Clinical isolate of Citrobacter freundii highly resistant to new quinolones

Aoyama, Hiroshi; Fujimaki, Kazuo; Sato, Kenichi; Fujii, Tatsuya; Inoue, Matsuhisa; Hirai, Keiji; Mitsuhashi, Susumu

doi:10.1128/aac.32.6.922

Cited by 37 publications

(21 citation statements)

References 23 publications

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“…(49), Salmonella spp. (18,43), and some other enteric bacilli (1,14,31,44). Although the resistance of E. coli strains to clinically achievable concentrations of newer fluoroquinolones has been documented in several instances (2,17,31,45), the incidence of such strains in large surveys conducted following the approval of fluoroquinolones for clinical use has remained extremely low (13,20,27).…”

Section: Discussionmentioning

confidence: 99%

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Emergence of fluoroquinolone-resistant Escherichia coli at a cancer center

Kern¹,

Andriof²,

Oethinger³

et al. 1994

Antimicrob Agents Chemother

189

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Prophylactic treatment with fluoroquinolones of patients with profound neutropenia has been found to be useful for preventing gram-negative bacteremia and has become a standard preventive-therapy strategy in many cancer centers, but the development of bacterial resistance is a cause of concern. During the past few years, we have observed an increasing number of patients with leukemia from whom fluoroquinolone-resistant strains of Escherichia coli were isolated. The increase was significant in this patient population, and among patients with other underlying diseases, the rates of isolation of such strains per number of discharges were significantly lower and did not increase. Most of the leukemia case patients (16 of 19) had been pretreated with an oral quinolone (ofloxacin), with cumulative doses until the first isolation of a resistant E. coli strain ranging from 0 to 97.8 g (median, 14.4 g). Repeated isolation of such strains was seen in 8 of 17 patients during a follow-up period of .4 weeks and in 1 of 6 patients during a follow-up period of .16 weeks. Ten patients developed bacteremia (mortality, 1 of 10). On the basis of the number of patients with leukemia admitted to the hematology-oncology service, the incidence of bacteremia caused by fluoroquinolone-resistant E. coli increased from <0.5% in 1988-1989 and 0.8% in 1990-1991 to 4.5% in 1992-1993 (P < 0.01). MICs for nine isolates obtained from cultures of blood from different patients ranged between 8 and 16 ,ig/ml (ciprofloxacin and PD 131628), 8 and 32 ,ug/ml (ofloxacin and BAY Y 3118), and 16 and 32 ,Lg/ml (sparfloxacin) and indicated resistance to trimethoprim-sulfamethoxazole, ampicillin, doxycycline, and chloramphenicol. Of nine isolates obtained from cultures of blood from different patients and that were subjected to genomic DNA typing by pulsed-field gel electrophoresis ofXbaI digests, seven were typeable. Among these, four different genotypes were identified, suggesting both the independent development and the horizontal spread of resistant clones ofE. coli.Several controlled studies have suggested that oral fluoroquinolones, particularly ciprofloxacin and ofloxacin, may be useful prophylactic antibacterial agents in neutropenic cancer patients (4,9,10,15,22,29,30,56). Fluoroquinolone treatment in these patients was associated with a significant reduction and virtual absence of infections caused by members of the family Enterobacteriaceae, with less fever (8, 39) and a shorter duration of antimicrobial therapy (22,29,39). Such beneficial effects were observed, even though such treatment has rapidly led to the emergence of resistance in gram-positive organisms not infrequently associated with clinical failures of prophylaxis and therapy (11, 16, 23-26, 34, 38, 52, 53, 55 (14,44), and Escherichia coli (2,17,31,35,45). Since enteric bacilli appear to be the primary target organisms of fluoroquinolone prophylaxis in neutropenic patients, increasing levels of resistance to fluoroquinolones in these species, particularly E. coli, would have a maj...

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Section: Discussionmentioning

confidence: 99%

“…There is now an increasing number of case reports documenting the development of clinical resistance to fluoroquinolones in gram-negative bacilli such as Citrobacter spp. (1), Salmonella spp. (18,43), Klebsiella pneumoniae (31), Serratia marcescens (14,44), and Escherichia coli (2, 17, 31,35,45).…”

mentioning

confidence: 99%

Emergence of fluoroquinolone-resistant Escherichia coli at a cancer center

Kern¹,

Andriof²,

Oethinger³

et al. 1994

Antimicrob Agents Chemother

189

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“…coli K-12 strains, several investigators have isolated drugresistant mutants associated with a reduction of drug uptake and with an alteration of the porin pathway of the outer membrane (1,3,14,15). In Pseudomonas aeruginosa, a less well-defined mechanism seems to be involved.…”

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confidence: 99%

“…Determinations of a DNA gyrase mutation by gene mapping with transduction and by use of a DNA supercoiling assay with purified DNA gyrase subunits have been done with both E. coli (2,15,19,31) and P. aeruginosa (16,20,28). Resistance in other bacteria has also been reported due to apparent reduced permeability or modified DNA gyrase or sometimes both (1,12,29,30).…”

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confidence: 99%

Contribution of permeability and sensitivity to inhibition of DNA synthesis in determining susceptibilities of Escherichia coli, Pseudomonas aeruginosa, and Alcaligenes faecalis to ciprofloxacin

Bédard

Chamberland

Wong

et al. 1989

Antimicrob Agents Chemother

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To examine the correlation between bacterial cell susceptibility to ciprofloxacin and the magnitude of uptake and cell target sensitivity, the relative contribution of ciprofloxacin accumulation in intact cells and its ability to inhibit DNA synthesis were investigated among strains of Escherichia coli, Pseudomonas aeruginosa, and Alcaligenesfaecalis. Uptake studies of ['4C] for the normally susceptible E. coli J53. The ID50 for P. aeruginosa obtained after EDTA treatment or in ether-permeabilized cells was higher than that obtained for the other two strains. The protonophore carbonyl cyanide m-chlorophenylhydrazone prevented killing by low ciprofloxacin concentrations, but sodium azide did not. The latter compound did not enhance killing in association with inhibition of a previously described energy-dependent efflux of ciprofloxacin. These results are consistent with the major determinant of ciprofloxacin susceptibility being the susceptibility to inhibition of DNA synthesis in E. coli, poor permeability associated with the small pore size of A. faecalis, and a combination of low permeability and reduced susceptibility of DNA synthesis to inhibition for P. aeruginosa.Studies have shown that there is a reasonable correlation between concentrations of some of the fluoroquinolone antimicrobial agents needed to inhibit DNA gyrase activity and the MICs for Escherichia coli (17) and Staphylococcus aureus (33) and for inhibition of early DNA synthesis of E. coli (7). However, this is not always so, for example, for Micrococcus luteus (39) and for several compounds examined as part of structure-function studies (11,22). Thus, it is possible for certain fluoroquinolones and bacteria that factors other than the concentration needed to produce a critical degree of inhibition of DNA gyrase activity go into the determination of the MIC. One of these is the accumulation of the quinolone agent.

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“…Widespread use of recently developed broad-spectrum cephems and new quinolones has resulted in the frequent isolation of multiple-antibiotic-resistant strains in hospitals, owing partly to reduced permeability of porins to antibiotics (1,2,11). Among these strains are Enterobacter isolates, which are some of the most important nosocomial pathogens.…”

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Molecular characterization of an Enterobacter cloacae gene (romA) which pleiotropically inhibits the expression of Escherichia coli outer membrane proteins

et al. 1990

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The introduction of a newly cloned Enterobacter cloacae chromosomal gene romA, into Escherichia coli and E. cloacae resulted in enhancement of resistance to quinolones, beta-lactams, chloramphenicol, and tetracycline. The primary effect of romA on a multicopy vector in E. coli was almost complete inhibition of OmpF expression in the outer membrane. From the experiments with ompR and envZ mutants or with ompF-lacZ and ompC-lacZ fusion plasmids, it was concluded that this inhibition is posttranscriptional. The introduction of romA on a multicopy vector into strains with micF deletion elicited only a moderate decrease in OmpF protein expression. This indicates that reduction of OmpF expression by romA is partly mediated posttranscriptionally by the activation of micF. Moreover, the overexpression of RomA protein from an isopropyl-beta-D-thiogalactopyranoside (IPTG)-inducible promoter resulted in nearly complete inhibition of expression of OmpC and OmpA, as well as OmpF. Taken together with an observation in a recent study that overexpressed OmpC inhibited the synthesis of OmpA and LamB, a possible inhibitory mechanism at the translational stage of the synthesis of outer membrane proteins should also be considered. By Southern hybridization, romA was generally detected in the chromosomes of all E. cloacae strains tested but not in the E. coli K-12 chromosome. Sequence data show that there is an open reading frame specifying 368 amino acids residues including a putative signal peptide. RomA appears to belong to the outer membrane protein family since it was extractable from an outer membrane preparation, but no sequence homology to other outer membrane proteins was detected.

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Clinical isolate of Citrobacter freundii highly resistant to new quinolones

Cited by 37 publications

References 23 publications

Emergence of fluoroquinolone-resistant Escherichia coli at a cancer center

Emergence of fluoroquinolone-resistant Escherichia coli at a cancer center

Contribution of permeability and sensitivity to inhibition of DNA synthesis in determining susceptibilities of Escherichia coli, Pseudomonas aeruginosa, and Alcaligenes faecalis to ciprofloxacin

Molecular characterization of an Enterobacter cloacae gene (romA) which pleiotropically inhibits the expression of Escherichia coli outer membrane proteins

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