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Clarence Sim Bench E 310816 Rothia dentocariosa
Classification
Higher order taxa
Bacteria: Terrabacteria: Actinobacteria: Actinobacteria: Micrococcales: Micrococcacae: Rothia
Species
Rothia dentocariosa ATCC 17931
Description and significance
Rothia dentocariosa was first isolated from decaying human teeth in 1949 by Onisi, going by the species name Actinomyces dentocariosus at that time[1]. It is a Gram positive bacterium that bears semblance to other Actinomyces species, but the Gram positivity of the bacteria has been noted to diminish in filamentous form [2]. Most isolates of R. dentocariosa come from the buccal cavity, but the microbe has been found in urine, cerebral spinal fluid and exudate from leg stumps [2] .
Microscopic examinations showed pleomorphic branched filaments that segment into coccoid or bacillus forms, not unlike the closely related Actinomyces genus. [1][2][3]
Immature colony morphology on trypticase soy agar show granular colonies in aerobic conditions, and similar granular colony formation with filamentous borders in anaerobic conditions. Mature colonies present either as smooth or rough colonies, and can both be present in the culture at the same time. Smooth colonies are convex with well-defined borders, whereas rough colonies appear to have cerebriform surfaces, or folded-edge looking appearances, on the surface of the colony R. dentocariosa show both coagulated and turbid growth in broth[1][2][3] .
Genome structure
Rothia dentocariosa ATCC 17931, complete genome available in GenBank database.
To date, 2126 genes have been identified from bioinformatics analysis of the 2.5Mbp genome [4].
Cell structure and metabolism
R. dentocariosa has a cell wall that is composed of galactose, alanine, glutamic acid and lysine. It is an aerobic organism and ferments most simple carbohydrates, catalase positive and indole negative. R. dentocariosa can reduce nitrites, but were shown to be more effective at it when the concentrations are not as high [3] . It is a non-motile organism that can be found in different biofilm communities, usually by coadhesion, but shown to have poor biofilm formation and growth when in isolation, even in saliva [5] [6].
Ecology
R. dentocariosa is a aerobe that is commonly found in abundance in oral biofilms on teeth and dental implants[7][8]. It has also been found, uncommonly, colonising blood vessels [9], joint replacements [10], and tonsils[11]. It is thought that R. dentocariosa is a commensal organism, but the relationship of the organism with humans is not clear.
Pathology
R. dentocariosa can colonise many locations in the body and cause infection, and have been found to cause endocarditis[9], prostheses[12] and joint infections[10]. To date, joint infections and endocarditic infections have been uncommon, but endocarditis in particular, is extremely serious and may require surgery to repair. However, as R. dentocariosa is susceptible to penicillin, it is relatively easy to clear infections caused by this offending organism
In the buccal cavity, R. dentocariosa is a normal microbe, but has been shown to cause tonsillitis, caries and other periodontal diseases[11]. It is also able to colonise prostheses resulting in early failure of the prosthesis and requiring repair or replacement. In a paper comparing biofilm formation on voice prostheses and their replacement rates, R. dentocariosa was found to be second only to Candida albicans in terms of causing prostheses failure[12].
Application to biotechnology
Organisms in the Rothia genus have been identified as gluten-degrading bacteria in the upper digestive tract [13]. Rothia mucilaginosa and Rothia aeria both possess a gliadin-digesting enzyme that has yet to be identified in R. dentocariosa.
Current research
A relatively recent and one of the pioneering researches on R. dentocariosa has linked the pathogenicity of the microbe to the human host’s immune response. In a paper by Katoaka et al, they have shown the mechanism of immune response induction by activation of toll-like receptors (TLR2) on human monocytic cell lines. TLR2 activation leads to production of the cytokine TNF-α, which is thought to play a role in periodontal inflammation[14].
References
4. Rothia dentocariosa (ID 1968) - Genome - NCBI
This page is written by Clarence Sim for the MICR3004 course, Semester 2, 2016