human intestinal strains of Bacteroides fragilis has assumed great importance in the last few years since this microorganism, like other members of the B. fragilis group, can be responsible for the spread of resistance determinants. It is possible that the presence of B. fragilis in polluted aquatic environments might contribute to the spread of resistance. The antimicrobial resistance profile of 44 clinical B. fragilis strains isolated from 1981-1988 and 1991-1998 from the University hospital of Rio de Janeiro, and of 17 faecal and 17 polluted aquatic environmental B. fragilis strains isolated between 1991 and 1998 was determined. The susceptibility tests against penicillin, cefoxitin, imipenem, meropenem, clindamycin, chloramphenicol and metronidazole were performed by Etest in Wilkins-Chalgren agar enriched with 5% sheep blood. Motivated by some high MIC values for cefoxitin and meropenem, the cfiA gene, which codes for a metallo-beta-lactamase, was investigated among all strains, using PCR amplification. The resistance to penicillin was high in the samples from 1981 to 1988 (92.9%) and also in those from 1991 to 1998 (100%), although the MIC90 decreased from 256 mg/L to 24 mg/L. An increase in the resistance level to clindamycin and cefoxitin was seen from one decade to the other, the MIC90 values changing from 4 mg/L to 12 mg/L and from 8 mg/L to 32 mg/L, respectively. The susceptibility profile for metronidazole, chloramphenicol, imipenem and meropenem remained stable, although two clinical strains showed MICs of 6 mg/L and 8 mg/L against meropenem. Almost all human intestinal strains were resistant to penicillin and all of them were susceptible to imipenem, meropenem, chloramphenicol and metronidazole. The MICs of meropenem against two strains isolated from a polluted aquatic environment were 6 mg/L and 32 mg/L. The cfiA gene was detected in five strains, two of which were isolated from clinical specimens against which the MIC values of cefoxitin were high and three from an aquatic environment, whose susceptibility to both cefoxitin and meropenem ranged from sensitive to resistant.
Pharmacodynamic modeling of carbapenems and fluoroquinolones against bacteria that produce extended-spectrum beta-lactamases.
BACKGROUND: Bacteria that produce extended-spectrum beta-lactamases (ESBLs) are resistant to penicillins,cephalosporins, and monobactams. The results of clinical studies suggest that the carbapenems imipenem and meropenem may be effective against bacteria that produce ESBLs, although it is not known whether the new once-daily carbapenem ertapenem or the fluoroquinolones are useful against infections caused by ESBL-producing bacteria. OBJECTIVE: The present study compared the simulated pharmacodynamics of the carbapenems imipenem,meropenem, and ertapenem; the simulated pharmacodynamics of the fluoroquinolones levofloxacin, gatifloxacin, and ciprofloxacin with those of the carbapenems; and the simulated pharmacodynamics of levofloxacin 750 mg with those of levofloxacin 500 mg, all against gram-negative isolates that did and did not produce ESBLs METHODS: Pharmacokinetic data were obtained from studies in healthy humans. Minimum inhibitory concentrationsMICs) for bacteria that did and did not produce ESBLs were determined in triplicate using broth-microdilution techniques as recommended by National Committee for Clinical Laboratory Standards guidelines. Monte Carlo simulation was used to construct pharmacodynamic models for imipenem, meropenem, ertapenem, levofloxacin, gatifloxacin, and ciprofloxacin. Pharmacodynamic measures of interest were the probability of the free concentration remaining above the MIC >-40% of the time (T>MIC > or =40%) for carbapenems and the likelihood of achieving a free AUC:MIC ratio > or =125 for fluoroquinolones. RESULTS: MICs were determined for 39 isolates that produced ESBLs and 45 isolates that did not Bacteria that did not produce ESBLs were > or =93% susceptible to all carbapenems and fluoroquinolones tested. Among bacteria that produced ESBLs, rates of susceptibility to the specific agents were as follows: imipenem, 100%; meropenem, 97%; ertapenem, 87%; levofloxacin, 54%; gatifloxacin, 44%; and ciprofloxacin, 36%. In the pharmacodynamic models, imipenem and meropenem had an equal likelihood of achieving a free T>MIC > or =40% against bacteria that produced ESBLs (> or =97%) and bacteria that did not produce ESBLs (> or =98%). In contrast, the likelihood of ertapenem achieving a free T>MIC > or =40% was lower against bacteria that produced ESBLs (78%) than against bacteria that did not produce ESBLs (94%). Similarly, the fluoroquinolones were less likely to achieve a free AUC:MIC ratio > or =125 against bacteria that produced ESBLs (2%-13%) than against bacteria that did not produce ESBLs (85%-91%). CONCLUSIONS: Carbapenems had superior in vitro activity against bacteria that produced ESBLs compared with fluoroquinolones. Pharmacodynamic modeling based on local ESBL-producing isolates and pharmacokinetic data from healthy humans indicated that imipenem and meropenem may have a greater likelihood of achieving pharmacodynamic targets against bacteria that produce ESBLs than ertapenem or fluoroquinolones.