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PubMed1999

Detection and reporting of organisms producing extended-spectrum beta-lactamases: survey of laboratories in Connecticut.

Extended-spectrum beta-lactamases (ESBLs) are enzymes produced in some gram-negative bacilli that mediate resistance to extended-spectrum cephalosporins and aztreonam. They are most common in Klebsiella spp. and Escherichia coli but are present in a variety of Enterobacteriaceae. Resistance mediated by these enzymes can be difficult to detect depending on the antimicrobial agents tested. AmpC beta-lactamases are related to the chromosomal enzymes of Enterobacter and Citrobacter spp. and also mediate resistance to extended-spectrum cephalosporins and aztreonam in addition to cephamycins, such as cefoxitin. Unlike ESBLs, however, AmpC beta-lactamases are not inhibited by clavulanic acid or other similar compounds. To assess the abilities of various antimicrobial susceptibility testing methods to detect ESBLs, we sent three ESBL-producing organisms, one AmpC-producing organism, and a control strain that was susceptible to extended-spectrum cephalosporins to 38 laboratories in Connecticut for testing. Eight (21.0%) of 38 labs failed to detect extended-spectrum cephalosporin or aztreonam resistance in any of the ESBL- or AmpC-producing isolates. Errors were encountered with both automated and disk diffusion methods. Conversely, seven (18.4%) labs categorized at least some of the four resistant isolates as potential ESBL producers and reported the results with the extended-spectrum cephalosporins and aztreonam as resistant as suggested by current National Committee for Clinical Laboratory Standards (NCCLS) guidelines. The percentage of laboratories that failed to detect resistance in the ESBL or AmpC isolates ranged from 23.7 to 31.6% depending on the type of enzyme present in the test organism. This survey suggests that many laboratories have difficulty detecting resistance in ESBL and AmpC-producing organisms and may be unaware of the NCCLS guidelines on modifying susceptibility testing reports for ESBL-producing strains.

Aztreonam↗

PubMed2002

Severe cellulitis/myositis caused by Stenotrophomonas maltophilia.

OBJECTIVE: To present a case of cellulitis/myositis due to Stenotrophomonas maltophilia in the absence of trauma and to discuss a potentially novel treatment option. CASE SUMMARY: A 57-year-old white man, having undergone an allogeneic bone marrow transplant, developed myositis with S. maltophilia of the left soleus muscle; there had been no trauma. Risk factors for infection included neutropenia, prolonged hospitalization and intensive care unit stay, and broad-spectrum antibiotic exposure. The affected area of muscle was resected and the patient successfully treated with trimethoprim/sulfamethoxazole (TMP/SMX), ticarcillin/clavulanate, and aztreonam. DISCUSSION: In severe myositis/cellulitis caused by S. maltophilia, TMP/SMX is considered the drug of choice. However, bacteriostatic agents such as TMP/SMX are less than ideal in neutropenic patients. The combination of ticarcillin/clavulanate plus aztreonam has been shown to improve activity in vitro against this organism compared with TMP/SMX. This is likely due to inhibition of the 2 beta-lactamases this organism produces by clavulanate and aztreonam. In our study of clinical isolates of S. maltophilia, this combination reduced the minimum inhibitory concentration at 90% by 128-fold and was synergistic against 10 of 12 isolates tested in time-kill analysis. CONCLUSIONS: S. maltophilia is emerging as an important pathogen in patients with compromised immunity, leading to severe infections that are difficult to treat. Based on in vitro synergy studied, we recommend considering ticarcillin/clavulanate plus aztreonam as a potential treatment option in immunocompromised patients with S. maltophilia infection.

Anti-Bacterial Agents↗

PubMed1996

Belgian multicentre study on the in vitro activity of cefepime against gram-negative bacilli.

The in vitro activity of cefepime has been compared with that of cefotaxime, ceftazidime, aztreonam, and piperacillin against 1826 Enterobacteriaceae including 537 inducible Enterobacteriaceae (Enterobacter spp., Serratia spp., Citrobacter spp,. Morganella morganii) and 572 non-fermenters, including 401 Pseudomonas aeruginosa and 111 Acinebacter spp. isolated from hospitalized patients in 28 Belgian hospitals. Overall, cefepime was found substantially more active than the third-generation cephalosporins, aztreonam and piperacillin against Enterobacteriaceae species producing inducible type I cephalosporinases. Notably, cefepime remained active against 96% of Enterobacteriaceae resistant to cefotaxime, ceftazidime or aztreonam while it displayed a similar activity against E. coli and the other Enterobacteriaceae. Against non-fermenters, cefepime was found less active than ceftazidime but more than cefotaxime or aztreonam.

Anti-Bacterial Agents↗

PubMed1998

Antimicrobial susceptibility testing for Klebsiella pneumoniae isolates resistant to extended-spectrum beta-lactam antibiotics.

Detection of Klebsiella pneumoniae strains with extended-spectrum beta-lactamase (ESBL)-related resistance phenotypes is becoming important in clinical microbiology laboratories. In this study, we investigated the usefulness of three screening methods, the Etest ESBL screen, the double-disk synergy test, and the ceftazidime disk test, for identifying ESBL-producing K. pneumoniae strains. The agar dilution method was used as the standard. We also determined the in vitro activity of several new antimicrobial agents against these organisms. Strains that exhibited an increase in the minimum inhibitory concentration (MIC) to the third-generation cephalosporins or aztreonam of 2 micrograms/mL or more, but were susceptible to the three cephamycins tested, were considered to have ESBL-related resistance phenotypes. The frequency of ESBL-producing K. pneumoniae isolates (according to the disk-diffusion method) has increased markedly in recent years, from 3.4% in 1993 to 10.3% in 1997. A total of 93 preserved isolates of K. pneumoniae collected from December 1995 through March 1997 were found to be resistant to at least one of the third-generation cephalosporins (cefotaxime and ceftazidime) or aztreonam using the routine disk diffusion method. Among these isolates, 35 were classified as having an ESBL phenotype using the agar dilution method. The remaining 58 isolates were classified as cephamycin resistant, which indicated resistance to both cephamycins and third-generation cephalosporins or aztreonam. The susceptibility rates of the ESBL-producing isolates were 11% for cefotaxime, 14% for ceftazidime, and 6% for aztreonam. The susceptibility rates of these 35 isolates to imipenem, ciprofloxacin, and ofloxacin were 100%, 80%, and 86%, respectively. Both the MIC50 and MIC90 of meropenem were 0.06 microgram/mL, while the MIC50 and MIC90 of BAY 12-8039 were 0.125 and 2 micrograms/mL, respectively. Thirty-two (91%) of the 35 isolates of K. pneumoniae with the ESBL-related resistance phenotype were detected by the Etest ESBL screen, while the ceftazidime disk screen test detected 77% of these isolates, and the double-disk synergy test detected 74%. The Etest ESBL screen appears to be an acceptable, convenient, and sensitive method for the detection of ESBL-producing isolates in the clinical microbiology laboratory.

Anti-Infective Agents↗

PubMed1988

The new monobactams: chemistry and biology.

The discovery of the monobactams led to the successful development of aztreonam as the first of this novel class of beta-lactam antibiotics to enter the clinical field. Continued structural modification on the monobactam nucleus has resulted in two additional compounds from this class that show interesting biologic properties. The first, SQ 83,360, is like aztreonam in exhibiting high activity against members of the Enterobacteriaceae but has the added characteristic of being exceptionally active against strains of Pseudomonas aeruginosa. Also, significant gains are made with SQ 83,360 in activity against Pseudomonas spp. and Acinetobacter. The second compound, tigemonam, is also like aztreonam, having good activity against Enterobacteriaceae, Haemophilus influenzae, and Neisseria gonorrhoeae and showing good beta-lactam stability. Tigemonam differs from aztreonam in being well absorbed orally by experimental laboratory animals.

Bacteria↗

PubMed1991

The monobactams.

The monobactam antibiotics are synthetic compounds, although monocyclic beta-lactam compounds have been found in nature in various soil bacteria. Although additional orally and parenterally administered monobactams are under investigation, the first marketed monobactam was aztreonam. This agent has an antimicrobial spectrum similar to that of gentamicin and tobramycin, aminoglycoside antibiotics. Aztreonam, however, is not nephrotoxic, is weakly immunogenic, and has not been associated with disorders of coagulation. Aztreonam may be administered intramuscularly or intravenously; absorption after oral administration is poor. The primary route of elimination is the urine. The serum half-life of the drug in patients with normal renal function is 1.5 to 2.1 hours; the recommended dosing interval in patients with normal renal function is every 8 hours. Dosage adjustment is necessary in patients with renal impairment. The strictly gram-negative aerobic spectrum of aztreonam limits its use as a single empiric agent. Approved indications for its use include infections of the urinary tract or lower respiratory tract, intra-abdominal and gynecologic infections, septicemia, and cutaneous infections caused by susceptible organisms. Concurrent initial therapy with other antimicrobial agents is recommended before the causative organism (or organisms) has been determined in patients who are seriously ill and at risk for gram-positive or anaerobic infections.

Humans↗

PubMed1991

Synergic post-antibiotic effect of mecillinam, in combination with other beta-lactam antibiotics in relation to morphology and initial killing.

The synergic in-vitro post-antibiotic effect (PAE) of mecillinam, in combination with either ampicillin, aztreonam, ceftazidime or piperacillin, on a reference strain of Escherichia coli was evaluated by bioluminescence assay of bacterial ATP. Ampicillin, ceftazidime and mecillinam alone induced a concentration dependent PAE (greater than 3 h) on E. coli, whereas aztreonam and piperacillin alone induced a short (less than 1 h) non-dose dependent PAE. At most concentrations, the combination of mecillinam and ampicillin, aztreonam, ceftazidime or piperacillin induced longer PAEs on E. coli than the sum of the individual antibiotics' PAEs. Long PAEs were seen concomitantly with the presence of spheroplasts. In addition to the synergistic PAE, the decrease in colony counts and changes in ATP values after a 2 h exposure to mecillinam, in combination with the other beta-lactam antibiotics, were more prominent than the respective values after exposure to the individual antibiotics. The change in ATP was generally less pronounced than the decrease in colony counts. This could be due to lysis of spheroplasts on agar plates, leading to an over-estimation of the initial killing when assayed by viable counting. Mecillinam, which induced long PAEs on E. coli at almost all concentrations in this study, has a high affinity for penicillin binding protein 2 (PBP 2) and induced spheroplast formation at all concentrations. However, mechanisms other than the affinity for PBP 2 and spheroplast formation are involved in the PAE of beta-lactam antibiotics on Gram-negative bacteria; since the PAE was prolonged when mecillinam was combined with ampicillin, aztreonam, ceftazidime or piperacillin, which bind preferentially to PBP 1 and 3.

Adenosine Triphosphate↗

PubMed1993

In-vitro susceptibility and in-vivo efficacy of antimicrobials in the treatment of intraabdominal sepsis in mice.

Cefoxitin, cefotetan, cefmetazole, ceftizoxime, imipenem plus cilastatin, ampicillin plus sulbactam and clindamycin alone or combined with gentamicin, ciprofloxacin, ofloxacin or aztreonam were compared in the therapy of intraabdominal infection in mice caused by Escherichia coli in combination with either Bacteroides fragilis or Bacteroides thetaiotaomicron. Mortality in the control group was 45%, and no animal receiving either imipenem, gentamicin, ciprofloxacin, ofloxacin or aztreonam died. Mortality in mice receiving cefoxitin, cefotetan, cefmetazole, or ceftizoxime was below 7% (P < 0.05%) and mortality following treatment with ampicillin-sulbactam was 23-27% (P > 0.05). The abscesses were examined ten days after inoculation. No abscesses were observed in mice treated with clindamycin or imipenem. Therapy with gentamicin, ciprofloxacin, ofloxacin, aztreonam or ceftizoxime alone did not prevent abscess formation by both Bacteroides sp. A significant reduction in abscess formation and number of E. coli and B. fragilis was observed with combination therapy of clindamycin with either ciprofloxacin, ofloxacin, aztreonam, or gentamicin and single agent therapy with either imipenem, cefoxitin, cefotetan, cefmetazole and ampicillin-sulbactam alone. However, cefotetan and cefmetazole did not reduce abscess formation or the number of B. thetaiotaomicron. These in-vivo data confirm the in-vitro activity of these antimicrobials.

Abdomen↗

PubMed1996

In-vitro susceptibility of Klebsiella oxytoca strains to 13 beta-lactams in the presence and absence of beta-lactamase inhibitors.

The susceptibility of Klebsiella oxytoca isolates was tested by an agar diffusion method (167 strains collected in six countries) and an agar dilution method (38 strains). Multivariate analysis of inhibition zone diameters by principal component analysis clearly individualised four susceptibility patterns, including the phenotype of strains overproducing beta-lactamase and resistant to penicillins, first-generation cephalosporins, cefuroxime and aztreonam, but susceptible to ceftazidime. This phenotype was different from that conferred by plasmid-mediated extended-spectrum beta-lactamases; strains expressing these enzymes were also resistant to ceftazidime and cefotaxime. The bla(oxy) gene from K. oxytoca was introduced into Escherichia coli and K. oxytoca recipients and conferred increased resistance to beta-lactams in the recipient cells. Clavulanic acid was effective in association with piperacillin (MIC decreased 36-fold), ceftriaxone (35-fold) and aztreonam (19-fold) against overproducing strains, in spite of a relatively high IC50 (0.3 microM). Sulbactam (IC50, 400 microM) was ineffective in this context when combined with piperacillin (MIC decreased 1.5-fold), ceftriaxone (1.6-fold) and aztreonam (1.6-fold). The inhibitory activity of tazobactam (IC50, 8.2 microM) was heterogeneous depending on the strain and the beta-lactam with which it was combined. When combined with piperacillin or ceftriaxone little potentiation in antibiotic activity occurred (MIC decreased 3.9-fold and 4.5-fold, respectively); however, tazobactam plus aztreonam resulted in a 50-fold decrease in MIC of antibiotic.

Enzyme Inhibitors↗

PubMed1999

Molecular and biochemical characterization of VEB-1, a novel class A extended-spectrum beta-lactamase encoded by an Escherichia coli integron gene.

A clinical isolate, Escherichia coli MG-1, isolated from a 4-month-old Vietnamese orphan child, produced a beta-lactamase conferring resistance to extended-spectrum cephalosporins and aztreonam. In a disk diffusion test, a typical synergistic effect between ceftazidime or aztreonam and clavulanic acid was observed along with an unusual synergy between cefoxitin and cefuroxime. The gene for VEB-1 (Vietnamese extended-spectrum beta-lactamase) was cloned and expressed in E. coli JM109. The recombinant plasmid pRLT1 produced a beta-lactamase with a pI of 5.35 and conferred high-level resistance to extended-spectrum (or oxyimino) cephalosporins and to aztreonam. Vmax values for extended-spectrum cephalosporins were uncommonly high, while the affinity of the enzyme for ceftazidime and aztreonam was relatively low. blaVEB-1 showed significant homology at the DNA level with only blaPER-1 and blaPER-2. Analysis of the deduced protein sequence showed that VEB-1 is a class A penicillinase having very low levels of homology with any other known beta-lactamases. The highest percentage of amino acid identity was 38% with PER-1 or PER-2, two uncommon class A extended-spectrum enzymes. Exploration of the genetic environment of blaVEB-1 revealed the presence of gene cassette features, i.e., (i) a 59-base element associated with blaVEB-1; (ii) a second 59-base element just upstream of blaVEB-1, likely belonging to the aacA1-orfG gene cassette; (iii) two core sites (GTTRRRY) on both sides of blaVEB-1; and (iv) a second antibiotic resistance gene 3' of blaVEB-1, aadB. blaVEB-1 may therefore be the first class A extended-spectrum beta-lactamase that is part of a gene cassette, which itself is likely to be located on a class 1 integron, as sulfamide resistance may indicate. Furthermore, blaVEB-1 is encoded on a large (> 100-kb) transferable plasmid found in a Klebsiella pneumoniae MG-2 isolated at the same time from the same patient, indicating a horizontal gene transfer.

Amino Acid Sequence↗

PubMed1988

Pseudomonas aeruginosa: in vitro susceptibility to antimicrobial drugs, single and combined, with and without defibrinated human blood.

Twelve clinical isolates of Pseudomonas aeruginosa of distinct pyocin type varied in susceptibility to 14 of 17 antimicrobial drugs. The 2 x MIC concentrations of 16 antimicrobial drugs combined with 55% (v/v) of fresh, defibrinated human blood yielded additive effects. Additive effects were noted with blood plus the MIC concentrations of all drugs tested except cefoperazone, gentamicin, and netilmicin. Blood combined with subinhibitory (1/2 MIC) concentrations of aztreonam, ceftazidime, ciprofloxacin, fleroxacin, imipenem, and tobramycin, respectively, yielded additive effects; indifferent effects were observed with the remaining 10 blood plus 1/2 MIC drug combinations. The following drug combinations additively augmented the antibacterial activity of 65% (v/v) of human blood against two selected isolates of P. aeruginosa: tobramycin (1 microgram/ml) plus the MIC or 2 x MIC concentrations of azlocillin, aztreonam, ceftazidime, ciprofloxacin, imipenem, norfloxacin, ofloxacin, piperacillin, and ticarcillin, respectively. Imipenem (8 micrograms/ml) combined with ceftazidime, cefoperazone, and piperacillin, but not aztreonam, enhanced the bactericidal activity of human blood. Rifampin (2 micrograms/ml) plus tobramycin (0.5-1 microgram/ml) combined with 8 or 16 micrograms/ml of azlocillin, aztreonam, cefoperazone, ceftazidime, imipenem, and piperacillin, respectively, enhanced blood-mediated killing of three representative multiple-drug-resistant P. aeruginosa isolates. Additional effective triple-drug combinations with human blood were rifampin + tobramycin + polymyxin B, rifampin + ciprofloxacin + imipenem, and rifampin + amikacin + imipenem. Ciprofloxacin (2 micrograms/ml) was the most potent intraphagocytic bactericidal drug of 16 tested agents (greater than or equal to 2 x MBC concentrations) against P. aeruginosa control strain ATCC 27853.

Anti-Bacterial Agents↗

PubMed1992

Lipopolysaccharide alterations responsible for combined quinolone and beta-lactam resistance in Pseudomonas aeruginosa.

Resistant variants of three clinical Pseudomonas aeruginosa isolates were obtained in the presence of aztreonam. The variants exhibited a four- to eightfold increase in the minimal inhibitory concentrations to beta-lactam antibiotics (except imipenem) to quinolones, such as norfloxacin and fleroxacin, chloramphenicol and tetracycline, but not to gentamicin and polymyxin B. beta-Lactamase production was barely detectable in both wild-type strains and the resistant clones. Only ampicillin, cefoxitin and imipenem increased the production of beta-lactamase, whereas various other beta-lactams did not. Penicillin-binding proteins remained unchanged in the aztreonam-resistant clones. The analysis of the outer membrane proteins did not reveal differences in the outer membrane proteins between the wild-type strains and the aztreonam-resistant clones. Two of the three antibiotic-resistant isogenic clones contained less lipopolysaccharides (LPSs) than their corresponding wild-type strains. Moreover, it could be demonstrated that the ratio of 2-keto-3-deoxy octonate to carbohydrate of the LPS changed in any case between the wild-type strains and the aztreonam-resistant clones. These alterations were accompanied by a decrease in surface hydrophobicity of the resistant clones as compared to the wild-type strains. Therefore, quantitative as well as qualitative alterations in the LPS may provide an explanation for the resistant phenotype observed.

4-Quinolones↗

PubMed1999

Extended-spectrum beta-lactamase producing strains of Enterobacter cloacae transferring resistance to cefotaxime and ceftazidime.

Transferability of ceftazidime resistance and of extended-spectrum beta-lactamase (ESBL) production was recorded in three strains of Enterobacter cloacae from Frankfurt University Clinics. All three strains were resistant to rifampicin, carbenicillin, cephaloridine, cefotaxime, ceftazidime, aztreonam, imipenem and meropenem. They transferred directly determinants of resistance to carbenicillin and cephaloridine to Escherichia coli K-12 No. 185 nal+ recipient strain. All transconjugant colonies also contained determinants of resistance to cefotaxime, ceftazidime and aztreonam. In the second cycle of transfers, determinants of resistance to carbenicillin, cephaloridine, cefotaxime, ceftazidime and aztreonam were transferred en bloc to the recipient Escherichia coli K-12 No. 3110 rif+ indicating that the "transfer factor" (tra+) mediating the process of conjugational transfer had also been co-transferred. Double-disk diffusion test showed the same pattern of production of ESBLs both in original strains and in transconjugants. Transfer of cefotaxime, ceftazidime and aztreonam was accompanied by the transfer of ESBL production.

Cefotaxime↗

PubMed1989

In vitro activity of tigemonam against urinary tract pathogens.

Tigemonam's in vitro activity was compared with that of aztreonam, cefotaxime, gentamicin, and norfloxacin. Thirty-two strains of Pseudomonas and 960 strains of Enterobacteriaceae were studied using the agar dilution method (including Escherichia coli, Klebsiella pneumoniae, Klebsiella oxytoca, Enterobacter sp., Serratia marcescens, Proteus mirabilis, Proteus vulgaris, Morganella morganii, and Salmonella enterica). Tigemonam displayed good activity against Enterobacteriaceae. Minimum inhibitory concentrations (MICs), were as follows: MIC50S were 0.01 mg/L for P. mirabilis and 0.5 mg/L for S. marcescens, MIC90S were 0.03 mg/L for P. mirabilis and P. vulgaris and 4 mg/L for Citrobacter freundii. Tigemonam inhibited E. coli and P. mirabilis, the most common strains of urinary pathogens. Despite MIC90S of 9.5 and 4 mg/L for Enterobacter and C. freundii, respectively, resistance to tigemonam was observed. Tigemonam was found to be inactive against Pseudomonas aeruginosa, with MIC50S and MIC90S higher than 128 mg/L (range, 64 to greater than 128 mg/L). Tigemonam's activity was found to be similar to that of cefotaxime, slightly less than that of norfloxacin and aztreonam, and substantially greater than that of gentamicin. Of all the drugs tested, only norfloxacin and aztreonam possessed activity profiles against P. aeruginosa that were compatible with their clinical usefulness (MIC90, 8 mg/L for norfloxacin; MIC50, 8 mg/L and MIC90, 32 mg/L for aztreonam). Cefotaxime and gentamicin showed no activity on more than 90% of the P. aeruginosa strains tested.

Enterobacteriaceae↗

PubMed1997

[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.

Enterobacteriaceae↗

PubMedDate not supplied

Antibiotic susceptibility profile of Xanthomonas maltophilia. In vitro activity of beta-lactam/beta-lactamase inhibitor combinations.

The susceptibility of 42 strains of Xanthomonas (Pseudomonas) maltophilia to 37 antibiotics (mainly beta-lactams, aminoglycosides, and fluorinated quinolones) was tested. Xanthomonas maltophilia was resistant to most beta-lactams, with ceftazidime, moxalactam, and ICI-194008 being the most active ones. Aminoglycosides had a very modest activity, with quinolones showing only moderate activity against this species. Trimethoprim/sufamethoxazole was effective against all strains tested. We also tested the synergy of several beta-lactam/beta-lactamase inhibitors against X. maltophilia. Only aztreonam/clavulanic acid at 3:1, 1:1 and, mainly, 2:1 combinations had synergistic activity, decreasing the rate of resistance from 92.8% for aztreonam alone to 32.4% for aztreonam-clavulanic acid at 1:1 and 0% for aztreonam-clavulanic acid at 2:1.

4-Quinolones↗

PubMed1988

Resistance-pattern-analysis--a step toward predictable differentiated antibiotic therapy.

The Resistance-Pattern-Analysis (RPA)-the procedure will be described- makes possible a comparison of susceptibility test results of different antibiotics independent of patient and test related factors. Using two examples, the comparative assessment of a more recent antibiotic with well-tried older antibiotics and the selection of antibiotics for an interventive therapy, whereby the pathogen being unknown the therapy is based upon the probable pathogen, the expected susceptibility and the localization of the infection the practicability will be illustrated. A RPA of 1526 bacterial isolates was carried out using aztreonam, gentamicin and amikacin. Aztreonam was superior to amikacin against all species tested. In comparison to gentamicin, aztreonam showed the best results against Pseudomonadaceae. Using common combinations of antibiotics for the initial interventive therapy the possible use of RPA for a cost-risk-analysis from a medical microbiological viewpoint will be demonstrated.

Amikacin↗

PubMed1997

Multicenter evaluation of antimicrobial resistance to six broad-spectrum beta-lactams in Colombia using the Etest method. The Colombian Antimicrobial Resistance Study Group.

The need for comprehensive and quantitative accurate antimicrobial resistance surveillance systems has become acute as a guide to problem recognition and to focus local interventions. A multilaboratory (10 medical centers) Colombia surveillance project was initiated in early 1997 to monitor the potency and spectrum of six (cefepime, cefotaxime, ceftazidime, cefoperazone/sulbactam, aztreonam, and imipenem) broad-spectrum antimicrobial agents tested against 100 organisms per participant center (802 strains). Ten groups of organisms were tested by a reference-quality method (Etest; AB BIODISK, Solna, Sweden) with results validated by concurrent quality control and additional challenge strain analysis. Results from nine qualifying medical centers were tabulated, and 95.7 to 96.8% of quality assurance tests were within expected ranges. Only cefepime (90.1-100.0% susceptible) and imipenem (96.3-100.0%) were active against all Enterobacteriaceae at > 90% of susceptible isolates using the breakpoint concentrations recommended by the National Committee for Clinical Laboratory Standards. Among ceftazidime- (or cefotaxime- or aztreonam-) resistant Enterobacter spp. and Citrobacter freundii, cefepime remained active, but not cefoperazone with sulbactam. Escherichia coli and Klebsiella spp. strains having resistance phenotypes consistent with extended spectrum beta-lactamase production were discovered in approximately 5 to 10% of isolates. All tested drugs except ceftazidime (31.8-57.7% susceptible) were active against > 94% of oxacillin-susceptible staphylococci. Similar rates of resistance (9.1-14.8%) were observed in Pseudomonas aeruginosa for five of six drugs (not cefotaxime; 15.9% of strains were susceptible). Acinetobacter spp. isolates were most susceptible to imipenem (95.8%), cefepime (86.1%), and cefoperazone/sulbactam (83.3%). Overall for the 1997 order of antimicrobial spectrums for these tested compounds was: imipenem (96.6%) > cefepime (93.6%) > cefoperazone/sulbactam (90.5%) > cefotaxime (74.9%) > aztreonam (74.3% for Gram-negative bacilli only) > ceftazidime (73.2%). These data should be used to guide empiric regimens in Colombia, and additionally will provide a resistance statistical baseline to which future studies in this nation can be compared.

Anti-Bacterial Agents↗