Prevotella oris

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Adrienne Agius Bench B 22/9/2017 [1]


Higher order taxa

Bacteria – Bacteroidetes – Bacteroidia – Bacteroidales – Prevotellaceae – Prevotella


Prevotella oris

Basonym: Bacteroides oris [1]

Type Strain: ATCC 33573[1], VPI D1A-1A[2], CCUG 15405, CIP 104480, DSM 18711, JCM 8540, JCM 12252, NCTC 13071

Strains: DSM 18711; C735 and F0302[3]

Description and significance

Prevotella oris is a gram-negative, nonpigmented, nonsporeforming, nonmotile and obligate anaerobe pleomorphic rod. It was originally classified as Bacteroides oris when first discovered in 1982 by Holdeman et al. from a patient with moderate periodontitis at the gingival suculus. Shah and Collins later reclassified this bacterium as Prevotella oris in 1990[1] [2].

P. oris has been isolated from many sites of the human body, but is most commonly found in the oropharyngeal mucosa or the gingival sulcus [1] [4]. This bacterium has successfully been cultured on blood agar plates that were anaerobically incubated[1]. This genus is frequently isolated from lesions of oral and some systemic infections, although the role of P. oris in relation to them is still unclear.

Genome structure

Prevotella oris DSM 18711T is utilized by NCBI as the reference genome at 3,077,999 bp in length and a genomic GC content of 43.8%. There is an estimation of 2,647 genes coding for: 654 pseudogenes, 4 rRNA’s, 1,939 proteins, 48 tRNA's and 2 other RNA’s[5].

Cell structure and metabolism

Biofilm formation is important for P. oris survival and pathogenicity. This bacterium has been found to be an early colonizer of periodontal pockets and acts as a target for P. gingivalis allowing biofilm formation[8]. P. oris was found to have high laminin binding rates which is a matrix protein that is associated with microbial invasiveness [4].

P. oris produces the pathogenic factors immunoglobulin A protease, hyalyronidase and beta-lactamase[6]. This gram-negative bacterium has produces acid in reaction to xylose, arabinose, salicin, cellobiose, sucrose, lactose and also have been found to have positive reactions to Esculin hydrolysis, alpha-Fucosidase, beta-N-acetyl-glucosamindase, beta-glucosidase and beta-xylosidase[2].


As P. oris is an obligate anaerobe it is generally isolated from regions with less oxygen, such as subgingival plaque and the oropharyngeal mucosa. P. oris has also been isolated from the human periodontal flora, intestinal tract as well as oral and systemic infections [1] [4].


As mentioned previously, P. oris has been isolated from many locations in the human body such as lesions from oral infections and systemic infections, generally arising from mucosal surfaces with diverse microbial communities[4]. Oral cavity isolates have been identified from dentoalveolar abscess, bacteremia, periodontal disease, endodontic infection and spreading odontogenic infections. On rarer instances, due to P. oris systemic infection, samples have been retrieved from empyema, meningitis and cervical spinal epidural abscess[6].

Application to biotechnology

P. oris has been found to activate ginseng, a crude oral drug that ha the capability to treat various diseases, in the gut. This bacteria is able to hydrolyse the ginsenoside Rb1 to the intestinal bacterial metabolite (IBM) 20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol, ginsenoside Rb2 to 20-O-[alpha-L-arabinopyranosyl-(1→6)-beta-D-glucopyranosyl]-20(S)-protopanaxadiol and ginsenoside Rc to 20-O-[alpha-L-arabinofuranosyl(1→6)-beta-D-glucopyranosyl]-20(S)-protopanaxadiol. These IBM’s affinity for the plasma membrane and inhibitory effects on multidrug resistance for bacteria and tumours as well as their inhibitory affect on the growth of tumour cells indicate the need for further research and development of this symbiotic relationship between the human gut microflora such as P. oris and the human gut [9].

Current research

Recent studies suggest that P. oris utilizes a unique 16kDa hemolysin, unaffected by trypsin treatment. It contains a heat-labile, proteinaceous substances as well as thiol-activated cytolytic activity and may consist of conjugated proteins such as lipoproteins. This P. oris hemolysis appears to differ from that caused by streptolysin O. Maximal hemolytic activity was found at pH 6.0 indicating that pus from infected sites increase the acidity of the lesion and inflamed site[6]. Further studies indicated that temperature-dependant binding of hemolysin-glycoprotein was occurring on the erythrocyte membranes before hemolysis. It was also found glyceraldehyde-3-phosphate dehydrogenase (GADPH) may cause damage to the cell when it is released from the erythrocyte cell membrane to the cytoplasm during hemolysis[7].


1. Holdeman L.V., Moore, W.E.C., Churn, P.J. and Johnson, J.L. (1982) Bacteroides oris and Bacteroides buccae New Species from Human Periodontitis and Other Human Infections. Int J Syst Bacteriol 32: 125-131.

2. Shah H.N. and Collins D.M. (1990) Prevotella, a new genus to include Bacteroides melaninogenicus and related species formerly classified in the genus Bacteroides. Int J Syst Bacteriol 40(2):205-208.

3. NCBI: Taxonomy

4. Eiring P., Waller K., Widmann A., and Werner H. (1998) Fibronectin and laminin binding of urogenital and oral prevotella species. Zentralbl Bakteriol 288: 361-372.

5. NCBI: Prevotella oris

6. Sato T., Kamaguchi A., and Nakazawa F. (2012) Purification and characterization of hemolysin from Prevotella oris. JOB 54: 113-118.

7. Sato T., Sulistyani H., Kamaguchi A., Miyakawa H., and Nakazawa F. (2013) Hemolysin of Prevotella oris: purification and characteristics. JOB 55: 149–154.

8. Sato T., and Nakazawa F. (2014) Coaggregation between Prevotella oris and Porphyromonas gingivalis. J Microbiol Immunol Infect 47: 182-186.

9. Hasegawa H., Sung J.-H., and Benno Y. (1997) Role of human intestinal prevotella oris in hydrolyzing ginseng saponins. Planta Medica 63: 436–440.

  1. MICR3004

This page is written by <Adrienne Agius> for the MICR3004 course, Semester 2, 2017