Selenomonas noxia

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Higher order taxa

Bacteria – Firmicutes – Negativicutes – Selenomonadales – Selenomonadaceae – Selenomonas [1]


“S. noxia” (ATCC 43541 = JCM 8546 = VPI D9B-5) [1]

Description and significance

“Selenomonas noxia” is gram-negative crescent-shaped bacteria included in the genus ““Selenomonas””. Antony Van Leeuwenhoek was the first person described the genus “Selenomonas” in 1683. Then the “motile, anaerobic and non-spore-forming” “S. noxia” was firstly discovered by Moore and her colleagues in 1987. “S. noxia” is normally present in human oral flora and can be isolated from the periodontal disease [2], [3] [4]. Three strains of “S. noxia” cultured in American Type Culture Collection (ATCC) were ATCC 43541, ATCC 51893 and ATCC 700225. Anaerobic culture approach for “S. noxia” is unrealistic as the obligate anaerobes are fastidious and the apparent discrepant bacterial presence in saliva and subgingival microbiota [2]. But the anaerobic strain can be fermented with lactate or glucose to produce sugars and different types of acids [9]. “S. noxia” was assumed as a new periodontal pathogen to initiate and develop periodontal diseases. The change in prevalence of “Selenomonas spp.” in healthy periodontium causes the conversion to either chronic periodontitis (CP) or generalized aggressive periodontitis (GAP) [2]. “Selenomonas spp.” was unexpected with high relative abundance in subgingival plaque samples from GAP patients, but the prevalence of “S. noxia” increased in diseased sites such as gingivitis and interproximal active sites, comparing to the normal sites [5]. Additionally, “S. noxia” is specific and sensitive to diagnose obese women, who are having periodontal diseases. If the median present of “S. noxia” is over 1.05% of the total sialic bacteria, 98.4% overweight persons can be identified and 80.2% healthy individuals without periodontal disease were diagnosed [6]. The rapid identification methods are required for “S. noxia” as its etiological and diagnostic importance to oral disease and obesity. The development of specific primer for quantitative PCR (qPCR)and the combinational use of 16S ribosomal RNA (rRNA) and qPCR enhance the higher specificity and sensitivity for “S. noxia” identification [5].

Genome structure

The DNA genome analyzed is a single “S. noxia” isolate. “S. noxia” has 2 assembled genome, one is F0398 and the other is ATCC 43541. “S. noxia” (ATCC 43541) is a motile, gram-positive bacillus preferentially living in anaerobic and mesophilic habitat. This strain is host-associated bacilli. The size of the genome is 2.05 Mb encompassing 1,993 genes. 1,876 proteins are encoded by genes. 5 rRNA, 56 tRNA, and 3 other RNA are incorporated. The GC content is 55.7%. No spanned gaps between scaffolds. 21 identified scaffolds are constituted by 56 contigs. Contig N50 is equal to 106,401 base-long, and there are 6 sequence contigs (contig L50) are longer than or equal to the length of contig N50. The contiguity (Scaffold N50) is 511,655 and the number of contigs (Scaffold L50) is 2. There’s no chromosome or plasmid involved. 35 spanned gaps with total assembly gap length, 15,526. The reference sequence is identical to the assemblies in the GenBank. “S. noxia” (F0398) is the closest genome with 89.9579% symmetrical identity to the “S. noxia” (ATCC 43541) [7].

Cell structure and metabolism

“S. noxia” is a gram-negative, obligate anaerobic and crescent bacillus with greater than or equal to one flagella emanated from the center of the concave side to the polar. The bacillus is approximately 1.1 µm in width and 1.1 to 3.2 µm in length. The gram-negative cell wall constituted by a thin peptidoglycan layer [4]. The building of “Selenomonas” biofilm is possessed by the adherence, cell-to-cell interactions, colonization, and coaggregation. Bacterial adherence proteins (adhesins) found in between bacterial cell wall and outer membrane can invade and localize on the mucosa of oral cavity. The primary colonization is induced via cell-to-cell interactions and then the second colonization is processed after the anchoring of primary colonization. Adhesins can interact with multiple targeted cell types simultaneously. Instead of interactions within “Selenomonad” colonizers, the secondary colonizers act as receptors to bind polysaccharides and then coaggregate with the adhesins of either gram-positive or gram-negative species, such as those from genera “Streptococcus”, “Actinomyces” and “Prevotella” [8]. However, some coaggregation are unimodal under the external intervention. When heating, lactose or acids (EDTA) is provided to “Selenomonad” pairs, the interactions between “Selenomonas spp.” and other bacterial strains will be interrupted. The coaggregation is completely prevented when heats the pairs at 85˚C over 30min. In contrast, same conditions exerted on the partner of “Selenomonad” contributes to tighter coaggregation. “Fusobacterium” is an exception that won’t be affected by lactose [9]. The subgingival biofilm formation of “Selenomonas” can be detected by specific probes. The spatial distribution of “Selenomonas” is relatively low in healthy individuals. By contrary, the increase in “S. noxia” prevalence may associate with the oral infections. Additionally, the “Selenomonas” species analyzed by fluorescence in-situ hybridization (FISH) is capable of organizing subgingival biofilm structures [10].


“S. noxia” is host-associated anaerobic bacteria mainly present in the human oral cavity. They are detected in salivary recovery and subgingival regions while the relative abundance of “S. noxia” is varied depending on their colonization sites [2]. The optimal environment for “S. noxia” to grow is in the anaerobic gas mixture (80% nitrogen gas with 10% carbon dioxide and hydrogen gas) at 37˚C. The lowest acceptable temperature is 22˚C and the maximum temperature is 50˚C. The anaerobic strain can ferment with lactate to produce lactic acids. Additionally, “S. noxia” can produce propionic acids and acetic acids by fermentation of glucose on PYG broth. Morphology of colonies is changed as the strain cultured on the different plates. In blood agar plate, the colony is circular, opaque and larger in size comparing to the colonizers on PYG broth, which is semi-transparent [11]. No cross-reactivity discovered in “Selenomonad” species but heterozygosity may occasionally present within the same genus. The “S. noxia” is reported as a potential indicator for the initiation of periodontitis. Though the strain is a putative pathogenic agent to GAP, CP or periodontitis-resistance (PR), the pathogenicity of “S. noxia” is still unclear [2]. “Selenomonad” can coaggregate with other bacterial genera in subgingival plaques in adults induces the periodontitis. But different types of bacterial strains are clustered and appears in both adults and adolescents’ mouth [9].


“S. noxia” is one of the bacterial species detected in “gingival crevice and periodontal pocket” which is associated to the GAP lesions, CP, and PR. As for periodontal infections, the “S. noxia” was found with inclined prevalence than that in healthy individuals. The loss of tooth attachment is possibly resulted by the initial periodontal lesions. “S. noxia” also disseminates in periodontal pocket whereas the colonization of “S. noxia” is not associated with the depth of the pocket [12]. The specific antibody, IgG surveils the condition of oral biofilms and is against mucosal microbiomes attributed by periodontal diseases, hypertension or plaques. Interestingly, the periodontal diseases are relevant to the presence of 8-isoprostane affected by different factors such as age, race, and smoking. Oxidative stress can induce the immune or inflammation. The enhanced oxidative stress or high concentration of 8-isoprostane will result in decreased the IgG level, therefore, the immune responses will be weaker associated to reduce “S. noxia” strains and relieve inflammation. Ultimately, the periodontal disease may be more severe with the higher prevalence of “S. noxia”. However, the association between 8-isoprostane concentration and declined level of antibodies was still unknown [13]. Additionally, the occurrence of “S. noxia” aids in diagnosing obese women who were already had oral inflammation. If the median percent of “S. noxia” was over 1.05% of the total sialic bacteria, there would be 98.4% certainty in identifying overweight females or 80.2% individuals were with normal weight as the median percentage is less than 1.05% [6].

Application to biotechnology

“S. noxia” is one of several hundred of bacteria living in the oral flora. The relatively low abundance of “S. noxia” can’t provide significance for periodontal disease diagnosis. Similar to the other species of “Selenomonad”, they are not effectively working as a biomarker [3]. But the strain might be able to act as an indicator to detect the variation of oral biofilms. From the other perspective, as mentioned above, the obesity in females who are diagnosed with periodontal symptoms can be accurately identified due to the sensitive and specific indication of the median percentages of “S. noxia”. Thus, the “S. noxia” is believed can be a biomarker to observe and possess the initiation and developmental status of obesity [6]. This is the novel idea to apply “S. noxia” into medical or biotechnological use for further accurate and rapid detection. In order to improve the diagnostic method, the anaerobic culture technique was tested while the presence of “S. noxia” in salivary samples and the tooth samples weren’t accordant. So, this technique wasn’t suitable.

Current research

The “S. noxia” is putatively used to identify the initiation of periodontitis. While the diagnostic strategies and treatment should be further discussed. Currently, a specific probe, SELE for “Selenomonad” and “Centipeda” was designed to analyze the oral bacteria. The combination of probe SELE to qPCR and 16S rRNA highly strengthened the specificity to 100% for “S. noxia” detection. Though the association between obesity, “S. noxia” and periodontal disease was identified, the etiology and pathogenicity of the strain and obesity is remained unknown [2], [6]. The “Selenomonas spp.” is relatively abundant in the oral biofilms that possibly disseminated to the gastrointestinal tract (GIT). Then “Selenomonas spp.” were found and isolated from the GIT mucosa. The “Selenomonas spp.” is morphologically similar to the “Helicobacter spp.”, which is responsible to cause gastric ulcer and gastritis. Thus, the similar structure in between “Selenomonas spp.” and “Helicobacter spp.” is deduced to share the similar function that the former can cause gastric inflammation. The specific species and the abundance of the related species in GIT microbiota are unclear [14]. In brief, the “S. noxia” is one of the abundant bacterial species living in salivary recovery and gingival crevice. It is believed as a pathogen causes periodontal diseases involving GAP, CP and PR [3]. The prevalence of “S. noxia” in healthy individuals is lower than the patients but is not significant enough to act as a biomarker for diagnosis [6]. The factors such as diet, environmental stress, smoking, and races could be the trigger to increase “S. noxia” levels and then result in diseases [15]. The association and mechanism between “S. noxia” and other genera of bacteria, the other diseases and practical therapies will be investigated in the future.


1. Taxanomy 2. Cruz P, Mehretu A.M., Buttner M.P., Trice T., Howard K.M. (2015) Development of a polymerase chain reaction assay for the rapid detection of the oral pathogenic bacterium, Selenomonas noxia. BMC Oral Health 1–8. 3. Drescher J., Schlafer S., Schaudinn C., Riep B., Neumann K., Friedmann A., Petrich A., Göbel U.B., Moter A. (2010) Molecular epidemiology and spatial distribution of Selenomonas spp. in subgingival biofilms. Eur J Oral Sci. 118:466-474. 4. Moore L.V.H., Johnson J.L., Moore W.E.C. (1987) Selenomonas noxia sp. nov., Selenomonas flueggei sp. nov., Selenomonas infelix sp. nov., Selenomonas dianae sp. nov., and Selenomonas artemidis sp. nov., from the Human Gingival Crevice. Int J Syst Bacteriol 37:271–280. 5. Tanner A., Maiden M.F., Macuch P.J., Murray L.L., Kent R.L. (1998) Microbiota of health, gingivitis, and initial periodontitis. J Clin Periodontol 25:85–98. 6. Goodson J.M., Groppo D., Halem S., Carpino E. (2009) Is Obesity an Oral Bacterial Disease? J Dent Res 88:519–523. 7. [1] 8. Kolenbrander P.E., London J. (1993) Adhere today, here tomorrow: Oral bacterial adherence. J Bacteriol 175: 3247-3252. 9. Kolenbrander P.E., Andersen R.N., Moore L.V.H. (1989) Coaggregation of Fusobacterium nucleatum, Selenomonas flueggei, Selenomonas infelix, Selenomonas noxia, and Selenomonas sputigena with strains from 11 genera of oral bacteria. Infect Immun 57:3194–3203. 10. Faveri M., Mayer M.P.A., Feres M., De Figueiredo L.C., Dewhirst F.E., Paster B.J. (2008) Microbiological diversity of generalized aggressive periodontitis by 16S rRNA clonal analysis. Oral Microbiol Immunol 23:112–118. 11. Kingsley, V.V., & Hoeniger, J.F. (1973) Growth, structure, and classification of Selenomonas. MMBR, 37:479-521. 12. Haffajee A.D., Cugini M., Tanner A., Pollack R.P., Smith C., Kent R.L., Socransky S.S. (1998) Subgingival microbiota in healthy, well-maintained elder and periodontitis subjects. J Clin Periodontol 25:346–353. 13. Singer R.E., Moss K., Beck J.D., Offenbacher S. (2009) Association of systemic oxidative stress with suppressed serum IgG to commensal oral biofilm and modulation by periodontal infection. Antioxid Redox Signal 11:2973–83. 14. Andersen L.P., Lange P., Tvede M. (2010) Selenomonas may puzzle the diagnosis of Helicobacter pylori in gastric mucosa. Eur J Clin Microbiol Infect Dis 29:891–892. 15. Tanner C.R., Paster B.J., Lu S.C., Kanasi E., Kent R., Van Dyke T., Sonis S.T. (2006) Subgingival and tongue microbiota during early periodontitis. J Dent Res 85:318–323.

This page is written by <Zheyi Wen> for the MICR3004 course, Semester 2, 2017