Understanding the role of different strain types of Fusobacterium necrophorum: biofilms, glycans and metabolic pathways
type: CreativeWork
description: Fusobacterium necrophorum an obligate Gram-negative anaerobe has been implicated in the cause of persistent severe throat infections and the systemic life-threatening Lemierre’s syndrome; a potentially fatal periodontal disease, which results in abscess formation in the tonsils. The use of antibiotics had led to decreased incidence of F. necrophorum infections to a point that the bacterium became a forgotten pathogen; however, there has recently been a rise in interest. F. necrophorum is thought to survive the aerobic oropharynx by biofilm formation. Studies of optimal conditions for biofilm formation could be useful in improving therapeutic options. This current study determined that strains ARU 01 and JCM 3718 formed the most biofilm at 37 °C, with reduction in biofilm observed at 26 °C and 42 °C. Strain JCM 3724 on the other hand, formed most biofilm at 26 °C and 42 °C; this is an indication that strain JCM 3724 but not JCM 3718 or ARU 01 was able to survive in extreme temperatures by forming biofilms; all strains produced more biofilm at pH 4. Biofilm formation was observed in both mono and dual species culture of F. necrophorum, in dual culture the organisms became resistant to penicillin and ciprofloxacin. As glycans are implicated in biofilm formation, bacterial adhesion to host cells and pathogenicity, the cell surface glycans and cell extracts of F. necrophorum were investigated using enzyme-linked lectin assays (ELLA) and lectin histochemical staining. No significant differences were seen in the staining patterns, but a patchy and variable staining was noted for Sambucus nigra that detects sialic acid. A surface lectin, the Galactose binding protein was identified and characterised as binding to unsubstituted beta galactosyl residues of the type carried by many bacteria suggesting a role in biofilm formation. Subsequent molecular and bioinformatic studies identified all but one key component of the lipid A pathway; lpxI was shown to substitute for lpxH in …
abstract: Fusobacterium necrophorum an obligate Gram-negative anaerobe has been implicated in the cause of persistent severe throat infections and the systemic life-threatening Lemierre’s syndrome; a potentially fatal periodontal disease, which results in abscess formation in the tonsils. The use of antibiotics had led to decreased incidence of F. necrophorum infections to a point that the bacterium became a forgotten pathogen; however, there has recently been a rise in interest. F. necrophorum is thought to survive the aerobic oropharynx by biofilm formation. Studies of optimal conditions for biofilm formation could be useful in improving therapeutic options. This current study determined that strains ARU 01 and JCM 3718 formed the most biofilm at 37 °C, with reduction in biofilm observed at 26 °C and 42 °C. Strain JCM 3724 on the other hand, formed most biofilm at 26 °C and 42 °C; this is an indication that strain JCM 3724 but not JCM 3718 or ARU 01 was able to survive in extreme temperatures by forming biofilms; all strains produced more biofilm at pH 4. Biofilm formation was observed in both mono and dual species culture of F. necrophorum, in dual culture the organisms became resistant to penicillin and ciprofloxacin. As glycans are implicated in biofilm formation, bacterial adhesion to host cells and pathogenicity, the cell surface glycans and cell extracts of F. necrophorum were investigated using enzyme-linked lectin assays (ELLA) and lectin histochemical staining. No significant differences were seen in the staining patterns, but a patchy and variable staining was noted for Sambucus nigra that detects sialic acid. A surface lectin, the Galactose binding protein was identified and characterised as binding to unsubstituted beta galactosyl residues of the type carried by many bacteria suggesting a role in biofilm formation. Subsequent molecular and bioinformatic studies identified all but one key component of the lipid A pathway; lpxI was shown to substitute for lpxH in …
author: Brimah, K.
date published: 2019
date modified: 2026-07-24T06:01:33Z
provider: University of Westminster
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: University of Westminster

PropertyValue
property ID: DOI
value: 10.34737/qzxy2