Fusobacterium

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Fusobacterium is a genus of obligate anaerobic, Gram-negative,[3] non-sporeforming bacteria[4] belonging to Gracilicutes. Individual cells are slender, rod-shaped bacilli with pointed ends.[5][6] Fusobacterium was discovered in 1900 by Courmont and Cade and is common in the flora of humans.[7][8]

Strains of Fusobacterium can cause several human diseases and infections, including periodontal diseases, Lemierre's syndrome,[9] oral, head, and neck infections, as well as colorectal cancer and topical skin ulcers.[10]

It has been tied[<span title="Script error: No such module "decodeEncode".">clarification needed] to HIV infection and suboptimal immune recovery.[11] Detection of Fusobacterium is typically through surgical retrieval of tissue, fecal tests, or blood tests in patients showing symptoms.[3] Early detection is preferred and helps to prevent further disease progression.[7]

Although older sources state that Fusobacterium is part of the normal flora of the human oropharynx, the current consensus is that Fusobacterium should always be treated as a pathogen.[12] There are thirteen described Fusobacterium strains; the predominant one affecting humans is F. nucleatum,[13] followed by F. necrophorum, which also affects animals, mainly cattle.[14]

Background

History

Although the genus was not discovered until 1900 by Courmont and Cade,[7] the first documented Fusobacterium infection was reported in 1898 by Veillon and Zuber, who described a case of systemic infection in a young child.[15] The genus was proposed by Knorr in 1923.[16] Fusobacterium has been classically considered a normal part of the human oral, gastrointestinal, and female genital flora, which is why infections are not commonly seen.[8]

Clinical relevance

Fusobacterium is often associated with ulcerative colitis.[17] Research of colon cancer has also shown an overrepresentation of Fusobacterium, both in feces of patients[18] and tumor tissue itself.[19] Fusobacterium has also been seen increased in individuals infected with HIV as well as in individuals with suboptimal immune recovery as compared to patients who were not infected and had optimal responses.[11]

Prevalent pathogenic species

F. nucleatum is found in humans more so than any other species of Fusobacterium.[13] It is commonly found in the oral cavity as well as in the intestinal tract.[10] Some of its pathogenic ties include its extraction from amniotic fluid sourced from spontaneous premature labor without reason/a given source.[13] A few additional sources of its pathogenic nature include its association with oral inflammation diseases, cancers such as pancreatic, oral, and colorectal, as well as infections of the head and neck. This association is due to the high increase in the prevalence of F. nucleatum in those infected areas. F. nucleatum can worsen or initiate colorectal cancer by stimulating other bacteria such as Streptococcus, Campylobacter spp. and Leptotrichia as well as cancerous gene expression from Beta-catenin signaling. F. nucleatum can be detected in tissues, genomic DNA, and feces using methods such as (FQ, q, and dd) polymerase chain reaction and fluorescence in situ hybridization. However, these are limited because tissues can only be tested after surgery and fecal matter can return false positive results.[10]

F. necrophorum has been found as a common pathogen in the diagnostic of peritonsillar abscess and is more prevalent than other bacteria regarding this infection. It is also the most frequent leading cause associated with Lemierre Syndrome and is not proven to be a normal part of the human oral bacterium population.[9] F. necrophorum commonly infects animals, causing liver abscesses and necrotic diseases, and can combine with other pathogenic bacteria to cause various infections such as foot rot[14] and uterine infections.[20]

Sources of other species of Fusobacterium

Source:[13]

  • F. ulcerans is very similar to F. varium and is commonly extracted from tropical ulcers.
  • F. necrogenes is also closely related to F. ulcerans and F. varium and has been found in chickens and ducks.
  • F. perfoetans is sourced from fecal matter. (F. perfoetans and F. necrogenes have not been sourced from any infections in humans or animals)
  • F. gonidiaformans is typically found in the intestines of humans and is not found orally like the other Fusobacterium.
  • F. russi is a common bacteria in canine and feline oral cavities and can lead to the infection of puncture wounds if transferred to humans from bites.
  • F. simae which can be sourced from monkeys.

Symptoms and treatment

Fusobacterium infections often cause clinical symptoms such as a fever, inflammation, and a diseased appearance. Further diagnosis can confirm suspicions of Fusobacterium infection through blood testing or culturing the tissue. Upon diagnosing the infection, action to treat it involves the application of antibiotics over a 2-week period which could be in the form of penicillin or other variants as well as using anaerobic antibiotics like clindamycin and metronidazole which work when the Fusobacterium can break down the Beta-lactams. Leaving Fusobacterium untreated could lead to more severe developments of the infection and early testing is recommended.[3] By testing early, fatal diseases such as Lemierre syndrome can be avoided. However, this requires the family physician to be conscious of the danger as infections such as Lemierre syndrome affects younger populations and especially those of male gender.[7] The bacterium is a big anchor for biofilms.[21][22] It is usually susceptible to clindamycin,[23] while approximately 20% of the clinical strains are resistant to penicillin.[24] In contrast to Bacteroides spp., Fusobacterium has a potent lipopolysaccharide.

Taxonomy

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Current species

Fusobacterium is divided into 13 different species, two of which each have their own set of subspecies (F. nucleatum and F. necrophorum).[13]

Reclassified species

Other previously declared species of Fusobacterium such as F. symbiosum, F. praecutum, F. plauti, F. alocis, F. sulci, and F. prausnitzii have since been reclassified due to containing different characteristics from the other Fusobacterium members. F. alocis has been reclassified into Filifactor alocis while F. sulci has been reclassified as Eubacterium sulci. F. prausnitzii is a part of the Clostridium leptum subgroup under Eubacterium-like organisms.[13] A few strains F. prausnitzii, a gut commensal associated with healthy patients, was completely reclassified as Faecalibacterium (Clostridiales:Ruminococcaceae) in 2002.

Phylogenic tree

16S rRNA based LTP_10_2024[25][26][27] 120 marker proteins based GTDB 10-RS226[28][29][30]

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Unassigned Fusobacterium:

  • "F. paranimalis" Sivertsen et al. 2025

See also

References

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  3. ^ a b c Page Module:Citation/CS1/styles.css has no content.Arane, Karen; Goldman, Ran (October 2016). "Fusobacterium infections in children". Canadian Family Physician. 62 (10): 813–814. PMC 5063768. PMID 27737977.
  4. ^ Page Module:Citation/CS1/styles.css has no content.Broadley, Marissa; Schweon, Steven J. (May 2017). "Get the facts about Fusobacterium". Nursing2023. 47 (5): 64–65. doi:10.1097/01.NURSE.0000515524.23032.d5. ISSN 0360-4039. PMID 28445341. S2CID 41693034.
  5. ^ Page Module:Citation/CS1/styles.css has no content.Madigan M; Martinko J, eds. (2005). Brock Biology of Microorganisms (11th ed.). Prentice Hall. ISBN 978-0-13-144329-7.
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  8. ^ a b Page Module:Citation/CS1/styles.css has no content.Garcia-Carretero, Rafael; Lopez-Lomba, Marta; Carrasco-Fernandez, Blanca; Duran-Valle, Maria Teresa (October 2017). "Clinical Features and Outcomes of Fusobacterium Species Infections in a Ten-Year Follow-up". Journal of Critical Care Medicine (Universitatea de Medicina Si Farmacie Din Targu-Mures). 3 (4): 141–147. doi:10.1515/jccm-2017-0029. PMC 5769905. PMID 29967887.
  9. ^ a b Page Module:Citation/CS1/styles.css has no content.Ehlers Klug, Tejs; Rusan, Maria; Fuursted, Kurt; Ovesen, Therese (15 November 2009). "Fusobacterium necrophorum: Most Prevalent Pathogen in Peritonsillar Abscess in Denmark". Clinical Infectious Diseases. 49 (10): 1467–1472. doi:10.1086/644616. PMID 19842975.
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