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We have reported the third case of Citrobacter endocarditis. Echocardiograms were invaluable in establishing the diagnosis. Ours is the first reported case of Citrobacter endocarditis to be cured by antimicrobial therapy alone.
Out of 19 strains belonging to the family Enterobacteriaceae only Escherichia coli and Citrobacter strains fermented fumarate exclusively to succinate. This fermentation was dependent on the presence of molecular hydrogen or formate. The inability of these micro-organisms to convert fumarate to succinate, acetate and CO2 correlated with their lack, or low activity, of oxaloacetate decarboxylase. Continuous culture experiments were performed with Citrobacter freundii in minimal or complex medium with fumarate + H2 of formate, and the growth parameters were determined. From the data obtained, a Ymax fumarate dissimilated value of 10.5 +/- 0.8 g dry wt per mol fumarate dissimilated was calculated. This value demonstrates that, per mol fumarate reduced, at least 0.6 +/- 0.05 mol ATP is produced and subsequently used for biosynthetic purposes.
Septic arthritis in an 8 month old infant due to Citrobacter freundii was treated successfully with a third generation cephalosporin. Infections due to Citrobacter are uncommon in this age group and are almost unknown as a cause of septic arthritis.
A 3-week-old infant developed left shoulder swelling and was found to have septic arthritis and osteomyelitis of the humerus caused by Citrobacter koseri (formerly C. diversus). Citrobacter species are Gram-negative rods that are best known for their propensity to cause neonatal meningitis, ventriculitis and concomitant brain abscess. Non-central nervous system infections are rare. The present case illustrates that neonatal osteomyelitis caused by unusual organisms can present to pediatricians in an inner-city setting, and can respond favorably to surgical and medical management.
O-specific-polysaccharide and core oligosaccharide were isolated from Citrobacter strain PCM 1487 lipopolysaccharide and purified. The polysaccharide was selectively devoid of 4-deoxy-D-arabinohexose residues. Covalent conjugates of the modified O-specific polysaccharide and of the core oligosaccharide with tetanus toxoid were prepared. Immunochemical characterization of these conjugates proved that they are strong immunogens. Using monospecific rabbit antisera raised against the conjugates, the antigenic relationships between lipopolysaccharides of various strains of Citrobacter, Shigella sonnei, and Shigella flexneri were studied by quantitative microprecipitin and quantitative microprecipitin inhibition and immunoblotting tests.
A Citrobacter sp. was reported previously to accumulate heavy metals as cell-bound heavy metal phosphates. Metal uptake is mediated by the activity of a periplasmic acid-type phosphatase that liberates inorganic phosphate to provide the precipitant ligand for heavy metals presented to the cells. Amino acid sequencing of peptide fragments of the purified enzyme revealed significant homology to the phoN product (acid phosphatase) of some other enterobacteria. These organisms, together with Klebsiella pneumoniae, previously reported to produce acid phosphatase, were tested for their ability to remove uranium and lanthanum from challenge solutions supplemented with phosphatase substrate. The coupling of phosphate liberation to metal bioaccumulation was limited to the metal accumulating Citrobacter sp.; therefore the participation of species-specific additional factors in metal bioaccumulation was suggested.
During the course of an antimicrobial resistance surveillance programme in Guangzhou, the People's Republic of China, single strains of Citrobacter youngae and Pseudomonas aeruginosa were identified which were resistant to imipenem and found to carry the carbapenemase gene bla(IMP). PCR screening of the citrobacter strain with specific primers for the bla(IMP) type genes gave a 587-bp product which when sequenced gave 100% homology with the bla(IMP-4) sequence reported recently from Acinetobacter spp. The determinant in the C. youngae strain was found to be located on a 156-kb plasmid capable of transfer to Escherichia coli UB1637 by conjugation. Sequencing of the bla(IMP-4) open reading frame in the C. youngae strain and adjacent sequences not only confirmed the presence of bla(IMP-4) but also identified that a conserved core site found within the 59-bp element of integrons was present and the same as the one described in the only other occurrence of bla(IMP-4) in Acinetobacter spp. isolated from an intensive care unit in Hong Kong. This is the second report of transferable carbapenemase genes in Enterobacteriaciae outside of Japan and the first in the People's Republic of China. Under the selective pressure of carbapenems and extended spectrum cephalosporins use we might expect this gene to spread and widespread surveillance should be instituted.
Citrobacter diversus is a cause of severe meningitis in neonates and infants. It is unique in its propensity to produce brain abscesses that play an important role in the poor prognosis associated with this condition. The recommended therapeutic regimen of third-generation cephalosporines, aminoglycosides and trimethoprim-sulfamethoxazole is usually disappointing. We describe the use of imipenemcilastatin in successfully treating Citrobacter diversus meningitis complicated by brain abscesses.
The resistance types of Citrobacter freundii were investigated. The strains were divided into three groups according to susceptibility to penicillin derivatives. Group 1, comprising the ampicillin-carbenicillin sensitive strains (A-s/Ca-s), constituted 22%. Group 2 (ampicillin-resistant (A-r)/Ca-s) constituted 45% and group 3 (A-r/Ca-r) 32%. Two strains (1%) were recorded as A-s/Ca-r. Group 3 contained a higher proportion of multi-resistant strains than groups 1 and 2. The log2IC50 with ampicillin, carbenicillin, cephalothin and mecillinam in the tube-dilution method were determined for 32 strains. Groups 1 and 2 differed only as regards cephalothin resistance. The strains of group 3 were more A-r than the group 2 ones. The mecillinam susceptibility did not differ between the three groups. No strains in group 2 could transfer A-resistance. In group 3 ten out of 16 strains were able to transfer A-resistance. Resistance to sulphonamide, tetracycline, and streptomycin was also transferred, but with low frequency. The A-r/Ca-r strains could be divided into two subgroups, probably reflecting different modes of developing beta-lactam resistance. One group was very A- and Ca-r, less cephalothin-r, more mecillinam-r and could transfer A-resistance. The other group had very high cephalothin-resistance and could not transfer A-resistance. Citrobacter freundii and Enterobacter cloacae are very similar as regards resistance conditions.
The predominant beta-lactam antibiogram of Citrobacter freundii resembles that of Enterobacter cloacae in demonstrating resistance to cephalothin and cefoxitin with susceptibility to the newer cephalosporins. Four representative strains of C. freundii were reversibly induced to high-level beta-lactamase production by cefoxitin, and mutants with stable, high-level production were selected with cefamandole. The mutants were resistant to several second- and third-generation cephalosporins. Comparisons of isoelectric points and substrate profiles of beta-lactamases from wild-type, induced wild-type, and mutant organisms suggested a close relationship to those from E. cloacae and indicated that C. freundii mutants, like those of E. cloacae, were derepressed for production of beta-lactamase. One primary isolate of C. freundii resembled the mutants in all characteristics. In contrast, most strains of Citrobacter diversus were susceptible to all cephalosporins, and two representative strains showed neither inducible nor mutational resistance. Cefoxitin induction to enhanced beta-lactamase production was demonstrated in a cephalothin-resistant isolate, and a derepressed mutant was selected with cefotaxime. The beta-lactamase from this C. diversus strain differed substantially in substrate profile from that of E. cloacae and C. freundii.
The in vitro activities of 16 antimicrobial agents against 14 clinical isolates of Citrobacter diversus and 27 isolates of Citrobacter freundii were studied. C. freundii isolates were more resistant, being susceptible only to amikacin, netilmicin, gentamicin, imipenem, ciprofloxacin, and enoxacin. C. diversus isolates were susceptible to many more of the agents tested.
The family of attaching and effacing (A/E) bacterial pathogens, which includes diarrheagenic enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC), remains a significant threat to human and animal health. These bacteria intimately attach to host intestinal cells, causing the effacement of brush border microvilli. The genes responsible for this phenotype are encoded in a pathogenicity island called the locus of enterocyte effacement (LEE). Citrobacter rodentium is the only known murine A/E pathogen and serves as a small animal model for EPEC and EHEC infections. Here we report the full DNA sequence of C. rodentium LEE and provide a comparative analysis with the published LEEs from EPEC, EHEC, and the rabbit diarrheagenic E. coli strain RDEC-1. Although C. rodentium LEE shows high similarities throughout the entire sequence and shares all 41 open reading frames with the LEE from EPEC, EHEC, and RDEC-1, it is unique in its location of the rorf1 and rorf2/espG genes and the presence of several insertion sequences (IS) and IS remnants. The LEE of EPEC and EHEC is inserted into the selC tRNA gene. In contrast, the Citrobacter LEE is flanked on one side by an operon encoding an ABC transport system, and an IS element and sequences homologous to Shigella plasmid R100 and EHEC pO157 flank the other. The presence of plasmid sequences next to C. rodentium LEE suggests that the prototype LEE resided on a horizontally transferable plasmid. Additional sequence analysis reveals that the 3-kb plasmid in C. rodentium is nearly identical to p9705 in EHEC O157:H7, suggesting that horizontal plasmid transfer among A/E pathogens has occurred. Our results indicate that the LEE has been acquired by C. rodentium and A/E E. coli strains independently during evolution.
A unique feature of Citrobacter koseri is the extremely high propensity to initiate brain abscesses during neonatal meningitis. Previous clinical reports and studies on infant rats have documented many Citrobacter-filled macrophages within the ventricles and brain abscesses. It has been hypothesized that intracellular survival and replication within macrophages may be a mechanism by which C. koseri subverts the host response and elicits chronic infection, resulting in brain abscess formation. In this study, we showed that C. koseri causes meningitis and brain abscesses in the neonatal rat model, and we utilized histology and magnetic resonance imaging technology to visualize brain abscess formation. Histology and electron microscopy (EM) revealed that macrophages (and not fibroblasts, astrocytes, oligodendrocytes, or neurons) were the primary target for long-term C. koseri infection. To better understand C. koseri pathogenesis, we have characterized the interactions of C. koseri with human macrophages. We found that C. koseri survives and replicates within macrophages in vitro and that uptake of C. koseri increases in the presence of human pooled serum in a dose-dependent manner. EM studies lend support to the hypothesis that C. koseri uses morphologically different methods of uptake to enter macrophages. FcgammaRI blocking experiments show that this receptor primarily facilitates the entry of opsonized C. koseri into macrophages. Further, confocal fluorescence microscopy demonstrates that C. koseri survives phagolysosomal fusion and that more than 90% of intracellular C. koseri organisms are colocalized within phagolysosomes. The ability of C. koseri to survive phagolysosome fusion and replicate within macrophages may contribute to the establishment of chronic central nervous system infection including brain abscesses.
Citrobacter freundii cells produce L-methionine gamma-lyase when grown on a medium containing L-methionine. The nucleotide sequence of the hybrid plasmid with a C. freundii EcoRI insert of about 3.0 kbp contained two open reading frames, consisting of 1,194 nucleotides and 1,296 nucleotides, respectively. The first one (denoted megL) encoded L-methionine gamma-lyase. The enzyme was overexpressed in Escherichia coli and purified. The second frame encoded a protein belonging to the family of permeases. Regions of high sequence identity with the 3'-terminal part of the C. freundii megL gene located in the same regions of Salmonella enterica serovar Typhimurium, Shigella flexneri, E. coli, and Citrobacter rodentium genomes were found.
Over a 6-month period, eight strains of Citrobacter diversus (Citrobacter koseri) resistant to extended-spectrum cephalosporins and monobactams were isolated from seven colonized and/or infected patients from the same intensive care unit. All strains harbored a single large conjugative plasmid which mediated an extended-spectrum beta-lactamase of the SHV-4 type (ceftazidimase phenotype; enzyme pI, 7.8; plasmid DNA hybridization with a blaSHV-specific probe). All strains were characterized by antibiotic resistance pattern analysis, beta-lactamase content analysis, plasmid profiling, ribotyping with EcoRI, and arbitrarily primed (AP)-PCR with primers O8 and O12. Among the eight C. diversus strains, strains Cd5 to Cd12, six isolates (isolates Cd6 to Cd11) were identical by all markers; one strain (strain Cd5) differed by two markers (antibiotype and AP-PCR pattern with primer O8), and the remaining strain (strain Cd12) differed by two other markers (ribotype and AP-PCR pattern with primer O12). Our results suggest that six of the eight SHV-4-producing C. diversus strains studied (strains Cd6 to Cd11) were a single epidemic strain. Strain Cd5 could be related to the epidemic strain; the origin of strain Cd12 remains uncertain.
We report bilateral cerebellar abscesses in a neonate with Citrobacter freundii meningitis. The mortality and morbidity of Citrobacter abscess is high. Rapidly developing drug resistance may play a role as illustrated by our case.
There are increasing reports of citrobacter central nervous system infections in neonates. These organisms cause brain abcesses in a high percentage of patients. They may be resistant to commonly used antibiotics. We report a term male infant with underlying meningo-myelocoele and hydrocephalus in whom Citrobacter diversus meningitis and ventriculitis developed. Initial antibiotic therapy including intraventricular amikacin failed to sterilize the ventricles or alter a deteriorating clinical course. Adding intravenous trimethoprim-sulfamethoxazole to the therapeutic regimen resulted in reversal of a progressively worsening condition and eventual recovery. Trimethoprim-sulfamethoxazole should be considered as a potentially useful alternative antibiotic for susceptible central nervous system infections.
A 4-month-old Maltese puppy and a 7.5-year-old Collie were diagnosed with septicemia associated with Citrobacter freundii. The puppy died soon, after developing weakness and mucohemorragic diarrhea. The Collie had immune-mediated hemolytic anemia and thrombocytopenia and was treated with immunosuppressive drugs before being euthanized. Gross examination of the puppy revealed mucohemorrhagic intestinal contents. Focal necrotic hepatitis, fibrinous peritonitis, interstitial pneumonia, and hemorrhagic gastrointestinal contents were observed in the older dog. Histologically, there was a diffuse, moderate, histiocytic meningitis in the puppy and a focal fibrinonecrotic hepatitis in the adult dog. Lesions in both dogs contained numerous gram-negative rods. Citrobacter freudii is a potential cause of monomicrobic bacteraemia-septicemia in puppies or immunocompromized adult dogs. The gastrointestinal tract is probably the main site of entry.