Citrobacter Freundii Isolates Research Articles

Clinical isolate of Citrobacter freundii highly resistant to new quinolones.

About 30% of 150 recent clinical isolates of Citrobacter freundii were resistant to greater than or equal to 3.13 micrograms of norfloxacin and ofloxacin per ml. Study of one quinolone-resistant strain for which the norfloxacin MIC was 100 micrograms/ml suggested that resistance was associated with both an altered A subunit of DNA gyrase and reduction in drug uptake accompanied by a decrease in an outer membrane protein.

DNA sequence of haemolysin genes fromCitrobacter freundii

The DNA sequence of a 2572-bp region containing genes encoding a hemolytic protein (citrolysin) cloned from an extra-intestinal clinical isolate of Citrobacter freundii, was determined. There were two open reading frames present on the same DNA strand, encoding predicted polypeptides of a molecular mass of 70.4 and 15.7 kDa. Based on the DNA sequence, a single putative promoter region is outlined, and a potential Shine-Dalgarno sequence precedes each of the two genes. However, structures typical of those involved in the rho-independent termination of transcription could not be detected between or within the two genes. The codon usage pattern and the low guanine-plus-cytosine content may suggest a non-Citrobacter origin for this hemolytic activity. An assay indicated the possible non-excretory nature of the C. freundii hemolysin, when expressed in E. coli.

Cloning of a haemolysin fromCitrobacter freundiiand its expression in phylogenetically related bacteria

The determinants for a haemolysin from an extraintestinal isolate of Citrobacter freundii have been cloned and expressed in both Escherichia coli K12 and phylogenetically related bacteria. Compared with E. coli, where the haemolytic determinants are encoded in 7.5 kb, the hemolysin determinants of C. freundii are located on a 2.5-kb HindIII fragment in the recombinant plasmid PJP71. Chicken embryo tests indicate that this haemolysin does contribute to the pathogenicity of C. freundii.

In vitro activity and beta-lactamase stability of two oral cephalosporins, ceftetrame (Ro 19-5247) and cefetamet (Ro 15-8074).

Ceftetrame (Ro 19-5247) and cefetamet (Ro 15-8074), two new orally administered aminothiazolyl imimomethoxy cephalosporins, inhibited hemolytic streptococci and Streptococcus pneumoniae at less than or equal to 0.5 micrograms/ml but were less active against staphylococci than were cephalexin and cefaclor. They did not inhibit S. faecalis, S. faecium, Listeria monocytogenes, Corynebacterium JK species, or Pseudomonas aeruginosa. Haemophilus influenzae, Branhamella catarrhalis, and Neisseria gonorrhoeae, including ampicillin-resistant isolates, were inhibited at less than 0.25 micrograms/ml. Both agents inhibited Escherichia coli, Klebsiella pneumoniae, K. oxytoca, Proteus mirabilis, Salmonella species, Shigella species, Citrobacter diversus, and Aeromonas hydrophila resistant to ampicillin, cephalexin, and cefaclor at less than or equal to 2 micrograms/ml, although many isolates of Enterobacter cloacae, Citrobacter freundii, and Serratia marcescens resistant to cefotaxime were not inhibited by these agents. A marked inoculum effect was noted for Enterobacteriaceae carrying the Richmond-Sykes type 1A chromosomally mediated beta-lactamases, but plasmid-mediated beta-lactamases did not hydrolyze the compounds. Both drugs inhibited the chromosomally mediated beta-lactamase of E. cloacae, P99.

Evidence for nonspecific induction of beta-lactamase in overproducing variants of Enterobacter cloacae and Citrobacter freundii.

Induction of chromosomally mediated beta-lactamases was studied in clinical isolates of Enterobacter cloacae and Citrobacter freundii. Whereas isolates resistant to ampicillin and cefoxitin exhibited an inducible enzyme, those sensitive to both agents did not. Cefoxitin and above all imipenem proved the most efficacious enzyme inducers. Variants among these inducible isolates which produced large amounts of beta-lactamase could be selected in the presence of cefamandole. In each of these selected variants constitutive enzyme production was markedly enhanced by induction, even with compounds lacking induction potency for the corresponding wild strains. Moreover, these variants could also be induced non-specifically, i.e. by non-beta-lactam compounds. Production of large amounts of enzyme was associated with resistance to all available beta-lactam compounds.

Evaluation of Rosco diagnostic beta-glucuronidase tablets in the identification of urinary isolates of Escherichia coli.

Rosco diagnostic beta-glucuronidase tablets have been evaluated as a method for the identification of urinary isolates of Escherichia coli. Results were compared with those from traditional biochemical testing. A total of 539 isolates were employed, representing a variety of Gram-negative species. Reproducibility testing was also performed. After 4h incubation, 86% of E. coli isolates (both lactose-positive and lactose-negative) gave a positive reaction. Some Salmonella, many Shigella and one Citrobacter freundii isolate also gave positive reactions. All other organisms gave negative reactions. Results were highly reproducible and not influenced by choice of primary medium. The tablets are suitable for routine use in the diagnostic laboratory for the identification of lactose-positive E. coli. A suitable diagnostic table has been suggested.

Beta-Lactamase inhibitory activity of iodopenicillanate and bromopenicillanate

Iodopenicillanate and bromopenicillanate were shown to be effective inhibitors of a variety of beta-lactamases. Staphylococcus aureus isolates were synergistically inhibited by iodopenicillanate and bromopenicillanate combined with ampicillin. Methicillin-resistant S. aureus was not synergistically inhibited. Escherichia coli which possessed TEM beta-lactamase activity had a reduction in ampicillin minimal inhibitory concentration, but an E. coli isolate which had chromosomal beta-lactamase and a low ampicillin minimal inhibitory concentration showed no reduction in ampicillin minimal inhibitory concentration with either iodopenicillanate or bromopenicillanate. Of the Klebsiella isolates tested, 80% were synergistically inhibited by both iodopenicillanate and bromopenicillanate. Most Morganella isolates were synergistically inhibited by either iodopenicillanate or bromopenicillanate combined with ampicillin, as were many Salmonella, Shigella, Citrobacter diversus, and Citrobacter freundii isolates. No Pseudomonas aeruginosa isolates were synergistically inhibited by iodopenicillanate or bromopenicillanate. Preincubation did not improve the inhibitory activity of iodopenicillanate or bromopenicillanate.

Phage-Host Specificity Tests using Levinea Phages and Isolates of Levinea spp. and Citrobacter freundii

Phage-host specificity tests were accomplished utilizing six serologically unrelated phages with 177 isolates of the genus Levinea and 44 Citrobacter freundii isolates. A total of 84% of the levineae were infected by at least one of the phages, and 21 phage-host patterns were obtained. Only 9% of the C. freundii isolates were infected. One phage, DM-21, only infected L. malonatica whereas the other phages showed no species specificity. Most of the infectivity patterns were specific for either L. amalonatica or L. malonatica, but some patterns showed no host specificity. A correlation was found between dulcitol fermentation and infectivity with DM-21. There was no evidence of a relationship between infectivity and source of isolation. The recommendation that the proposed genus Levinea be accepted rather than the inclusion of these organisms within the genus Citrobacter is discussed.