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Gabriel Tai

Classification

Higher order taxa

Bacteria – Actinobacteria – Actinobacteria – Actinomycetales – Micrococcaceae – Rothia

Species

Rothia dentocariosa

Type strain: ATCC 17931, CCUG 35437, CIP 81.83, DSM 43762, DSM 46363, NBRC 12531, NCTC 10917, NRRL B-8017.

Description and significance

RRothia dentocariosa is a described as a pleomorphic, gram-positive bacteria most commonly found residing as part of the human micoflora in the oral cavity and the pharynx.[1] First discovered in 1949, R. dentocariosa was first isolated from dental plaques and caries in oral cavity of humans. R. dentocariosa is included in the family, Actinomycetaceae due to its filamentous, pleomorphic morphology.[6] Due to the bacterium being pleomorphic, its morphology can be differentiated into a coccal, bacillary, or diptheroidal cells.[5] The morphology and physiology of R. dentocariosa is closely related to Actinomyces as well as several species from the genus Nocardia.[6] Cultured colonies on blood-heart infusion agar plates are off-white in color and can either appear smooth or rough.[1]

Genome structure

Representative genome: Rothia dentocariosa ATCC 17931. R. dentocariosa ATCC 17931 was isolated from the oral cavity for complete genome sequencing. ATCC 17931 strain comprises of a circular genome 2,506,025 base pairs in length.[3] The genome consists of 2,126 genes with 2,040 coding regions for protein production.[3]

Cell structure and metabolism

R. dentocariosa is characterized as non-acid-fast, non-pigmented, non-spore-forming, and non-haemolytic bacterium.[4]. The peptidoglycan of R.dentocariosa is type A3a, having a D-alanine found in position 4, and an L-lysine in position 3. The cell wall is mainly comprised of galactose, fructose, glucose, and ribose.[2] The major glycolipid of the bacterium consists of mannose, glycerol and fatty acids.[10] R. dentocariosa undergoes glucose metabolism in a fermentative manner, with the terminal products being lactic and acetic acids.[4]

Ecology

R. dentocariosa, being mainly an aerobic bacterium, can still grow in anaerobic conditions in a slower rate hindered by the presence of CO2.[4] Known to be a natural residence of the human microflora, increasing R. dentocariosa isolates from supragingival dental plaque have been reported.[10] Furthermore, the bacterium is identified to be linked with periodontal diseases.[10]

Pathology

Reports of clinical infections arise to the primary infection of R. dentocariosa are rare.[8] Although R. dentocariosa is indicated to have low virulence, it can raise complications such as periodontal disease when established with other bacteria of the oral microflora.[5] The presence of anaerobic and facultative anaerobic microbes isolated along with R. dentocariosa from pericoronal pockets can suggest severe pericoronitis.[5] Peridontal disease is therefore a risk factor for individuals infected with R. dentocariosa.[5] In addition to oral infections, R. dentocariosa is also associated with other complications such as bacteraemia, septic arthritis, and pneumonia. Though rare, severe infections caused by R. dentocariosa can lead to the development of infective endocarditis in infected individuals.[7] Individuals suffering from prior heart conditions are frequently found to develop endocarditis caused by R. dentocariosa.[2]

Application to biotechnology

Given the fact that R. dentocariosa are typically of low virulence and is sensitive to a wide range of β-lactam antimicrobials, treatment and therapy is usually successful with rare reports of deaths.[9] There are no current studies that have suggested the organism in biotechnology and bioengineering.

Current research

Recent studies have indicated R. dentocariosa as an opportunistic pathogen responsible for the involvement of inflammatory process in several complications. A research was conducted in 2014 demonstrating the role of Toll-like receptor 2 being a primary receptor for the induction of tumor necrosis factor α follow an exposure to R. dentocariosa.[10] Future research aims to determine the immunological responses that lead to inflmmation upon detection of R. dentocariosa in the absence of Toll-like receptor 2.[10]

References

1. [Boudewigns, M., Magerman, K., Verhaegen, J., Debrock, G., Peetermans, W.E., Donkersloot, P., Mewis, A., Peeters, V., Rummens, J.L., Cartuyvels, R. 2003. Rothia dentocariosa, endocarditis and mycotic aneurysms: case report and review of the literature. Clinical Microbiology and Infection 9:222-229]

2. [National Center for Biotechnology Information, Rothia dentocariosa overview, viewed 20-09-2016]

3. [National Center for Biotechnology Information, Rothia dentocariosa ATCC 17931 complete genome, viewed 20-09-2016]

4. [Von Graevenitz, A. 2004. Rothia dentocariosa: taxonomy and differential diagnosis. Clinical Microbiology and Infection. 10:399-402]

5. [Droz, S., Zbinden, Reinhard, Rothia dentocariosa, viewed 19-09-2016]

6. [Hammond, B.F. 1970. Isolation and Serological Characterization of a Cell Wall Antigen of Rothia dentocariosa. Journal of Bacteriology. 103:634-640.]

7. [Medscape, Rothia dentocariosa Endocarditis Complicated by Multiple Intracranial Hemorrhages, viewed 19-09-2016]

8. [Larkin, J., Montero, J., Targino, M., Powers, A., Accurso, C., Campbell, M. 2001. Rothia dentocariosa Endocarditis. Clinical Microbiology Newsletter. 23:13-15]

9. [Al Habib, K., Werb, R., Conway, B. 1999. Rothia dentocariosa Bacteremia in a Patient with End-Stage Renal Disease. Infectious Diseases in Clinical Practice. 8:170-173.]

10. [Kataoka, H., Taniguchi, M., Fukamachi, H., Arimoto, T., Morisaki, H., Kuwata, H. 2013. Rothia dentocariosa induces TNF-alpha production in a TLR2-dependent manner. Pathogens and Disease. 71: 65-68.]

11. [Pasciak, M., Ekiel, I., Grzegorzewicz, A., Mordarska, H., Gamian, A. 2002. Strucutre of the major glycolipid from Rothia dentocariosa. Biochimica et Biophysica Acta (BBA) - Protein Structure and Molecular Enzymology. 1594:199-205]


This page is written by Gabriel Tai for the MICR3004 course, Semester 2, 2016