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PubMedDate not supplied

Some properties of Serratia marcescens, Salmonella paratyphi A, and Enterobacter cloacae with non-enzyme-dependent multiple resistance to beta-lactam antibiotics, aminoglycosides, and quinolones.

Non-enzyme-dependent multiple-drug resistance occurs preferentially in some genera of Enterobacteriaceae, such as Serratia, Klebsiella, Enterobacter, and Salmonella. Susceptibility to beta-lactam antibiotics, aminoglycosides, quinolones, trimethoprim, and chloramphenicol may be affected in various combinations in different mutants. Proteins from the outer and inner membranes and lipopolysaccharides may be altered concomitantly. Although porin alterations have been observed in all resistant mutants studied, these modifications alone do not seem sufficient to explain the various cross-resistance phenotypes.

4-Quinolones↗
PubMed1992

Molecular analysis provides evidence for the endogenous origin of bacteremia and meningitis due to Enterobacter cloacae in an infant.

We analyzed the restriction fragment length polymorphism (RFLP) of total DNA and of ribosomal DNA regions (ribotyping) to document the occurrence of endogenous, systemic bacteremia and meningitis due to Enterobacter cloacae in a newborn. Five strains of E. cloacae were isolated from this newborn. Three of these strains were recovered from stool at counts of 10(8), 10(9), and 10(9) organisms/g of feces, respectively; one strain was isolated from blood; and one strain was isolated from cerebrospinal fluid. In addition, five epidemiologically unrelated strains of E. cloacae were studied for comparison. Our study clearly shows the genetic relatedness of the strains isolated sequentially from cultures of stool, blood, and cerebrospinal fluid. RFLP analysis of total DNA and ribotyping seem particularly well suited to the study of the epidemiology of nosocomial E. cloacae strains.

Bacteremia↗
PubMed1979

Enterobacter cloacae septicemia in a burn center: epidemiology and control of an outbreak.

An outbreak of infections due to Enterobacter cloacae occurred in the burn center at the Medical College of Virginia (Richmond, Virginia) in 1976. Fifteen patients had bacteremia due to E. cloacae; 10 cases of bacteremia occurred during a six-week period in January and February. The development of bacteremia was significantly related to the extent of third-degree burn and to admission to the burn center in January and February but not to the presence of an intravenous cannula, underlying disease, or antimicrobial therapy. E. cloacae was spread by contaminated hands of personnel and by cross-contamination of hydrotherapy water. A shortage of staff appeared to be an important factor in the occurrence of the outbreak. Control measures included an increase in the number of personnel, instruction of personnel in proper aseptic technique, and adoption of a new hydrotherapy protocol.

Adolescent↗
PubMed1982

Resistance to cefamandole: derepression of beta-lactamases by cefoxitin and mutation in Enterobacter cloacae.

Studies were performed to characterize resistance to cefamandole in two strains of Enterobacter cloacae. Susceptible wild-type cells were exposed either to cefamandole to select stably resistant mutants or to cefoxitin to induce unstable resistance. The two types of resistant cells inactivated cefamandole, and their beta-lactamases had identical isoelectric focusing patterns and substrate profiles. Studies of the beta-lactamases of these resistant cells indicated that the enzymes belonged to the Richmond and Sykes Group I and suggested that their production in wild-type cells is under repressor control. The resistant mutants appeared to be stably derepressed at the locus for beta-lactamase expression, whereas cefoxitin-induced cells were reversibly derepressed wild-type cells. Transfer of plasmids from one mutant colony to recipient Escherichia coli cells did not transfer resistance. These two types of resistance to cefamandole may explain the widely discrepant results obtained during in vitro and in vivo studies, as well as the rapid emergence of resistance that has been observed during clinical use.

Cefamandole↗
PubMed1983

Retrospective analysis of plasmid patterns in a study of burn unit outbreaks of infection due to Enterobacter cloacae.

To evaluate the usefulness of plasmid pattern analysis as an epidemiologic tool and to determine the mechanism of resistance to silver sulfadiazine and mafenide acetate, silver sulfadiazine-resistant, mafenide acetate-resistant Enterobacter cloacae isolates from a 1976 outbreak of infections in a burn unit (group I) were analyzed retrospectively. These strains were compared with various E cloacae isolates (groups II-V), including E cloacae isolates from a more recent (1982) burn unit outbreak (group V). Agarose gel electrophoresis (AGE) of DNA isolated from "epidemic" strains of E cloacae revealed a uniform pattern of four plasmid DNA bands, ranging in molecular size from 66 to 2 megadaltons. No such plasmid pattern was seen in silver sulfadiazine-, mafenide acetate-susceptible isolates of E cloacae in groups II, III, and V. Analysis of non-E cloacae coisolates suggested that silver sulfadiazine resistance was associated with the 55-megadalton plasmid. Plasmid pattern analysis easily separated "epidemic" E cloacae isolated in 1976 from those isolated in 1982.

Burns↗
PubMed1985

Cross-resistance to nalidixic acid, trimethoprim, and chloramphenicol associated with alterations in outer membrane proteins of Klebsiella, Enterobacter, and Serratia.

We studied in vitro mutants of Klebsiella, Enterobacter, and Serratia cross-resistant to nalidixic acid, trimethoprim, and chloramphenicol that were similar to mutants found in vivo. The sole mechanism for this type of resistance appeared to be a reduction in permeability of the cell envelope. The mutants had significantly lower rates of uptake of glucose and chloramphenicol, but binding of chloramphenicol to ribosomes was normal. In addition, the amounts of dihydrofolate reductase were similar in both wild-type and cross-resistant mutants of Klebsiella. Examination of the bacterial outer membrane revealed that the amount of at least one major protein, with a molecular size of approximately 40 kilodaltons, was decreased in the mutants. Therefore the resistance seemed likely to be due to the reduction in quantity of these outer membrane proteins, possibly porins, in the mutant bacteria.

Anti-Bacterial Agents↗
PubMed1987

Factors that influence the evolution of beta-lactam resistance in beta-lactamase-inducible strains of Enterobacter cloacae and Pseudomonas aeruginosa.

Induction ratios were determined for beta-lactamase-inducible strains of Enterobacter cloacae and Pseudomonas aeruginosa by using 10 beta-lactam agents. For E. cloacae, pre-incubation with ceftriaxone, cefoxitin, cefamandole, cefoperazone, or imipenem produced significantly larger amounts of beta-lactamase than did pre-incubation with moxalactam, clavulanate, ceftazidime, or aztreonam. For P. aeruginosa, imipenem was the best inducer, whereas ceftriaxone, piperacillin, cefoperazone, cefamandole, clavulanate, and aztreonam were poor beta-lactamase inducers. The rate of emergence of resistance by E. cloacae p99 and P. aeruginosa ATCC 27853 did not correlate with the induction ratio of the selecting agent; however, a strong correlation was noted between the mutation rate and the ratio of the MIC to the concentration of selecting antibiotic used. Emergence of resistance is related to the MIC of the antibiotic and the concentration of antibiotic used to select for resistance and is independent of the efficacy of the beta-lactam inducer. Resistant mutants arise through both beta-lactamase-dependent and -independent mechanisms.

Anti-Bacterial Agents↗
PubMed1987

Emergence of resistance to ceftazidime during therapy for Enterobacter cloacae infections.

The mechanism of resistance to ceftazidime in two clinical isolates of Enterobacter cloacae that emerged during therapy with broad-spectrum beta-lactam antibiotics was studied. Both isolates acquired broad resistance to advanced-spectrum beta-lactam drugs other than imipenem. Biotyping confirmed strain identity in both cases, and no new plasmids were detected in the resistant isolates. Both resistant isolates produced beta-lactamase constitutively. Slow but definite hydrolysis of ceftazidime was demonstrated by using purified beta-lactamase in a spectrophotometric assay. Further evidence that beta-lactamase is responsible for resistance in these organisms was provided by the demonstration that cefoxitin, a potent inducer of beta-lactamase, antagonized the activity of ceftazidime against these isolates. This antagonism could be prevented by inhibition of derepression of beta-lactamase with clindamycin. Clindamycin also prevented regrowth of ceftazidime-treated cells in time-kill studies and markedly reduced production of beta-lactamase in induced cultures at concentrations as low as 2 micrograms/ml.

Adult↗
PubMed1985

Effect of beta-lactamase induction on susceptibility to cephalosporins in Enterobacter cloacae and Serratia marcescens.

For Enterobacter cloacae GN5797 and Serratia marcescens 72-2, which produce inducible beta-lactamases and respond antagonistically to many combinations of cephalosporins, the changes in beta-lactamase activity and sensitivity to cephalosporins were examined during semi-continuous cultivation in which the concentration of inducers was decreased by two-fold dilution of the culture every 30 min starting from 1 h after the addition of inducers. The levels of beta-lactamase, which peaked at 0.5-2 h after induction, decreased concomitantly with the disappearance of the inducers in the culture, and returned to the uninduced levels by 6 h. The ability of cefoxitin and cefmetazole to induce beta-lactamases was more potent than that of cefazolin and cefotiam. The sensitivity to some cephalosporins, judged by the MIC and bactericidal effect, was slightly decreased at an early stage of induction, and reverted to the uninduced levels within several hours after the inducers were depleted.

Cephalosporins↗
PubMed1987

Properties of spontaneous Enterobacter cloacae mutants with temperature-conditional derepression of type I beta-lactamase synthesis.

Spontaneous mutants, with temperature-conditional derepression of chromosomally-encoded Type I beta-lactamase synthesis, were derived from two independent clinical isolates of Enterobacter cloacae. At the permissive temperature (28 degrees C) the mutants' beta-lactamase activity was equivalent to that of their respective parents but at restrictive temperatures (above 40 degrees C) the activity increased many hundred-fold. The increased beta-lactamase expression correlated with reduced beta-lactam susceptibility. In temperature shift-up experiments, the initial rate of beta-lactamase synthesis closely paralleled that of the parent strains induced with cefoxitin. Maximal beta-lactamase activity in the mutants was attained after about 3 h growth at restrictive temperatures and was significantly higher than that of the cefoxitin-induced parents. However, the level was not as high as that observed in isogenic temperature-stable derepressed mutants, under the same conditions. All temperature-conditional mutants showed hyper-induction of beta-lactamase synthesis at permissive temperatures. Our findings are discussed in relation to a positive control model for regulation of Type I beta-lactamase synthesis in Ent. cloacae.

Anti-Bacterial Agents↗
PubMed1987

Selection of enhanced cefotaxime resistance in Enterobacter spp.

Four strains of Enterobacter spp. with different chromosomal beta-lactamase expression (inducible, constitutive or negligible) were grown in broth containing either cefoxitin or cefotaxime, then plated on to agar containing 20 mg cefotaxime per litre to quantitate the cefotaxime-resistant mutants present in the population. Spontaneous resistant mutants were initially isolated from each strain at frequencies of 10(-4) to 10(-5). These high frequencies of spontaneous mutation suggested that more than one type of mutational event could yield cefotaxime resistance. Induction of a high level of beta-lactamase in broth cultures was not in itself sufficient to confer a high level of cefotaxime resistance on the population, and increased resistance following selection of resistant mutants did not necessarily correlate with any significant increase in beta-lactamase activity.

Cefotaxime↗
PubMed1987

Treatment failures of cefotaxime and latamoxef in meningitis caused by Enterobacter and Serratia spp.

Despite the apparent success of several new cephalosporins in the treatment of Gram-negative bacterial meningitis, four treatment failures with cefotaxime or latamoxef were encountered (two caused by Enterobacter and two by Serratia spp.) In-vitro parameters of susceptibility of these clinical isolates were compared with those of a meningeal Ent. cloacae isolate from a successfully treated patient. The MIC and MBC values, degrees of inoculum effect, and amounts of beta-lactamase produced correlated poorly with the observed clinical outcome. However, the extent to which an isolate was killed by the cephalosporin used for treatment, in a 6-h in-vitro incubation, showed good correlation. We suggest that such a test should be used to predict clinical outcome of therapy because the other parameters such as the MIC and MBC values are not sufficiently discriminatory.

Adult↗
PubMed1988

Comparison of glycine enhancement with cefoxitin induction of class 1 beta-lactamase production in Enterobacter cloacae ATCC 13047.

The presence of either glycine or cefoxitin in the growth medium resulted in an increase in the beta-lactamase activity of cultures of Enterobacter cloacae ATCC 13047. Although the beta-lactamases produced as a result of either glycine enhancement or cefoxitin induction were identical there were striking differences in the kinetics of beta-lactamase production. The increased production of beta-lactamase which resulted from enhancement by glycine occurred late in the growth cycle whereas, with cefoxitin induction, the maximum production of beta-lactamase occurred early in logarithmic-phase growth. After the peak activity was reached the beta-lactamase activity appeared to decline with both processes. However, the mechanism of the apparent fall in the intracellular beta-lactamase activity was different with glycine enhancement and cefoxitin induction. In glycine enhanced cultures the fall presumably was due to leakage of intracellular beta-lactamase into the culture medium whereas with cefoxitin induced cultures there was dilution of beta-lactamase activity by bacterial protein derived from an increase in cell numbers after the cessation of induction. High extra-cellular levels of beta-lactamase activity were observed in cultures enhanced by glycine, whereas little beta-lactamase activity was detected in the medium when the cultures were induced by cefoxitin. The findings demonstrate that there are considerable differences between glycine enhancement and cefoxitin induction, but a final mechanism common to both processes exists which results in the production of identical beta-lactamases by E. cloacae ATCC 13047.

Cefoxitin↗
PubMed1988

Inactivation of beta-lactamases from Enterobacter cloacae by monophosphams.

Amongst the monocyclic beta-lactam antibiotics, selected monophosphams were potent mechanism-based inactivators of the P99 and E2 cephalosporinases of Enterobacter cloacae. Inhibition of these enzymes was time-dependent with second order rate constants for inactivation of 100,000 to 20,000,000 l/mol/min. After incubation for 24 h at least 99% of the enzymatic activity was inhibited when enzyme was exposed to a ten-fold excess of inactivator. Amongst the monophosphams three classes of inhibitors were seen: irreversible inactivators as described above, transient inactivators and competitive (inhibitory) substrates.

Anti-Bacterial Agents↗
PubMed1989

Enhanced in-vitro bactericidal activity of amikacin combined with latamoxef, cefotaxime and aztreonam against multi-resistant Enterobacter cloacae.

The in-vitro interactions of amikacin with latamoxef, cefotaxime and aztreonam were studied for 20 multiresistant strains of Enterobacter cloacae isolated from clinical specimens of nosocomial origin. All the strains were resistant to amikacin, cefotaxime and aztreonam while 14 were resistant and six sensitive to latamoxef. Interactions were studied simultaneously by the killing curve technique after exposure to 16 mg/l of each antibiotic, whenever the MIC was above 16 mg/l and 1/4 the MICs whenever the MIC was less than or equal to 16 mg/l. Enhanced killing was defined as a greater than or equal to 2 log increase in bactericidal effect after three or five and a half or 24 h incubation with both drugs, as compared to the single most effective antibiotic alone. Aztreonam enhanced the rate of killing by amikacin for 13 strains, latamoxef for 12 strains and cefotaxime for 11 strains. For seven strains, all interactions exhibited enhanced killing over time. No antagonism was observed. The interaction results were independent of the MICs as well as of the underlying resistance mechanism to either of the combined antibiotics. The significance of these in-vitro results requires confirmation in vivo.

Amikacin↗
PubMed1989

A comparison of aztreonam and imipenem induction of class I beta-lactamase in Enterobacter cloacae ATCC 13047.

Aztreonam and imipenem were shown to induce Class I beta-lactamase in Enterobacter cloacae ATCC 13047 to a similar extent. Quantitatively, however, aztreonam was far less efficient as an inducer than imipenem. Optimum induction by aztreonam required a concentration of 200 mg/l, which was 800-fold greater than the concentration of 0.25 mg/l of imipenem which resulted in the optimum induction. The differences in the concentrations of aztreonam and imipenem that gave optimum induction were related to the inherent antibacterial activities of the antibiotics when these were determined under the conditions of broth culture. The beta-lactamase activity of sonicated cell samples following induction was inhibited by the presence of aztreonam but not by imipenem. The inhibition was overcome by first washing the cell samples from induced cultures and then incubating the sonicates for a prolonged period at 4 degrees C. It is proposed that the phenomena of an optimum inducing concentration and the interference with the assay of beta-lactamase by the presence of residual antibiotic demonstrated in this study with aztreonam and imipenem would be of relevance when applied more broadly to studies of beta-lactamase induction. In particular these would have a profound effect on the results of studies which attempt to compare the efficacy of beta-lactams as inducers of Class I beta-lactamase.

Aztreonam↗
PubMed1990

Enhanced resistance to cefotaxime and imipenem associated with outer membrane protein alterations in Enterobacter aerogenes.

Mutants exhibiting enhanced resistance to cefotaxime and imipenem were selected by plating a strain of Enterobacter aerogenes, which already produced chromosomal beta-lactamase constitutively, on to varying concentrations of different beta-lactam antibiotics. Frequencies of mutation varied from 10(-5) to 10(-8), depending upon the particular antibiotic and concentration used for selection. Only minor variations in beta-lactamase specific activities were observed and these could not be directly correlated with changes in resistance when compared with the original strain. In the majority of mutants, the selection of an enhanced level of resistance to cefotaxime was associated with a significant increase in resistance to imipenem, but no increase in resistance to the non-beta-lactam antibiotics tested was observed. Examination of outer membrane protein profiles revealed a number of complex changes in the mutants when directly compared to the original strain. In one mutant imipenem/cefotaxime resistance was directly associated with almost total loss of a 42K protein which was non-covalently associated with peptidoglycan and therefore possibly a porin protein.

Cefotaxime↗
PubMed1993

Effect of ampicillin versus cefuroxime on the emergence of beta-lactam resistance in faecal Enterobacter cloacae isolates from neonates.

Enterobacter cloacae strains dominated the aerobic faecal flora of 8.3% of 953 infants discharged from 32 Swedish neonatal intensive care units and the susceptibility of these strains to seven beta-lactam antibiotics was determined. Isolates from infants treated with cefuroxime showed slightly increased MICs only to ampicillin, cephalexin and cephalothin as compared to isolates from untreated infants matched for ward and time of sampling (P = 0.02). In contrast, E. cloacae isolates from ampicillin treated infants showed markedly elevated MICs of all agents tested including piperacillin, cefuroxime, cefotaxime and ceftazidime as compared to those from control neonates (P values between 0.001 for ampicillin and 0.017 for cefotaxime). Thus, E. cloacae with cefotaxime MICs as high as 512 mg/L were isolated only after ampicillin therapy. The resistant strains were negative in a colony DNA hybridization assay using gene probes for the plasmid beta-lactamases TEM-1, OXA-1 and SHV-1. The resistant strains also showed only one beta-lactamase band when crude cell sonicates were analysed by isoelectric focusing, and were not found in other infants in the same ward. The results indicate that the selection of chromosomal E. cloacae mutants, presumably with stably derepressed beta-lactamase production, in the faecal flora of neonates is rare during treatment with cefuroxime and more common during ampicillin therapy.

Ampicillin↗