Filifactor alocis

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Domain: Bacteria
Phylum: Firmicutes
Class: Clostridia
Order: Clostridiales
Family: Peptostreptococcaceae
Genus: Filifactor
Species: F. alocis

Filifactor alocis is one of two known members of the genus ''Filifactor''.[1] F. alocis was first isolated from gingival sulci of patients with gingivitis or periodontitis in 1985. F. alocis is a gram-negative, non-spore forming, rod-shaped bacterium. The cells are typically 0.4 to 0.7 by 1.5-7.0 µm and they have rounded to tapered ends. Cells generally occur singularly, in pairs, or in short chains. Motility is rare, though some strains have been observed exhibiting twitching or end-over-end movement. Flagella are not observed.[2] F. alocis has been identified as a potentially pathogenic agent in many forms of periodontal disease.

History

Filifactor alocis was first identified in 1985, though it was initially classified as Fusobacterium alocis on the basis of phenotypic characteristics that were similar to the Fusobacterium genus.[3] A phylogenetic analysis of F. alocis was performed in 1999. The 16S ribosomal RNA (rRNA) gene of F. alocis was found to have 74-76.9% sequence similarity with species of the Fusobacterium genus. In contrast, the 16S rRNA gene sequence was 92.6% similar to Filifactor villosus, a member of an entirely different phylum (Firmicutes rather than Fusobacteria). Fusobacterium alocis was consequently reclassified as Filifactor alocis.[4] F. alocis and F. villosus remain the only two identified species in the Filifactor genus.

Growth and Metabolism

Laboratory growth of F. alocis is challenging as the bacteria are slow-growing, and the exact nutritional requirements of the bacteria are unknown.[5] Growth optimally occurs at 37ºC, though only moderate growth is observed. Slight growth is observed at 25ºC and 45ºC.[6] Growth pH conditions are unknown. F. alocis is an obligate anaerobe. Growth is better in a 10% CO2–90% N2 environment than in a 100% CO2 environment.[7] While F. alocis is anaerobic, its growth seems to be stimulated under oxidative stress conditions, specifically in the presence of hydrogen peroxide.[8] F. alocis is relatively biochemically inert and not responsive to most typical biochemical assays. It has been shown to produce butyrate and acetate as fermentation products when grown in culture in peptone yeast glucose (PYG) broth, an enriched medium. Additionally, F. alocis appears to metabolize the amino acid arginine into butyrate and ammonia.[9] Hydrogen gas (H2) is detected when there is sufficient growth in PYG broth.[10] Fermentation is assumed to be the process by which F. alocis generates ATP, and as there is no evidence of carbon fixation by the bacteria, it is assumed to be a chemoheterotroph. Further characterization of the bacteria is necessary to confirm this designation.

Microbial Physiology

The initial characterization of F. alocis was as a gram-negative staining bacteria.[11] There are, however, conflicting reports in the literature, as some more recent papers identify F. alocis as gram-positive.[12],[13],[14] The only other identified member of the Filifactor genus, ''Filifactor villosus'', exhibits variable gram staining[15], which and that could similarly be the case with F. alocis. Additionally, bacteria of the Firmicutes phylum generally stain gram-positive. Regardless, the content and structure of the cell wall and cell membrane of F. alocis remain undetermined.

Genome

The genome of the type strain of F. alocis has been sequenced. The genome has genes encoding 1,616 presumed proteins.[16] The genome appears to contain at least fifteen proteases and superoxide reductase.[17] Not much research has been done characterizing and confirming these proteins in the genome. The G-C content of the type strain is reported to be 34 mol%.[18]

Response to Antibiotics

All tested strains of F. alocis have shown susceptibility to the antibiotics chloramphenicol, clindamycin, erythromycin, and tetracycline. Most, though not all, strains are also susceptible to penicillin.[19]

Periodontal Disease

Around the early 2000s, evidence emerged that F. alocis might play a pathogenic role in the development of periodontal disease.[20] F. alocis has been associated with infection of the tooth pulp and is specifically a prevalent phenotype when typical treatment fails. The bacteria has also been identified in lesions around the apex of the tooth root. It is found more frequently and at higher levels in patients with dental disease than in healthy patients. There are several unique characteristics of F. alocis that are likely important to its role in periodontal disease.[21] One key aspect of periodontal disease is the presence of biofilm due to bacterial growth. F. alocis was found to be a major component of biofilms associated with periodontal disease.[22] Additionally, when co-cultured with Porphyromonas gingivalis'', another bacteria implicated in periodontal disease, formation of a biofilm was enhanced. This enhancement increases the virulence potential of both F. alocis and P. gingivalis.[23] Another characteristic of F. alocis that might contribute to its pathogenicity is its stimulated growth under oxidative stress. This is likely important to the microbial community involved in periodontal disease as F. alocis could protect other species from the harmful effects of oxidative stress.[24] F. alocis has also been shown to modulate neutrophil activity, therefore reducing the effectiveness of the immune system in combating bacterial growth.[25] The presence of proteases in the F. alocis genome, as well as the proteome of the periodontal microenvironment suggest that F. alocis might also play a role in the breakdown of tissue associated with periodontal disease.

References

  1. ↑ Jalava, J. & Eerola, E. Filifactor. in Bergey’s Manual of Systematics of Archaea and Bacteria 1–5 (American Cancer Society, 2015). doi:10.1002/9781118960608.gbm00667.
  2. ↑ CATO, E. P., MOORE, L. V. H. & MOORE, W. E. C. Fusobacterium alocis sp. nov. and Fusobacterium sulci sp. nov. from the Human Gingival Sulcus. Int. J. Syst. Evol. Microbiol. 35, 475–477 (1985).
  3. ↑ CATO, E. P., MOORE, L. V. H. & MOORE, W. E. C. Fusobacterium alocis sp. nov. and Fusobacterium sulci sp. nov. from the Human Gingival Sulcus. Int. J. Syst. Evol. Microbiol. 35, 475–477 (1985).
  4. ↑ Jalava, J. & Eerola, E. Phylogenetic analysis of Fusobacterium alocis and Fusobacterium sulci based on 16S rRNA gene sequences: proposal of Filifactor alocis (Cato, Moore and Moore) comb. nov. and Eubacterium sulci (Cato, Moore and Moore) comb. nov. Int. J. Syst. Evol. Microbiol. 49, 1375–1379 (1999).
  5. ↑ Siqueira, J. F. & Rôças, I. N. Detection of Filifactor alocis in endodontic infections associated with different forms of periradicular diseases. Oral Microbiol. Immunol. 18, 263–265 (2003).
  6. ↑ Cato, E. P., Moore, L. V. H. & Moore, W. E. C. Fusobacterium alocis sp. nov. and Fusobacterium sulci sp. nov. from the Human Gingival Sulcus. Int. J. Syst. Evol. Microbiol. 35, 475–477 (1985).
  7. ↑ Cato, E. P., Moore, L. V. H. & Moore, W. E. C. Fusobacterium alocis sp. nov. and Fusobacterium sulci sp. nov. from the Human Gingival Sulcus. Int. J. Syst. Evol. Microbiol. 35, 475–477 (1985).
  8. ↑ Aruni, A. W., Roy, F. & Fletcher, H. M. Filifactor alocis has virulence attributes that can enhance its persistence under oxidative stress conditions and mediate invasion of epithelial cells by porphyromonas gingivalis. Infect. Immun. 79, 3872–3886 (2011).
  9. ↑ Uematsu, H., Sato, N., Hossain, M. Z., Ikeda, T. & Hoshino, E. Degradation of arginine and other amino acids by butyrate-producing asaccharolytic anaerobic Gram-positive rods in periodontal pockets. Arch. Oral Biol. 48, 423–429 (2003).
  10. ↑ Cato, E. P., Moore, L. V. H. & Moore, W. E. C. Fusobacterium alocis sp. nov. and Fusobacterium sulci sp. nov. from the Human Gingival Sulcus. Int. J. Syst. Evol. Microbiol. 35, 475–477 (1985).
  11. ↑ Cato, E. P., Moore, L. V. H. & Moore, W. E. C. Fusobacterium alocis sp. nov. and Fusobacterium sulci sp. nov. from the Human Gingival Sulcus. Int. J. Syst. Evol. Microbiol. 35, 475–477 (1985).
  12. ↑ Kumar, P. S., Griffen, A. L., Moeschberger, M. L. & Leys, E. J. Identification of Candidate Periodontal Pathogens and Beneficial Species by Quantitative 16S Clonal Analysis. J. Clin. Microbiol. 43, 3944–3955 (2005).
  13. ↑ Moffatt, C. E., Whitmore, S. E., Griffen, A. L., Leys, E. J. & Lamont, R. J. Filifactor alocis interactions with gingival epithelial cells. Mol. Oral Microbiol. 26, 365–373 (2011).
  14. ↑ Griffen, A. L. et al. Distinct and complex bacterial profiles in human periodontitis and health revealed by 16S pyrosequencing. ISME J. 6, 1176–1185 (2012).
  15. ↑ Love, D. N., Jones, R. F. & Bailey, M. Clostridium villosum sp. nov. from Subcutaneous Abscesses in Cats. Int. J. Syst. Evol. Microbiol. 29, 241–244 (1979).
  16. ↑ Filifactor alocis (strain ATCC 35896 / D40 B5) (Fusobacterium alocis). https://www.uniprot.org/proteomes/UP000007468.
  17. ↑ Aruni, W., Chioma, O. & Fletcher, H. M. Filifactor alocis: The Newly Discovered Kid on the Block with Special Talents. J. Dent. Res. 93, 725–732 (2014).
  18. ↑ Cato, E. P., Moore, L. V. H. & Moore, W. E. C. Fusobacterium alocis sp. nov. and Fusobacterium sulci sp. nov. from the Human Gingival Sulcus. Int. J. Syst. Evol. Microbiol. 35, 475–477 (1985).
  19. ↑ Cato, E. P., Moore, L. V. H. & Moore, W. E. C. Fusobacterium alocis sp. nov. and Fusobacterium sulci sp. nov. from the Human Gingival Sulcus. Int. J. Syst. Evol. Microbiol. 35, 475–477 (1985).
  20. ↑ Moore, W. E. C. & Moore, L. V. H. The bacteria of periodontal diseases. Periodontol. 2000 5, 66–77 (1994).
  21. ↑ Aruni, W., Chioma, O. & Fletcher, H. M. Filifactor alocis: The Newly Discovered Kid on the Block with Special Talents. J. Dent. Res. 93, 725–732 (2014).
  22. ↑ Schlafer, S. et al. Filifactor alocis--involvement in periodontal biofilms. BMC Microbiol. 10, 66 (2010).
  23. ↑ Aruni, A. W., Roy, F. & Fletcher, H. M. Filifactor alocis has virulence attributes that can enhance its persistence under oxidative stress conditions and mediate invasion of epithelial cells by porphyromonas gingivalis. Infect. Immun. 79, 3872–3886 (2011).
  24. ↑ Aruni, W., Chioma, O. & Fletcher, H. M. Filifactor alocis: The Newly Discovered Kid on the Block with Special Talents. J. Dent. Res. 93, 725–732 (2014).
  25. ↑ Armstrong, C. L. et al. Filifactor alocis Promotes Neutrophil Degranulation and Chemotactic Activity. Infect. Immun. 84, 3423–3433 (2016).
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