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PubMed2002

Mutations in Flavobacterium johnsoniae gldF and gldG disrupt gliding motility and interfere with membrane localization of GldA.

Flavobacterium johnsoniae moves rapidly over surfaces by a process known as gliding motility. The mechanism of this form of motility is not known. Four genes that are required for F. johnsoniae gliding motility, gldA, gldB, gldD, and ftsX, have recently been described. GldA is similar to the ATP-hydrolyzing components of ATP binding cassette (ABC) transporters. Tn4351 mutagenesis was used to identify two additional genes, gldF and gldG, that are required for cell movement. gldF and gldG appear to constitute an operon, and a Tn4351 insertion in gldF was polar on gldG. pMK314, which carries the entire gldFG region, restored motility to each of the gldF and gldG mutants. pMK321, which expresses GldG but not GldF, restored motility to each of the gldG mutants but did not complement the gldF mutant. GldF has six putative membrane-spanning segments and is similar in sequence to channel-forming components of ABC transporters. GldG is similar to putative accessory proteins of ABC transporters. It has two apparent membrane-spanning helices, one near the amino terminus and one near the carboxy terminus, and a large intervening loop that is predicted to reside in the periplasm. GldF and GldG are involved in membrane localization of GldA, suggesting that GldA, GldF, and GldG may interact to form a transporter. F. johnsoniae gldA is not closely linked to gldFG, but the gldA, gldF, and gldG homologs of the distantly related gliding bacterium Cytophaga hutchinsonii are arranged in what appears to be an operon. The exact roles of F. johnsoniae GldA, GldF, and GldG in gliding are not known. Sequence similarities of GldA to components of other ABC transporters suggest that the Gld transporter may be involved in export of some material to the periplasm, outer membrane, or beyond.

ATP-Binding Cassette Transporters↗
PubMed2004

GldI is a lipoprotein that is required for Flavobacterium johnsoniae gliding motility and chitin utilization.

Cells of Flavobacterium johnsoniae glide rapidly over surfaces by an unknown mechanism. Seven genes (gldA, gldB, gldD, gldF, gldG, gldH, and ftsX) that are required for gliding motility have been described. Complementation of the nonmotile mutants UW102-41, UW102-85, and UW102-92 identified another gene, gldI, that is required for gliding motility. gldI mutants formed nonspreading colonies, and individual cells were completely nonmotile. They were also resistant to bacteriophages that infect wild-type cells, and they failed to digest chitin. Introduction of wild-type gldI on a plasmid restored colony spreading, cell motility, phage sensitivity, and the ability to digest chitin to the gldI mutants. gldI encodes a predicted 199-amino-acid protein that localized to the membrane fraction. Labeling studies with [(3)H]palmitate indicated that GldI is a lipoprotein. GldI is similar to peptidyl-prolyl cis/trans-isomerases of the FK506-binding protein family and may be involved in folding cell envelope protein components of the motility machinery.

Amino Acid Sequence↗
PubMed2005

Flavobacterium johnsoniae gliding motility genes identified by mariner mutagenesis.

Cells of Flavobacterium johnsoniae glide rapidly over surfaces. The mechanism of F. johnsoniae gliding motility is not known. Eight gld genes required for gliding motility have been described. Disruption of any of these genes results in complete loss of gliding motility, deficiency in chitin utilization, and resistance to bacteriophages that infect wild-type cells. Two modified mariner transposons, HimarEm1 and HimarEm2, were constructed to allow the identification of additional motility genes. HimarEm1 and HimarEm2 each transposed in F. johnsoniae, and nonmotile mutants were identified and analyzed. Four novel motility genes, gldK, gldL, gldM, and gldN, were identified. GldK is similar in sequence to the lipoprotein GldJ, which is required for gliding. GldL, GldM, and GldN are not similar in sequence to proteins of known function. Cells with mutations in gldK, gldL, gldM, and gldN were defective in motility and chitin utilization and were resistant to bacteriophages that infect wild-type cells. Introduction of gldA, gldB, gldD, gldFG, gldH, gldI, and gldJ and the region spanning gldK, gldL, gldM, and gldN individually into 50 spontaneous and chemically induced nonmotile mutants restored motility to each of them, suggesting that few additional F. johnsoniae gld genes remain to be identified.

Bacteriophages↗
PubMed2005

Flavobacterium johnsoniae GldJ is a lipoprotein that is required for gliding motility.

Cells of Flavobacterium johnsoniae glide rapidly over surfaces by an unknown mechanism. Eight genes required for gliding motility have been described. Complementation of the nonmotile mutant UW102-48 identified another gene, gldJ, that is required for gliding. gldJ mutants formed nonspreading colonies, and individual cells were completely nonmotile. Like previously described nonmotile mutants, gldJ mutants were deficient in chitin utilization and were resistant to bacteriophages that infect wild-type cells. Cell fractionation and labeling studies with [(3)H]palmitate indicated that GldJ is a lipoprotein. Mutations in gldA, gldB, gldD, gldF, gldG, gldH, or gldI resulted in normal levels of gldJ transcript but decreased levels of GldJ protein. Expression of truncated GldJ protein in wild-type cells resulted in a severe motility defect. GldJ was found in regular bands that suggest the presence of a helical structure within the cell envelope.

Bacteriophages↗
PubMed1967

Aflatoxin B 1 uptake by Flavobacterium aurantiacum and resulting toxic effects.

Removal of aflatoxin B(1) from liquid cultures by resting and growing cells of Flavobacterium aurantiacum NRRL B-184 was studied. Spectrophotometic and thin-layer techniques served as aflatoxin assays. Cells grown in the presence of 5 ppm or higher levels of aflatoxin developed aberrant morphological forms. These toxin concentrations partially inhibited growth, and the nature of the inhibition suggested that aflatoxin interfered with cell wall synthesis. Incubation of 1.0 x 10(11) resting cells per milliliter with 7.0 mug/ml of aflatoxin B(1) during a 4-hr period facilitated complete toxin removal from a buffered aqueous medium. Autoclaved cells and cell wall preparations could remove a fraction of the aflatoxin of a test system. However, the toxin removed by autoclaved cells and cell walls could be extracted by washing with water but the aflatoxin B(1) removed by intact cells could not be extracted into the liquid phase. The uptake of aflatoxin B(1) by resting cells was sensitive to temperature and pH. Ruptured preparations of F. aurantiacum were not able to remove or modify the aflatoxin in an aqueous solution.

Aflatoxins↗
PubMed1983

Patterns of extracellular proline-specific endopeptidases in Legionella and Flavobacterium spp. demonstrated by use of chromogenic peptides.

Some Legionella strains possess a strong extracellular proline-specific endopeptidase (PSE) activity. Using an enlarged selection of chromogenic peptides representing a variety of N-terminal amino-acids binding to a -prolyl-proline, paranitroanilide chain, PSE activity of Legionella and Flavobacterium strains was examined. Differences in PSE activity emphasized the importance of the chemical structure at the nonchromogenic end of the peptide substrates. There seem to be distinct patterns of N-terminal specificity of PSE in the two bacterial groups.

Chromogenic Compounds↗
PubMed1990

Recovery of an unusual Flavobacterium group IIb-like isolate from a hand infection following pig bite.

An unusual gram-negative rod (RMA 1571) was isolated from a hand infection following a pig bite. This unclassified isolate was characterized by growth requirements, microscopic examination, biochemical characteristics, antimicrobial susceptibility tests, and cellular fatty acid analysis. It was indole positive and produced yellow-pigmented growth, which placed it in the genus Flavobacterium, but its other features, including cellular fatty acid analysis, did not appear to be those of a named species.

Animals↗
PubMed1994

Flavobacterium meningosepticum, a pathogen in birds.

Five bacterial isolates were recovered from various diseased birds (chickens, a pigeon, and a zebra finch) and were identified as Flavobacterium meningosepticum. Four of them were isolated in pure or nearly pure culture of samples from internal organs, and one strain was isolated in mixed culture of a tarsal joint fluid sample. Except for the last case, there was no evidence of other disease agents. By using phenotypic, chemotaxonomic, and genomic methods, the strains were taxonomically characterized and could not be differentiated from the human clinical reference strains of the species. Two avian strains were different in their phenotypic behaviors and constituted another genotypic subgroup. In general, all F. meningosepticum strains constituted a single species which was easily differentiated from biochemically similar species and phylogenetically closely related taxa.

Animals↗
PubMed1994

Ribotyping for differentiating Flavobacterium meningosepticum isolates from clinical and environmental sources.

On the basis of DNA-DNA hybridization data, two main genomic relatedness groups (I and II) have been reported for a geographically varied collection of 52 strains of Flavobacterium meningosepticum. Herein, we have shown that genomic group II can be further divided into four subgroups (II:1 to II:4). To examine the taxonomic relevance of the ribosomal patterns of the 52 F. meningosepticum strains, the patterns were compared with existing DNA-DNA hybridization data with restriction enzymes PstI and HindIII. Ribotyping of the 52 F. meningosepticum strains showed banding patterns that could identify them correctly to one of the five genomic groups or subgroups. To assess the value of ribotyping for the interpretation of epidemiological data, the discriminatory power of the method was investigated for the 52 F. meningosepticum strains. With one to four restriction enzymes (PstI, HindIII, ClaI, EcoRI), a discriminatory index of 0.95 to 0.97 was found. The value of ribotyping in an epidemiological setting was assessed for three clinical isolates of F. meningosepticum from an outbreak of meningitis and bacteremia in the neonatal intensive care unit, Rigshospitalet, Copenhagen, Denmark. The three clinical isolates were shown to belong to the same ribotype, characteristic of genomic subgroup II:1. This ribotyping method will prove to be a useful tool for epidemiological studies concerning F. meningosepticum in the future.

Bacteremia↗
PubMed1996

Clinical and microbiological characteristics of Flavobacterium indologenes infections associated with indwelling devices.

Clinical infections caused by Flavobacterium indologenes have never been documented. Thirteen isolates derived from seven patients with indwelling device-associated F. indologenes infections were identified from 1 April through 30 November 1995. The antimicrobial susceptibilities to 20 antimicrobial agents of the isolates, the cellular fatty acid chromatograms for the isolates, and the random amplified polymorphic DNA (RAPD) patterns generated by arbitrarily primed PCR of the isolates were studied. The antibiotypes and RAPD patterns differed among the isolates recovered from different patients. However, both antibiotypes and RAPD patterns were identical among the five isolates from one patient with multiple episodes of central venous catheter-associated bacteremia within a 1.5-month period and between the two isolates from another patient suffering from two episodes of catheter-related bacteriuria at an interval of 14 days. It is documented that the recurrent infections in each of these two patients were caused by a single F. indologenes clone, respectively. Identical antibiotypes and RAPD patterns were also demonstrated between two isolates from a patient with ventilator-associated pneumonia, one recovered from an endotracheal aspirate and the other derived from a blood specimen 10 days later, indicating the invasive nature of F. indologenes. Two cellular fatty acid chromatograms were identified among these isolates. All of the isolates showed in vitro resistance to cephalothin, cefotaxime, ceftriaxone, moxalactam, aztreonam, aminoglycosides, erythromycin, clindamycin, vancomycin, and teicoplanin. F. indologenes should be included as an etiologic agent of infections associated with the use of indwelling devices.

Adult↗
PubMed1997

Comparison of Etest and agar dilution method for antimicrobial susceptibility testing of Flavobacterium isolates.

The Etest was evaluated as a possible alternative to the standard agar dilution method for susceptibility testing of nine antimicrobial agents against Flavobacterium species. In studies of 100 clinical isolates, the agreement between the MICs (+/-1 log2 dilution) obtained by the two methods was acceptable for cefotaxime, ceftazidime, amikacin, minocycline, ofloxacin, and ciprofloxacin (> 90%). Conversely, the agreement between the results obtained for piperacillin was limited (84%). The overall agreement was 92.5%.

Anti-Bacterial Agents↗
PubMed1977

Two outbreaks of Flavobacterium meningosepticum type E in a neonatal intensive care unit.

Two separate outbreaks due to Flavobacterium meningosepticum type E occurred in a neonatal intensive care unit in March-April and July 1975. The first outbreak involved all five infants in the unit. Two infants developed meningitis, one had bacteremia, and two were colonized. During the second outbreak, five of seven infants were colonized but none developed disease. The upper respiratory tract was colonized first in most instances, and the organism persisted at this site for a mean of 17.3 days. Duration of colonization was more prolonged in infants receiving antibiotics than in untreated infants. Extensive environmental surveillance failed to demonstrate a reservoir, however, F. meningosepticum was recovered from three nasoendotracheal tubes and from an aerosol tube before colonization of four infants. The organism was resistant to most antimicrobial colonization of four infants. The organism was resistant to most antimicrobial agents tested and developed resistance to others during the treatment course of one infant. Although F. meningosepticum was not recovered from cultures of transport vehicles, several other gram-negative bacteria were isolated and were also resistant to multiple antibiotics.

Anti-Bacterial Agents↗
PubMed1984

Trimethoprim sulphamethoxazole in neonatal Flavobacterium meningosepticum infection.

During an outbreak of Flavobacterium meningosepticum septicaemia in a neonatal intensive care unit 9 infants were treated with intravenous trimethoprim sulphamethoxazole. Bacteriological cure was achieved in 8 patients; one infant died of massive intraventricular haemorrhage on the first day of treatment. Apart from prolonged persistence of pre-existing thrombocytopenia there was no evidence of side effects. Trimethoprim sulphamethoxazole should be considered in the treatment of neonatal F meningosepticum sepsis in view of its activity against this organism, good penetration of the blood brain barrier, and the absence of serious side effects.

Bacterial Infections↗
PubMed1973

Flavobacterium meningosepticum from cases of meningitis in Botswana and England.

Two strains of Flavobacterium meningosepticum isolated from cases of meningitis are described. One was isolated in Botswana from a man with an aplastic anaemia, the other in the UK from an infant who was probably infected in Bangladesh. The severity of the infection, the characterization of the organism, and the possibility that infection may be found in the UK are discussed.

Adult↗
PubMed1976

Flavobacterium meningosepticum in the hospital environment.

Ten strains of Flavobacterium meningosepticum were isolated from routine clinical material during a period of two years. Of a number of antibiotics tested, clindamycin was the only one to which they were fully sensitive. The organism was found in chlorhexidine gluconate (Hibitane) solutions in use on the wards for the storage of thermometers and for routine disinfection.

Adolescent↗