Kingella kingae strain:F41215CHC
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ABSTRACT:
PROVIDER: PRJNA577516 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Kingella kingae KKC2005004457 Genome sequencing
| PRJNA174413 | ENA
Project description:Kingella kingae 11220434 Genome sequencing and assembly
| PRJNA88539 | ENA
Project description:Whole genome sequenceing of Kingella kingae isolates from New Zealand.
| PRJNA644230 | ENA
Project description:Genome sequence of Kingella kingae septic arthritis isolate PYKK081
| PRJNA85111 | ENA
Project description:Kingella negevensis is a newly described gram-negative bacterium in the Neisseriaceae family and is closely related to Kingella kingae, an important cause of pediatric osteoarticular infections and other invasive diseases. Like K. kingae, K. negevensis can be isolated from the oropharynx of young children, although at a much lower rate. Due to the potential for misidentification as K. kingae, the burden of disease due to K. negevensis is currently unknown. Similarly, there is little known about virulence factors present in K. negevensis and how they compare to virulence factors in K. kingae. Using a variety of approaches, we show that K. negevensis produces many of the same putative virulence factors that are present in K. kingae, including a polysaccharide capsule, a secreted exopolysaccharide, a Knh-like trimeric autotransporter, and type IV pili, suggesting that K. negevensis may have significant pathogenic potential.
| S-EPMC7598479 | biostudies-literature
Project description:Kingella kingae is a betaproteobacterium from the order Neisseriales, and it is an agent of invasive infections in children. We sequenced the genome from the septic arthritis strain 11220434. It is composed of a 1,990,794-bp chromosome but no plasmid, and it contains 2,042 protein-coding genes and 52 RNA genes, including 3 rRNA genes.
| S-EPMC3486087 | biostudies-literature
Project description:Kingella bonacorsii strain:Marseille-Q4569 Genome sequencing and assembly
| PRJNA685311 | ENA
Project description:Cell-free extracts prepared from Kingella kingae colony biofilms were found to inhibit biofilm formation by Aggregatibacter actinomycetemcomitans, Klebsiella pneumoniae, Staphylococcus aureus, Staphylococcus epidermidis, Candida albicans, and K. kingae. The extracts evidently inhibited biofilm formation by modifying the physicochemical properties of the cell surface, the biofilm matrix, and the substrate. Chemical and biochemical analyses indicated that the biofilm inhibition activity in the K. kingae extract was due to polysaccharide. Structural analyses showed that the extract contained two major polysaccharides. One was a linear polysaccharide with the structure ?6)-?-d-GlcNAcp-(1?5)-?-d-OclAp-(2?, which was identical to a capsular polysaccharide produced by Actinobacillus pleuropneumoniae serotype 5. The second was a novel linear polysaccharide, designated PAM galactan, with the structure ?3)-?-d-Galf-(1?6)-?-d-Galf-(1?. Purified PAM galactan exhibited broad-spectrum biofilm inhibition activity. A cluster of three K. kingae genes encoding UDP-galactopyranose mutase (ugm) and two putative galactofuranosyl transferases was sufficient for the synthesis of PAM galactan in Escherichia coli. PAM galactan is one of a growing number of bacterial polysaccharides that exhibit antibiofilm activity. The biological roles and potential technological applications of these molecules remain unknown.
| S-EPMC3147541 | biostudies-literature
Project description:The Gram-negative bacterium Kingella kingae is part of the normal oropharyngeal mucosal flora of children <4 years old. K. kingae can enter the submucosa and cause infections of the skeletal system in children, including septic arthritis and osteomyelitis. The organism is also associated with infective endocarditis in children and adults. Although biofilm formation has been coupled with pharyngeal colonization, osteoarticular infections, and infective endocarditis, no studies have investigated biofilm formation in K. kingae. In this study we measured biofilm formation by 79 K. kingae clinical isolates using a 96-well microtiter plate crystal violet binding assay. We found that 37 of 79 strains (47%) formed biofilms. All strains that formed biofilms produced corroding colonies on agar. Biofilm formation was inhibited by proteinase K and DNase I. DNase I also caused the detachment of pre-formed K. kingae biofilm colonies. A mutant strain carrying a deletion of the pilus gene cluster pilA1pilA2fimB did not produce corroding colonies on agar, autoaggregate in broth, or form biofilms. Biofilm forming strains have higher levels of pilA1 expression. The extracellular components of biofilms contained 490 ?g cm-2 of protein, 0.68 ?g cm-2 of DNA, and 0.4 ?g cm-2 of total carbohydrates. We concluded that biofilm formation is common among K. kingae clinical isolates, and that biofilm formation is dependent on the production of proteinaceous pili and extracellular DNA. Biofilm development may have relevance to the colonization, transmission, and pathogenesis of this bacterium. Extracellular DNA production by K. kingae may facilitate horizontal gene transfer within the oral microbial community.
| S-EPMC5384882 | biostudies-literature