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PubMed1981

Plasmid specification of resistance to antibacterial compounds in environmental Citrobacter freundii.

Citrobacter freundii from an environmental source displayed resistance to a wide variety of antibacterials. Some of these resistances could be transferred by conjugation with frequencies as high as 10(-2). The complexity of plasmid involvement in the antibacterial resistance of this species was demonstrated by isolation of plasmid DNA from two isolates. In one strain, resistance to beta-lactam antibiotics was specified by a 55 x 10(6) molecular weight plasmid, whereas kanamycin and neomycin resistance was specified by a 7 x 10(6) molecular weight plasmid. Resistance to chloramphenicol and tetracycline was not plasmid mediated. The other strain contained plasmids of molecular weight 113 x 10(6) and 80 x 10(6), which specified resistance to chloramphenicol, neomycin, kanamycin, tetracycline, and mercury.

Anti-Bacterial Agents↗
PubMed1989

Septic pulmonary embolization caused by Citrobacter diversus.

Citrobacter diversus is an unusual human pathogen. This organism has never been reported as a cause of septic pulmonary embolization. We report a case of septic pulmonary embolization caused by C. diversus in a relatively healthy young woman following an otherwise uncomplicated cesarean section.

Adult↗
PubMed1991

Successful treatment of neonatal Citrobacter freundii meningitis with ceftriaxone.

Citrobacter meningitis is an uncommon enteric gram-negative infection that afflicts neonates and young children. Approximately 30 percent of children treated or untreated die from the infection. We report a case of C. freundii meningitis that was resistant to ampicillin and was successfully treated with ceftriaxone, a third-generation cephalosporin. A 13-day-old, full-term baby was admitted to the hospital with a one-day history of fever up to 38.8 degrees C. On admission the infant had a temperature of 39.2 degrees C, pulse of 140 beats/min, and a respiratory rate of 32 breaths/min. Except for a slightly bulging fontanelle, the rest of the physical examination was within normal limits. Complete blood count revealed a white blood cell (WBC) count of 12.5 x 10(9)/L, with 0.66 polymorphonuclear cells, 0.10 bands, 0.18 lymphocytes, and 0.06 monocytes. A stat lumbar puncture showed 10 WBCs per high-power field with gram-negative rods. Empiric therapy with ampicillin 225 mg q12h and gentamicin 11 mg q8h was started. Both antibiotics were discontinued after culture and sensitivity results were positive for C. freundii in the blood and spinal fluid. The patient was successfully treated with nine days of ceftriaxone 250 mg q12h.

Ceftriaxone↗
PubMed2005

Preinoculation with the probiotic Lactobacillus acidophilus early in life effectively inhibits murine Citrobacter rodentium colitis.

Enteropathogenic Escherichia coli (EPEC) is a common pathogen in infantile diarrhea, causing a characteristic histopathologic attaching and effacing (A/E) lesion in the intestinal mucosa. The mouse pathogen Citrobacter rodentium causes a similar A/E lesion in the murine intestine. Like EPEC, C. rodentium infection results in colonic crypt hyperplasia, goblet cell depletion, epithelial proliferation, and mucosal disruption. Using this murine model, we tested the hypothesis that preinoculation of murine gut with Lactobacillus acidophilus early in life can enhance host defense against enteric bacterial infection and attenuate bacteria-mediated colitis. Two-week old BALB/c mice were inoculated with L. acidophilus twice per week for 4 weeks before C. rodentium infection or concomitantly with the exposure to C. rodentium at 6-8 weeks of age. The probiotics were administered twice weekly thereafter. We observed that L. acidophilus inoculation in mice inhibits C. rodentium-induced colitis, which is associated with a decrease in C. rodentium colonization and translocation, an increase in its clearance, and a suppression of colonic myeloperoxidase (MPO) activity. Probiotic treatment also stimulates regulatory cytokine expression in the colon [transforming growth factor beta (TGF-beta), interleukin (IL)-10]. Preinoculation with L. acidophilus is more effective than concomitant use of probiotics in the induction of intestinal IgA secretion and in the downregulation of proinflammatory cytokine expression [tumor necrosis factor alpha (TNF-alpha), IL-6, and IL-12]. These observations suggest that inoculation with probiotics can effectively prevent bacteria-induced colitis by limiting enteric bacteria infection and promoting mucosal protective regulatory immune responses. This study may have ramifications for prevention of infectious diarrhea in human infants and children, particularly in developing countries.

Animals↗
PubMed1994

Characterization of the lactose transport system in Citrobacter freundii.

The lactose transport system of Citrobacter freundii was characterized. Both the lactose transport system and beta-galactosidase were induced with either lactose or isopropyl-beta-D-thiogalactopyranoside (IPTG), the latter being the better inducer. The Km values for methyl-beta-D-thiogalactopyranoside (TMG) transport and lactose transport were 0.61 mM and 1.1 mM, respectively, and the Vmax values were 53 nmol/min/mg cell protein and 12 nmol/min/mg cell protein, respectively. Thus, TMG is a better substrate than lactose. Thiogalactopyranoside (TDG) was a very potent competitive inhibitor. Neither Na+ nor Li+ had a significant effect on the TMG transport or the lactose transport. Proton/substrate cotransport (symport) via this system was observed.

Citrobacter freundii↗
PubMed1990

Urethane-hydrolyzing enzyme from Citrobacter sp.

Urethane, a cancer-causing chemical, was reported to contaminate alcoholic beverages such as whisky, liquor, wine and sake. Enzymatic removal of urethane would be a possible approach to remove this potentially hazardous chemical from alcoholic beverages. We found that Citrobacter sp. isolated from mouse feces stoichiometrically decomposed urethane to ethanol and ammonia. We named this enzyme "urethanase." Partially purified urethanase could hydrolyze several carbamates and some amides. However, urea, N-alkyl ureas and ethyl esters of organic acids were not hydrolyzed at all. These results suggest that urethanase belongs to the category of amidase. The enzyme was inactive in high concentrations of alcohol and at acidic pH and was practically ineffective for the elimination of urethane from alcoholic beverages.

Animals↗
PubMed2006

Characterization of arylsulfatase formed by derepressed synthesis in Citrobacter braakii.

Arylsulfatase activity was detected in a bacterial strain, Citrobacter braakii 69-b, isolated from soil by enrichment cultivation using porcine gastric mucin. The production of arylsulfatase was derepressed markedly in a synthetic medium by the addition of tyramine. The purified enzyme hydrolyzed 4-nitrophenyl sulfate, 4-nitrocatechol sulfate, and 3-indoxyl sulfate, and was classified as type I arylsulfatase.

Arylsulfatases↗
PubMed1992

Characterization of membrane-bound spermidine dehydrogenase of Citrobacter freundii.

Spermidine dehydrogenase found in the membrane fraction of Citrobacter freundii IFO 12681 was solubilized with Triton X-100 and further purified to homogeneity. The properties of the membrane enzyme were almost identical to those obtained from the soluble fraction of the organism with respect to molecular and catalytic properties. Thus, binding properties of the enzyme to the bacterial membrane were checked. The ratio of enzyme activity found in the soluble fraction to the membrane fraction was dependent on salt concentration during cell disruption. A hydrophobic interaction was largely involved in anchoring the enzyme to the membrane fraction. Purified spermidine dehydrogenase from the soluble fraction was readily adsorbed into the membrane fraction in the presence of salt. Spermidine dehydrogenase appeared to be a membrane-bound enzyme localized in the cytoplasmic membranes in a manner that makes a partial release of the enzyme possible during mechanical cell disruption. When spermidine oxidation was done with the resting cells of C. freundii, a stoichiometric formation of two reaction products, 1,3-diaminopropane and gamma-aminobutyraldeyde, was observed without any lag time. These facts indicate that the enzyme is localized on the outer surface of the cytoplasmic membranes or in the periplasmic space of the organism.

Amino Acids↗
PubMed2002

Myocarditis in sibling boxer puppies associated with Citrobacter koseri infection.

Two sibling Boxer puppies presented with severe suppurative myocarditis in the absence of additional disseminated suppurative foci. The identification of gram-negative bacteria within areas of myocarditis in both puppies and the pure growth of large numbers of Citrobacter koseri from the myocardial lesions in one of the dogs were consistent with a bacterial etiology. The fact that C. koseri is an opportunist pathogen suggested intercurrent immunosuppression. The finding of a concomitant bacterial myocarditis in two canine siblings is novel. The case is also unusual in that syncope could be related to the myocardial injury.

Animals↗
PubMed2004

Detection of ticarcillin-clavulonic acid susceptibility with microdilution method in Citrobacter, Hafnia, Proteus and some gram negative bacteria.

The broth dilution method has been regarded as a good alternative test for detection of susceptibilities to antimicrobial agents. In this study, the antimicrobial activity of ticarcillin-clavulonic acid (TIM) was investigated by the minimal inhibitory concentration (MIC) method on strains of Aeromonas, Citrobacter, Hafnia, Morganella, Proteus, Pseudomonas and gram negative bacteria isolated from raw milk. The isolate collection included 91 gram negative strains. Fifty-one (56.04%) isolates were found sensitive (MIC < or = 8 microg/ml), 12 (13.19%) isolates were found intermediately sensitive (MIC 16-32 microg/ml), and 28 (30.77%) isolates were found resistant (MIC > or = 64 microg/ml) to TIM.

Aeromonas↗
PubMed2001

Comparison of bacteriological, genetic and pathological characters between Escherichia coli O115a,c:K(B) and Citrobacter rodentium.

Murine pathogenic Escherichia coli O115a,c:K(B) (MPEC) is the causative agent of mouse megaenteron, the pathology of which resembles that of transmissible murine colonic hyperplasia caused by Citrobacter rodentium. We compared their genetic and pathological features to reveal the relationship between these two bacteria. To evaluate the genetic distances, 16S rDNA genes were sequenced and biochemical reactions were tested. Mouse strain susceptibility tests, using CF1 MPEC-susceptible germfree mice and BALB/cA(Jic) resistant mice were performed. MPEC strains and C. rodentium showed more than 99.6% identity by comparison of 16S rDNA gene sequences. All results from biochemical reactions and the mouse strain susceptibility tests were identical. It is proposed that MPEC should be reclassified as C. rodentium.

Animals↗
PubMed2006

Diffuse pneumocephalus in neonatal Citrobacter meningitis.

Pneumocephalus, intracranial air or gas collection, associated with neonatal meningitis is extremely rare. We report the first case in the United States and the second case in the world of intracranial gas accumulation in a neonate with Citrobacter koseri meningitis. The clinical presentation was acute with pneumocephalus demonstrated by cranial sonography and computed tomography. The clinical course was fatal despite the prompt administration of antibiotics.

Citrobacter koseri↗
PubMed2000

Brain abscess by citrobacter diversus in infancy: case report.

Citrobacter diversus is closely related to brain abscess in newborn infants. We describe a case of brain abscess by this bacteria in a newborn infant and his clinical and cranial computed tomographic evaluation until the fourth month of life and discuss therapeutic management of this patient.

Brain Abscess↗
PubMed1980

Effect of a combination of benzylpenicillin or ampicillin and dicloxacillin on peptidoglycan synthesis in a cell-free enzyme system from a beta-lactamase producing strain of Citrobacter freundii.

The membrane fraction prepared from beta-lactamase producing Citrobacter freundii GN346 catalyzed in vitro peptidoglycan synthesis from uridine-5'-diphosphate-N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelyl- D-alanyl-D-alanine and uridine-5'-diphosphate-N-acetylglucosamine, which was accompanied by the release of alanine from the carboxyl terminal end of the former substrate. Though this reaction was inhibited by benzylpenicillin (PCG) and ampicillin (ABPC), the reaction was relatively insensitive compared with that catalyzed by the membrane fraction from a derived beta-lactamaseless mutant strain GN346/16. In contrast, the enzyme activity of the parent strain was strongly inhibited by a combination of PCG or ABPC and dicloxacillin (MDIPC). The beta-lactamase present in the membrane fraction from the parent strain showed stronger activity than that from the mutant strain, and the activity was inhibited by MDIPC as in the case of the soluble enzyme localized in the periplasmic space.

Ampicillin↗
PubMed1986

Delayed inactivation of Citrobacter freundii cephalosporinase by 6 beta-[3-(2-chlorophenyl)-5-methyl-4-isoxazolyl]penicillin sulfone.

When Citrobacter freundii cephalosporinase was incubated with 6 beta-[3-(2-chlorophenyl)-5-methyl-4-isoxazolyl]penicillin sulfone (cloxacillin sulfone) in phosphate buffer, the enzyme was suddenly inactivated just after the completion of enzymatic degradation of the cloxacillin sulfone. Such delayed inactivation was due to a secondary inhibitor formed from cloxacillin sulfone during the incubation period. The inactivation was delayed due to the protection of the enzyme by cloxacillin sulfone from the attack of the secondary inhibitor. Phosphate anions were essential for the formation of the secondary inhibitor. However, once the secondary inhibitor was formed, the inactivation occurred in the absence of phosphate anions although the degree of the inactivation depended on the length of the preincubation period with phosphate anions. The main species (more than 80%) of the inactivated enzyme was detected as a single protein band with a slightly lower pI value than that of the native enzyme on isoelectric focusing on a plate.

Buffers↗
PubMed1995

Effects of tazobactam on the frequency of the emergence of resistant strains from Enterobacter cloacae, Citrobacter freundii, and Proteus vulgaris (beta-lactamase derepressed mutants).

When Enterobacter cloacae, Citrobacter freundii, and Proteus vulgaris were treated with piperacillin (PIPC) in combination with tazobactam (TAZ), the in vitro frequency of emergence of resistant strains (beta-lactamase producing mutants) was lower than with PIPC or ceftazidime (CAZ) treated bacteria. In a mouse intraperitoneal infection model caused by E. cloacae, beta-lactamase derepressed mutants were detected following therapy with PIPC or CAZ, although no derepressed mutants were detected after treatment with PIPC in combination with TAZ. This suppression of the selection of derepressed mutants, which produce large amounts of beta-lactamases, by the combination of TAZ and PIPC suggests that the combination delays the increase of resistant mutants compared with PIPC alone.

Animals↗
PubMed2000

Comparison of antimicrobial susceptibility of Citrobacter freundii isolates in two different time periods.

Citrobacter freundii was first identified in 1932, since then it has been reported to cause a variety of infections in aged, immunocompromised, and debilitated patients. With the use of broad-spectrum antibiotics, C. freundii has become increasingly resistant to antimicrobial agents. In order to determine the chronological changes in susceptibility and current susceptibility status of C. freundii, we compared the antimicrobial susceptibility of C. freundii in two different time periods, from 1987 to 1988 and from 1997 to 1998. In both time periods, 61 isolates of C. freundii were randomly selected for study from all clinical isolates at National Taiwan University Hospital. The minimum inhibitory concentrations and susceptible rates of 15 antimicrobial agents were compared, and it was found that most C. freundii isolates were resistant to anti-pseudomonal penicillins, first, second, and third generation cephalosporins, gentamicin, tobramycin, and aztreonam. The results indicate that the susceptible rates of C. freundii to aminoglycosides and ciprofloxacin decreased markedly during the period from 1987 to 1998. Cefepime, cefpirome, imipenem, and meropenem remained the most active agents against C. freundii.

Citrobacter freundii↗