8.11E: Fusobacteria - Biology

8.11E: Fusobacteria - Biology

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Fusobacterium are anaerobic, non-spore forming, gram-negative bacteria that are associated with periodontal disease and Lemierre’s syndrome.

Learning Objectives

  • Describe the role of Fusobacterium in Lemierre’s syndrome

Key Points

  • Fusobacterium flourish in anaerobic conditions.
  • Fucosbacterium necrophorum are responsible for causing Lemierre’s syndrome which is characterized by thrombophlebitis.
  • Identification of Fusobacterium within the laboratory is difficult due to their asaccharolytic nature; however, advancements in molecular technology has resulted in identification of numerous species.

Key Terms

  • periodontal disease: disease surrounding a tooth
  • asaccharolytic: incapable of metabolizing carbohydrates
  • septicemia: presence of pathogenic organisms in the bloodstream leading to sepsis

Fusobacteria are a genus of bacteria categorized as gram-negative with similarities to Bacteroides. Fusobacteria are rod-shaped bacilli capable of thriving in anaerobic conditions. However, in contrast to Bacteroides, Fusobacterium have a potent lipopolysaccharide that can function as an endotoxin. The Fusobacterium are associated with infection and disease including periodontal diseases, topical skin ulcers and Lemierres’s syndrome. Fusobacterium are difficult to identify in the laboratory due to their asaccharolytic nature. However, the use of novel molecular biology techniques has allowed for the the identification of new species that are included in Fusobacterium. The diseases attributed to Fusobacterium infection involve symptoms that include tissue necrosis, septicemia, intra-amniotic infections and ulcers.

A specific disease caused by Fusobacteria includes Lemierres’s syndrome. Lemierres’s syndrome is also known as postanginal sepsis and is a form of thrombophlebitis. Thrombophlebitis is inflammation caused by a blood clot. In individuals infected with Fusobacterium necrophorum and additonal Fusobacterium as well, a sore develops in the throat due to infection by a bacterium of the Streptococcus genus. Once this sore develops into a peritonsillar abscess, the pocket is filled with pus and bacteria in close proximity to the tonsils. At this point, bacteria which are capable of thriving in anaerobic conditions, such as Fusobacterium necrophorum can flourish deep in the abscess. At this point, the bacteria are able to pass into the neighboring jugular vein and cause an infected clot to form. The bacteria are then able to circulate throughout the body via the bloodstream and pieces of the blood clot will dissociate from the original site and travel to the lungs. The pieces of the clot will settle in the lungs and block branches of the pulmonary artery, resulting in shortness of breath, chest pain and pneumonia. Fusobacteria are normal flora within the oropharyngeal and can clearly result in disease if conditions are optimal.

Functional profiles of coronal and dentin caries in children

Background: Dental caries results from a dysbiosis of tooth-associated biofilms and frequently extends through enamel into dentin which has a different structure and composition.

Objective: To evaluate the metatranscriptome of caries to determine the metabolic potential of caries communities compared with health.

Design: Samples from children, caries-free (CF: n = 4) or with coronal (CC: n = 5) or dentin (DC: n = 5) caries were examined for gene expression potential. Functional profiling was performed using HUMAnN2 (HMP Unified Metabolic Analysis Network).

Results: There was increased gene expression diversity in DC compared with CC and CF. Genes in CF included alcohol dehydrogenase from Neisseria sicca, methylenetetrahydrofolate reductase from Streptococcus sanguinis and choline kinase from streptococci. Genes in CC mapped mainly to Streptococcus mutans. Arginine deiminase in DC mapped to S. sanguinis and Actinomyces naeslundii. Glycerol kinase genes mapped to S. sanguinis in all groups whereas glycerol kinase in DC were from Rothia, Prevotella and streptococci. Uracil-DNA glycosylase in DC mapped to Prevotella denticola and Actinomyces. Repressor LexA in DC mapped to Scardovia wiggsiae, Dialister invisus and Veillonella parvula.

Conclusions: Functional profiling revealed enzyme activities in both caries and caries-free communities and clarified marked differences between coronal and dentin caries in bacterial composition and potential gene expression.