Surveillance of Pseudomonas aeruginosa sensitivity to antibiotics in France and distribution of beta-lactam resistance mechanisms: 1998 GERPB study

In a prospective study carried out during a three-week period in October 1998 in 13 teaching hospitals, 735 non-repetitive isolates of Pseudomonas aeruginosa were collected. In patients presenting cystic fibrosis (70 strains), the main serotypes isolated were O:6 (14.3%) and O:1 (14.3%). Serotypes O:11 and O:12 were exceptional. In other patients (665 strains), the most frequent serotypes were O:6 (15.9%), O:11 (15.6%), O:1 (10.7%) and O:12 (9.2%). The antibiotic susceptibility rates were as follows (respectively, non-cystic fibrosis and cystic fibrosis strains): ticarcillin, 55 and 59%, piperacillin, 71 and 67%, ceftazidime, 75 and 67%, cefepime, 56 and 43%, cefpirome, 37 and 21%, aztreonam, 57 and 56%, imipenem, 83 and 70%, amikacin, 69 and 33%, ciprofloxacin, 56 and 61% and fosfomycin, 33 and 43%. Serotype O:12 was the least susceptible to antibiotics. Forty-five percent of the non-cystic fibrosis strains presented intermediate susceptibility or resistance to ticarcillin. The most frequent mechanisms of resistance were: non-enzymatic resistance (14.3%), overproduction of the constitutive cephalosporinase (13.8%), production of transferable beta-lactamase (8.6%) and a combination of these mechanisms (4.2%). Among cystic fibrosis strains, resistance to beta-lactam antibiotics was mainly due to overproduction of the constitutive cephalosporinase (18.6%), whereas production of a transferable beta-lactamase was rare (1.4%). Susceptibility to aminoglycosides and fluoroquinolones was less frequent in isolates producing transferable beta-lactamases and/or overproducing cephalosporinase. Decreased susceptibility to imipenem was more frequent in strains presenting a high level of cephalosporinase production. Among the cephalosporins, cefepime was the least affected by the overproduction of constitutive cephalosporinase. Ceftazidime remained the most efficient antibiotic against both susceptible isolates and strains presenting a non-enzymatic or PSE-1 penicillinase-producing mechanism.     

Survey of the antibiotic sensitivity of Pseudomonas aeruginosa in France and the distribution of beta-lactam resistance mechanisms: the GERPB 1999 study

A prospective survey was carried out in october 1999 in 15 french teaching hospitals. Average susceptibility rates, determined by minimal inhibitory concentrations, for the 738 non-repetitive strains of P. aeruginosa isolated were: ticarcillin, 58%, ticarcillin + clavulanic acid, 56%, piperacillin, 73%, piperacillin + tazobactam, 82%, ceftazidime, 76%, cefepime, 53%, cefpirome, 36%, aztreonam, 58%, imipenem, 81%, amikacin, 62%, tobramycine, 71% and, ciprofloxacin, 60%. Among the 75% serotypable strains, the most frequent serotypes were: O:6 (15.3%), O:11 (14.5%), O:1 (10.4%), O:3 (7.9%), O:4 (6.1%) and O:12 (6.1%). The serotype O:12 was the most resistant to antibiotics. Forty-two percent of the strains were resistant or presented an intermediate susceptibility to ticarcillin. Mechanisms were as follow: 14.5% non enzymatic mechanism, 12.5% overproduction of the constitutive cephalosporinase, 7.1% transferable betalactamase and, 6.9% combination of these mechanisms. Among the 67 transferable betalactamases: 48 (71.6%) were PSE-1, 12 (19.4%) TEM-2 and 6 (7.5%) oxacillinases. One extended spectrum betalactamase was characterized. Among the cephalosporines tested, cefepime was less affected by the overproduction of constitutive cephalosporinase. Ceftazidime, remained the best cephalosporin except against the strains overexpressing the chromosomal type 1 beta-lactamase. Resistance to tobramycin was mainly due to enzymatic mechanisms with a high level of resistance. Decreased susceptibility was more frequent for amikacin than for tobramycin. This was probably related with non enzymatic mechanisms.     

Changes in resistance of Pseudomonas aeruginosa to beta-lactams in a general intensive care unit over a three-year period. Role of piperacillin

Nosocomial infections by Pseudomonas aeruginosa seen in a general intensive care unit from January 1987 through December 1989 were studied. Use of piperacillin, ticarcillin, cefsulodine, ceftazidime, and imipenem over the same period were recorded. Rate of infection by P. aeruginosa among the 1,844 patients admitted during the study period was 3.2%; 32% of all nosocomial infections during this period were due to P. aeruginosa. The proportion of P. aeruginosa strains exhibiting in vitro susceptibility to ticarcillin rose from 45.5% in 1987 to 59% in 1988 and 86% in 1989. Concomitantly, the proportion of P. aeruginosa strains simultaneously resistant to ticarcillin, piperacillin, cefsulodine and ceftazidime fell from 32% to 18.5% then 0%. A statistically significant correlation was found between the decrease in piperacillin use and the fall in penicillinase-producing ticarcillin-resistant strains of P. aeruginosa. Because piperacillin has undesirable effects on the intestinal flora and promotes the emergence of resistant strains of P. aeruginosa, the authors now use narrow spectrum antimicrobial agents as first line treatment of nocosomial infections.     

Comparative antibacterial activity of a new monobactam, carumonam (RO 17-2301, AMA 1080) on hospital bacteria resistant to beta lactams

In vitro activity of a new monobactam, carumonam (RO 17-2301, AMA 1080) was tested against 370 hospital bacterial isolates. Results were compared to aztreonam, cefotaxime, cefmenoxime, latamoxef, ceftazidime, ceftriaxone, pefloxacin against Enterobacteriaceae, to aztreonam, piperacillin, cefoperazone, cefsulodin, ceftazidime, imipenem and pefloxacin against P. aeruginosa. All Enterobacteriaceae strains produced cephalosporinases and all P. aeruginosa strains were ticarcillin resistant. MIC 90% of carumonam against Enterobacteriaceae strains was lower than 0.25 mg/l for P. mirabilis, P. vulgaris, P. stuartii, Salmonella sp., ranged from 0.25 to 0.5 mg/l for Klebsiella sp. and S. marcescens, from 1 to 2 mg/l for E. coli and P. morganii, and from 4 to 8 mg/l for C. freundii and E. cloacae. The rate of strains inhibited with 4 mg/l of carumonam was 95.3%. So carumonam was at the second place from eight tested products, after latamoxef (97.5% of susceptible strains). Carumonam was active against second generation cephalosporins resistant strains when these strains were susceptible or intermediate to cefotaxime. Strains resistant to this compound escaped to its action. Its activity against A. calcoaceticus was weak (22.6% of strains inhibited by 4 mg/l), but was superior to that of cefsulodin against ticarcillin resistant P. aeruginosa strains (54.5 versus 16.1% of susceptible strains). However carumonam was less active against this last species than ceftazidime or imipenem (92.6 and 91% of susceptible strains respectively).     

Pseudomonas aeruginosa: acquired in vitro resistance to beta-lactams

The development of resistance acquired in vitro to 5 semi-synthetic penicillins: carbenicillin, ticarcillin, azlocillin, mezlocillin, piperacillin and to 5 cephalosporins: cefotaxime, cefoperazone, moxalactam, cefsulodin and ceftazidime, was compared in 6 strains of Pseudomonas aeruginosa. The strains were selected on the basis of their phenotypic resistance: 3 were susceptible to all the betalactam antibiotics tested, 1 was resistant to carbenicillin and ticarcillin but remained susceptible to the others, 2 were susceptible to cefsulodin and ceftazidime but resistant to the others. The development of resistance was investigated by subsequent passages in liquid medium: up to 15 passages or up to an MIC of 4 096 mg/l for a penicillin or 512 mg/l for the cephalosporins. Irrespectively of the phenotypic resistance, for all cephalosorins the MIC became greater than or equal to 64 mg/l and very often greater than or equal to 512 mg/l after 1 to 3 passages. For the penicillin susceptible strains very high MICs were obtained more rapidly with azlocillin and piperacillin (1-2 passages) than with carbenicillin or ticarcillin (5-9 passages). These results are not in favour of a monotherapy with betalactam antibiotics, especially cephalosporins, in the treatment of Pseudomonas aeruginosa infections, but suggest the preferential use of carbenicillin and especially ticarcillin for sensitive isolates.     

Which betalactam antibiotic use as a marker of multiresistance in Pseudomonas aeruginosa?

The determination of an indicating antibiotic for multiresistance, as methicillin in staphylococci, can be useful for Pseudomonas aeruginosa. Until now, the majority of the hygienists used ticarcillin, ceftazidim or imipenem in their investigations as markers of multiresistance for this species. Piperacillin has never been proposed for this purpose. To evaluate this choice, 2098 non-repetitive P. aeruginosa strains collected from 15 teaching hospitals in 1997-1999 were analysed, for eight antibiotics (ticarcillin, piperacillin, ceftazidim, imipenem, tobramycin, amikacin, ciprofloxacin, fosfomycin) according (i) to the results of the minimal inhibiting concentrations obtained by dilution in Mueller-Hinton agar, (ii) to their susceptibility following the criteria of Comité de l'antibiogramme de la Société Fran?aise de Microbiologie and (iii) to the determination of the mechanisms of resistance to the beta-lactam antibiotics. The low rates of sensitivity to the beta-lactam antibiotics, aminoglycosides, ciprofloxacin and fosfomycin were more frequent for piperacillin-resistant strains than for ceftazidim-resistant ones. Resistance to the other beta-lactam antibiotics are poor markers of multiresistance. In the light of the presented data, piperacillin seems to be, among the beta-lactam antibiotics, the best candidate as a marker of multiresistance for P. aeruginosa, followed by ceftazidim. This multiresistance is mainly found in strains overproducing AmpC cephalosporinase or transferable beta-lactamases. These mechanisms are well detected by resistance to piperacillin.     

Sensitivity of Pseudomonas aeruginosa to beta-lactam antibiotics. Apropos of 338 strains isolated at the Regional Hospital Center at Nantes in 1984

The MIC of 338 Pseudomonas aeruginosa strains isolated in 1984, in a French hospital, was determined by an agar dilution method, using seven beta-lactam antibiotics: ticarcillin, azlocillin, piperacillin, cefoperazone, ceftriaxone, cefsulodin and ceftazidime. The MIC50-MIC90 were respectively: 32-64, 8-32, 8-16, 8-16, 16-64, 4-16, 2-4 mg/l. Ticarcillin was the most frequently effective compound (95% of the strains were susceptible), 90% of the strains were susceptible to ceftazidime or piperacillin, 87% to azlocillin and 84% to cefsulodin. Cefoperazone and ceftriaxone were much less effective (43% and 19% of the strains, respectively). The study of the resistance patterns showed a higher percentage (80%) of strains susceptible to all the penicillins than the percentage of strains susceptible to cephalosporins, most of them however were susceptible to both cefsulodin and ceftazidime. It also showed the relatively low frequency of resistant strains by inducible cephalosporinase or decreased permeability. Serovar 0.12 was characterized by its multi-resistance to beta-lactam antibiotics.     

Diversity of β-lactamases in Pseudomonas aeruginosa isolates producing metallo-β-lactamase in two Tunisian hospitals

This study was conducted to identify the β-lactamase content of 30 metallo-β-lactamase-producing Pseudomonas aeruginosa isolated in 2007 from two Tunisian hospitals and to investigate their genetic relatedness. All these isolates produced VIM-2. bla(PER-1), bla(PSE-1), bla(OXA-2), and bla(OXA-10) were identified in 17, 5, 21, and 1 isolates, respectively. These enzymes were often associated in the same isolate: 26 isolates had at least two β-lactamases. The predominant serotype was O12. Pulsed-field gel electrophoresis revealed genetic diversity among the metallo-β-lactamase-producing P. aeruginosa isolates. This is the first report on the existence of bla(PER-1), bla(PSE-1), bla(OXA-2), and bla(OXA-10) in Tunisia.     

Evaluation of the VITEK 2 system for the identification and susceptibility testing of three species of nonfermenting gram-negative rods frequently isolated from clinical samples

VITEK 2 is a new automatic system for the identification and susceptibility testing of the most clinically important bacteria. In the present study 198 clinical isolates, including Pseudomonas aeruginosa (n = 146), Acinetobacter baumannii (n = 25), and Stenotrophomonas maltophilia (n = 27) were evaluated. Reference susceptibility testing of cefepime, cefotaxime, ceftazidime, ciprofloxacin, gentamicin, imipenem, meropenem, piperacillin, tobramycin, levofloxacin (only for P. aeruginosa), co-trimoxazole (only for S. maltophilia), and ampicillin-sulbactam and tetracycline (only for A. baumannii) was performed by microdilution (NCCLS guidelines). The VITEK 2 system correctly identified 91.6, 100, and 76% of P. aeruginosa, S. maltophilia, and A. baumannii isolates, respectively, within 3 h. The respective percentages of essential agreement (to within 1 twofold dilution) for P. aeruginosa and A. baumannii were 89.0 and 88.0% (cefepime), 91.1 and 100% (cefotaxime), 95.2 and 96.0% (ceftazidime), 98.6 and 100% (ciprofloxacin), 88.4 and 100% (gentamicin), 87.0 and 92.0% (imipenem), 85.0 and 88.0% (meropenem), 84.2 and 96.0% (piperacillin), and 97.3 and 80% (tobramycin). The essential agreement for levofloxacin against P. aeruginosa was 86.3%. The percentages of essential agreement for ampicillin-sulbactam and tetracycline against A. baumannii were 88.0 and 100%, respectively. Very major errors for P. aeruginosa (resistant by the reference method, susceptible with the VITEK 2 system [resistant to susceptible]) were noted for cefepime (0.7%), cefotaxime (0.7%), gentamicin (0.7%), imipenem (1.4%), levofloxacin (2.7%), and piperacillin (2.7%) and, for one strain of A. baumannii, for imipenem. Major errors (susceptible to resistant) were noted only for P. aeruginosa and cefepime (2.0%), ceftazidime (0.7%), and piperacillin (3.4%). Minor errors ranged from 0.0% for piperacillin to 22.6% for cefotaxime against P. aeruginosa and from 0.0% for piperacillin and ciprofloxacin to 20.0% for cefepime against A. baumannii. The VITEK 2 system provided co-trimoxazole MICs only for S. maltophilia; no very major or major errors were obtained for co-trimoxazole against this species. It is concluded that the VITEK 2 system allows the rapid identification of S. maltophilia and most P. aeruginosa and A. baumannii isolates. The VITEK 2 system can perform reliable susceptibility testing of many of the antimicrobial agents used against P. aeruginosa and A. baumannii. It would be desirable if new versions of the VITEK 2 software were able to determine MICs and the corresponding clinical categories of agents active against S. maltophilia.     

Epidemic Pseudomonas aeruginosa serotype O16 bacteremia in hematology-oncology patients.

From 1 August 1978 through 31 December 1982, 98 hematology-oncology patients had positive cultures for Pseudomonas aeruginosa serotype O16; 22 of these patients developed bacteremia, and this bacteremia was associated with the occurrence of extensive perineal cellulitis in 10 patients (45.5%). Seventeen bacteremic patients died. The epidemic strain differed from other P. aeruginosa organisms isolated at the hospital by its resistance to all antibiotics available at that time (ticarcillin, piperacillin, azlocillin, tobramycin, ceftizoxime, ceftriaxone, moxalactam, ceftazidime, and fosfomycin). Univariate analysis showed the following factors to be significantly associated with P. aeruginosa O16 bacteremia: the severity of granulocytopenia at the time of the bacteremia, more days with fever, the administration of ticarcillin or an aminoglycoside, the receipt of a greater number of antimicrobial agents for a longer period of time before documentation of the bacteremia, and the occurrence of cellulitis. Logistic regression analysis showed that duration of fever, duration of bacteremia, and the number of antimicrobial agents administered before documentation of the bacteremia were the best predictors of P. aeruginosa O16 bacteremia. In a prospective study of the acquisition of P. aeruginosa by hematology-oncology patients, 1,149 specimens (throat and rectal swabs) from 270 patients and 201 specimens from their washbasin drains were collected. On only three occasions was the epidemic strain isolated from both the patient and his or her washbasin, but in each case the colonization of the patient preceded the isolation of the strain from the washbasin. The transmission of any P. aeruginosa organism from washbasin drain to patient could not be documented. Contact isolation precautions from the Centers for Disease Control were used for all hematology-oncology patients colonized or infected with P. aeruginosa after 7 January 1983. No case of P. aeruginosa O16 bacteremia has occurred at Hotel Dieu since July 1984.     

In vitro activity of tazobactam and piperacillin combination against 224 strains of Pseudomonas aeruginosa according to the production of beta-lactamase]

Piperacillin (PIP) alone and combined with 4 mg/l, 8 mg/l of tazobactam (TAZ) were tested by MIC determination on Mueller-Hinton agar against 224 clinical strains of P. aeruginosa: "wild type" (BLA-), 32 producing a constitutive cephalosporinase (CEP), 41 producing the PSE-1 type beta-lactamase, 7 PSE-2, 8 PSE-3, 9 PSE-4, 13 TEM-1, 24 TEM-2, 13 OXA-1, 22 OXA-2, 5 OXA-3. The combination with 8 mg/l was more effective than that one with 4 mg/l. Combinations of PIP-TAZ 8 mg/l reduced the MICs of PIP for the resistant strains (MICs greater than 64 mg/l) to the susceptible ot the moderately susceptible range (MICs less than or equal to 64 mg/l) for 31% of the CEP producing strains, 63% of the PSE-1, 15% of the PSE-2, none of the PSE-3, 34% of the PSE-4, 39% of the TEM-1, 30% of the TEM-2, 23% of the OXA-1, 14% of the OXA-2, 27% of the OXA-3, TAZ is the first beta-lactamase inhibitor effective against the constitutive cephalosporinase of P. aeruginosa; it is also very effective against the most frequently found PSE-1 beta-lactamase in P. aeruginosa.     

Sensitivity of Pseudomonas aeruginosa to beta-lactam antibiotics and effects of beta-lactamases

The activities of carbenicillin, ticarcillin, piperacillin, cefsulodin, ceftriaxone, azlocillin, ceftazidime and apalcillin were evaluated against 128 hospital isolates of Pseudomonas aeruginosa. Against the 85 isolates that were susceptible to carbenicillin, apalcillin had the best minimal inhibitory concentrations, the median MIC being 1, 1 microgram/ml. Against the 43 isolates resistant to carbenicillin, ceftazidime inhibited 90% of organisms at a concentration of 16 micrograms/ml. A constitutive beta-lactamase, was found in 27 of the 43 resistant isolates. All the 128 isolates, but one, were producers of an inducers of an inducible beta-lactamase. Ceftriaxone, piperacillin and azlocillin were highly antagonized by cefoxitin. The extent of antagonism was lower with ticarcillin and carbenicillin.     

PSE-4 beta lactamase: a serotype-specific enzyme in Pseudomonas aeruginosa

PSE-4 enzyme is the most common plasmidic beta lactamase in Pseudomonas aeruginosa but its production is invariably non-transferable by conjugation. Of 20 PSE-4+ isolates from 10 separate sources, 16 were serotype O:16 and two belonged to the related O:2(b) serotype. One of the two remaining organisms was not O-typable and the other was agglutinated by several unrelated antisera. Examination of additional O:16 strains confirmed the unusual frequency of PSE-4 enzyme in this serotype. None of the PSE-4+ strains was able to transfer carbenicillin resistance in mating experiments and none contained extrachromosomal DNA. Two explanations of the relationship between enzyme production and O antigenicity are proposed. PSE-4 production may be transmissible, perhaps by transduction, between strains of O:16 or related serotypes, or PSE-4+ P. aeruginosa may represent a disseminated subtype. A third hypothesis, that the PSE-4 coding element carried serotype determinants, was discounted. PSE-4+ and PSE-4- P. aeruginosa strains of O:16 and related serotypes were found to represent a definite cluster by their phage-susceptibility pattern and pyocin type (type 1). The only characters linked to PSE-4 production were resistance to spectinomycin, streptomycin and sulphonamide and the genes responsible for these characters seemed to occur on the PSE-4 coding element.     

Risk factors for antimicrobial resistance and influence of resistance on mortality in patients with bloodstream infection caused by Pseudomonas aeruginosa

This study was conducted to evaluate risk factors for antimicrobial resistance and influence of resistance on mortality in Pseudomonas aeruginosa bacteremia. Data on 190 patients with P. aeruginosa bacteremia were analyzed retrospectively. Antimicrobial resistance to antipseudomonal antibiotics was evaluated. The main outcome measure was 30-day mortality. In P. aeruginosa bacteremia, resistance rates to piperacillin (PIP), ceftazidime (CAZ), ciprofloxacin (CIP), and imipenem (IPM) were 29 (56/190), 19 (36/190), 17 (32/190) and 15% (28/190), respectively. Prior uses of fluoroquinolones or carbapenems were independent risk factors for resistance to CIP and IPM, and prior use of extended-spectrum cephalosporins was a risk factor for PIP-R. An indwelling urinary catheter was a risk factor for PIP-R, CAZ-R, and CIP-R. An invasive procedure was a risk factor for CIP-R and IPM-R. The 30-day mortality rate was 44% (33/75) in patients infected by strains resistant to any of the antipseudomonal antibiotics, but 33.9% (39/115) in those by strains susceptible to all antipseudomonal antibiotics (p = 0.161). Among patients with bloodstream infection due to antimicrobial-resistant P. aeruginosa, those infected by IPM-R strains had the highest mortality (IPM-R, 53.6% vs. CAZ-R, 47.2% vs. CIP-R 46.9%, PIP-R, 39.3%). In this study regarding P. aeruginosa bacteremia, prior uses of fluoroquinolones, carbapenems, or extended-spectrum cephalosporins, a prior invasive procedure, and an indwelling urinary catheter were found to be associated with antimicrobial resistance. The patients with bloodstream infection caused by antimicrobial-resistant P. aeruginosa, especially to imipenem, had a tendency toward higher mortality than those infected by susceptible strains.     

Comparative activities of 15 beta-lactam antibiotics against 590 strains of Klebsiella pneumoniae according to the production of beta-lactamase

In October 1988, all non repetitive strains of K. pneumoniae isolated in 17 hospitals have been studied. Among these 590 strains: 451 (76%) only produce the specific beta-lactamase of the species SHV-1 (pI 7,7) or SHV-1 type (pI 7,1), while 74 (12.5%) produce a TEM-1 or TEM-2 type beta-lactamase, and 65 (11%) an extended broad spectrum beta-lactamase: 22 CTX-1, 5 SHV-2, 4 SHV-3, 26 SHV-4, 8 SHV-5. The minimum inhibitory concentrations of the following antibiotics were performed by a liquid micro dilution technic: amoxicillin (AMX), amoxicillin + clavulanic acid (CL), 5 mg/l, ticarcillin (TIC), piperacillin (PIP), cefazolin (CEZ), cefamandole (CFM), cefoperazone (CFP), cefotaxime (CTX), cefotaxime + clavulanic acid 5 mg/l, cefotaxime + sulbactam (SUL) 5 mg/l, cefpirome (CPI), ceftazidime (CAZ), azthreonam (AZT), latamoxef (MOX), cefoxitin (FOX), cefotetan (CTT), temocillin (TMO), imipenem (IMI). The "wild" strains with SHV-1 beta-lactamase are resistant to AMX and have a decreased susceptibility to TIC and PIP, but are susceptible to other antibiotics. The TEM producing strains are more resistant to PIP and TIC, have a decreased susceptibility to CEZ and CFM but are susceptible to other antibiotics. For the extended broad-spectrum beta-lactamase producing strains, the MIC of penicillin antibiotics (AMX, TIC, PIP) are very high and also the MIC of CEZ, CFM and CFP. The MIC of CTX are higher for CTX-1 or SHV-4 producing strains, than for SHV-2, SHV-3, or SHV-5 producing strains. The combination with CL is more efficacious than the one with SUL to reduce the MIC of CTX in susceptibility area.(ABSTRACT TRUNCATED AT 250 WORDS)     

Choice of a rapidly bactericidal beta-lactamin-aminoglycoside combination in the treatment of Pseudomonas aeruginosa infections at a child intensive care unit

Morbidity and mortality among children with Pseudomonas aeruginosa infection in Pediatric Intensive Care Unit remains high. Delays in bacterial killing may be responsible for the poor outcome. Antimicrobial sensitivity and timed-killing assays were determined for ticarcillin, azlocillin, piperacillin, cefsulodin, ceftazidime, gentamicin, tobramycin and amikacin alone and in combination against 40 strains of Pseudomonas aeruginosa isolated from blood cultures and tracheal aspirate. Antibiotic concentrations used were at clinically achievable level. None bactericidal effect was observed with each beta-lactamin alone. However with the combinations azlocillin or piperacillin or cefsulodin or ceftazidime plus amikacin a bactericidal effect was observed at 4.5 hours.     

Risk factors for mortality in patients with Pseudomonas aeruginosa bacteremia: clinical impact of antimicrobial resistance on outcome

Despite the high prevalence of antimicrobial resistance among Pseudomonas aeruginosa bacteremia, the clinical consequence of resistance remains unclear. The purpose of this study was to identify predictors of mortality and evaluate the clinical impact of antimicrobial resistance on outcome in P. aeruginosa bacteremia. A retrospective cohort study including patients with P. aeruginosa bacteremia was performed. The risk factors for antimicrobial resistances were evaluated, and the impact of the respective resistances on mortality was assessed. Of 202 P. aeruginosa bacteremia cases, the resistance rates to ceftazidime, piperacillin, imipenem, fluoroquinolone, and aminoglycoside were 36.6%, 22.3%, 22.8%, 23.8%, and 17.8%, respectively. A prior use of fluoroquinolones and an indwelling urinary catheter were common risk factors for all types of antimicrobial resistance. The overall 30-day mortality rate was 25.2% (51/202), and the risk factors for mortality were corticosteroid use, nosocomial acquisition, polymicrobial infection, an increasing Charlson's weighted co-morbidity index, and intensive care unit care (p?相似文献   

Evaluation of the VITEK 2 cards for identification and antimicrobial susceptibility testing of non‐glucose‐fermenting Gram‐negative bacilli

We evaluated VITEK 2 cards (NGNC and AST‐GN10) for the accuracy of identification (ID) and antimicrobial susceptibility testing (AST) of non‐glucose‐fermenting Gram‐negative bacilli (NGF‐GNB). In a total of 201 strains, 190 strains (94.5%) were correctly identified, seven strains (3.5%) showed low discrimination, four strains (2.0%) had discrepancies, and no strain remained unidentified. Reference AST of amikacin, aztreonam, cefepime, cefotaxime, ceftazidime, ciprofloxacin, imipenem, levofloxacin, piperacillin‐tazobactam, and trimethoprim‐sulfamethoxazole was performed by the agar dilution method. Approximately 82.5% of ID and 72.9% of AST were completed within 7 and 14 h, respectively. For NGF‐GNB, other than Pseudomonas aeruginosa, Acinetobacter spp., Stenotrophomonas maltophilia, and the Burkholderia cepacia group, essential agreements (EAs) were 93.6–100.0%. Severe disagreements (resistant by the reference method to susceptible by AST‐GN10) were observed for amikacin (0.9%), cefepime (1.8%), cefotaxime (1.8%), imipenem (0.9%), and piperacillin‐tazobactam (0.9%). One major disagreement (susceptible to resistant) was observed for ceftazidime (0.1%). For P. aeruginosa, EAs were 85.7–100%, with severe disagreements observed for cefepime (4.8%) and piperacillin‐tazobactam (4.8%). For Acinetobacter spp., EAs were 86.4–100% without disagreements. The VITEK 2 cards appear to be promising for rapid ID and reliable AST for most species of NGF‐GNB.     

Comparative bactericidal activity of imipenem and other antibiotics against Pseudomonas aeruginosa

The bactericidal activity of imipenem (IM), ticarcillin (TIC), ceftazidime (CEZ), amikacin (AMK) or tobramycin (TOB), ciprofloxacin (CIP), was compared on 6 P. aeruginosa: 1 ticarcillin, susceptible strain (TICs), 5 constitutive beta-lactamases producing strains (PSE, TEM, OXA1, OXA2, cephalosporinase (CEP). The time-kill-curves method was performed. Bacteria were incubated with antibiotics at M.I.C. X2 and at concentrations obtained in vivo with usual therapeutic doses: IM 4-8 mg/l, TIC 64-128, CEZ 4-32, TOB 2-8, AMK 4-16, CIP 1-4. The bactericidal activity of IM was independent of the concentration. A 5 Log10 reduction in viability was observed at 3 h for strains TICs, TEM and PSE, 3 Log10 for strains OXA and CEP. This bactericidal activity was also observed in a non growing system. The bactericidal activity of TIC (strain TICs) and CEZ was slower and weaker: 1-2 Log10 at 6 h, 2-3 Log10 at 24 h. It is not observed in a non growing system. On the other hand, the bactericidal activity of aminoglycosides and ciprofloxacin was rapid: 3-4 Log10 at 3 h, 5 Log10 at 6 h for all strains in growing and non growing systems. IM is the only beta-lactam antibiotic bactericidal on growing and non growing cells of P. aeruginosa like aminoglycosides and new quinolones.