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Bench E
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310816
310816
<ref>MICR3004</ref>
<i>Rothia dentocariosa</i>


==Classification==
==Classification==
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==Description and significance==
==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<sup>[[#References|[1]]]</sup>.  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 <sup>[[#References|[2]]]</sup>. 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 <sup>[[#References|[2]]]</sup> .
<i>Rothia dentocariosa</i> was first isolated from decaying human teeth in 1949 by Onisi, going by the species name <i>Actinomyces dentocariosus</i> at that time<sup>[[#References|[1]]]</sup>.  It is a Gram positive bacterium that bears semblance to other <i>Actinomyces</i> species, but the Gram positivity of the bacteria has been noted to diminish in filamentous form <sup>[[#References|[2]]]</sup>. Most isolates of <i>R. dentocariosa</i> come from the buccal cavity, but the microbe has been found in urine, cerebral spinal fluid and exudate from leg stumps <sup>[[#References|[2]]]</sup> .


Microscopic examinations showed pleomorphic branched filaments that segment into coccoid or bacillus forms, not unlike the closely related Actinomyces genus. <sup>[[#References|[1]]]</sup><sup>[[#References|[2]]]</sup><sup>[[#References|[3]]]</sup>
Microscopic examinations showed pleomorphic branched filaments that segment into coccoid or bacillus forms, not unlike the closely related <i>Actinomyces</i> genus. <sup>[[#References|[1]]]</sup><sup>[[#References|[2]]]</sup><sup>[[#References|[3]]]</sup>


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<sup>[[#References|[1]]]</sup><sup>[[#References|[2]]]</sup><sup>[[#References|[3]]]</sup> .
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 <i>R. dentocariosa</i> show both coagulated and turbid growth in broth<sup>[[#References|[1]]]</sup><sup>[[#References|[2]]]</sup><sup>[[#References|[3]]]</sup> .


==Genome structure==
==Genome structure==
Line 28: Line 28:
==Cell structure and metabolism==
==Cell structure and metabolism==


Cell wall, biofilm formation, motility, metabolic functions.  
<i>R. dentocariosa</i> 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. <i>R. dentocariosa</i> can reduce nitrites, but were shown to be more effective at it when the concentrations are not as high <sup>[[#References|[3]]]</sup> .  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 <sup>[[#References|[5]]]</sup> <sup>[[#References|[6]]]</sup>.


==Ecology==
==Ecology==


Aerobe/anaerobe, habitat (location in the oral cavity, potential other environments) and microbe/host interactions.
<i>R. dentocariosa</i> is a aerobe that is commonly found in abundance in oral biofilms on teeth and dental implants<sup>[[#References|[7]]]</sup><sup>[[#References|[8]]]</sup>. It has also been found, uncommonly, colonising blood vessels <sup>[[#References|[9]]]</sup>, joint replacements <sup>[[#References|[10]]]</sup>, and tonsils<sup>[[#References|[11]]]</sup>. It is thought that <i>R. dentocariosa</i> is a commensal organism, but the relationship of the organism with humans is not clear.


==Pathology==
==Pathology==


Do these microorganisms cause disease in the oral cavity or elsewhere?
<i>R. dentocariosa</i> can colonise many locations in the body and cause infection, and have been found to cause endocarditis<sup>[[#References|[9]]]</sup>, prostheses<sup>[[#References|[12]]]</sup> and joint infections<sup>[[#References|[10]]]</sup>. 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 <i>R. dentocariosa</i> is susceptible to penicillin, it is relatively easy to clear infections caused by this offending organism
 
In the buccal cavity, <i>R. dentocariosa</i> is a normal microbe, but has been shown to cause tonsillitis, caries and other periodontal diseases<sup>[[#References|[11]]]</sup>. 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, <i>R. dentocariosa</i> was found to be second only to <i>Candida albicans</i> in terms of causing prostheses failure<sup>[[#References|[12]]]</sup>.


==Application to biotechnology==
==Application to biotechnology==


Bioengineering, biotechnologically relevant enzyme/compound production, drug targets,…
Organisms in the <i>Rothia</i> genus have been identified as gluten-degrading bacteria in the upper digestive tract <sup>[[#References|[13]]]</sup>. <i>Rothia mucilaginosa</i> and <i>Rothia aeria</i> both possess a gliadin-digesting enzyme that has yet to be identified in <i>R. dentocariosa</i>.


==Current research==
==Current research==


Summarise some of the most recent discoveries regarding this species.
A relatively recent and one of the pioneering researches on <i>R. dentocariosa</i> 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<sup>[[#References|[14]]]</sup>.


==References==
==References==


References examples
1. [http://ijs.microbiologyresearch.org/content/journal/ijsem/10.1099/00207713-24-2-154 Georg LK, Brown JM. 1967. Rothia, gen. nov. an aerobic genus of the family Actinomycetaceae. Int J Syst Bacteriol <b>17</b>:79–88.]
 
2. [http://www.ncbi.nlm.nih.gov/pubmed/4886858 Brown JM, Georg LK, Waters LC. 1969. Laboratory identification of Rothia dentocariosa and its occurrence in human clinical materials. Appl Microbiol <b>17</b>:150–6.]
 
3. [http://ijs.microbiologyresearch.org/content/journal/ijsem/10.1099/00207713-24-2-154 Lesher RJ, Gerencser MA, Gerenscer VF. 1974. Morphological, Biochemical, and Serological Characterization of Rothia dentocariosa. Int J Syst Bacteriol <b>24</b>:154–159.]
 
4. [http://www.ncbi.nlm.nih.gov/genome/?term=rothia+dentocariosa Rothia dentocariosa (ID 1968)  - Genome - NCBI]
 
5. [http://aem.asm.org/cgi/doi/10.1128/AEM.01826-14 Ruhl S, Eidt A, Melzl H, Reischl U, Cisar JO. 2014. Probing of Microbial Biofilm Communities for Coadhesion Partners. Appl Environ Microbiol <b>80</b>:6583–6590.]
 
6. [http://aem.asm.org/lookup/doi/10.1128/AEM.01111-16 Zhou Y, Yang J, Zhang L, Zhou X, Cisar JO, Palmer RJ. 2016. Differential Utilization of Basic Proline-Rich Glycoproteins during Growth of Oral Bacteria in Saliva. Appl Environ Microbiol <b>82</b>:5249–5258.]
 
7. [http://www.ncbi.nlm.nih.gov/pubmed/25518856 Schaumann S, Staufenbiel I, Scherer R, Schilhabel M, Winkel A, Stumpp SN, Eberhard J, Stiesch M. 2014. Pyrosequencing of supra- and subgingival biofilms from inflamed peri-implant and periodontal sites. BMC Oral Health <b>14</b>:157.]
 
8. [http://aem.asm.org/lookup/doi/10.1128/AEM.03984-15 Heller D, Helmerhorst EJ, Gower AC, Siqueira WL, Paster BJ, Oppenheim FG. 2016. Molecular Characterization of the Microbial Diversity in the Early, In Vivo -Formed, Dental Biofilm. Appl Environ Microbiol <b>82</b>:AEM.03984-15.]
 
9. [http://link.springer.com/10.1007/s15010-011-0087-7 Shakoor S, Fasih N, Jabeen K, Jamil B. 2011. Rothia dentocariosa endocarditis with mitral valve prolapse: case report and brief review. Infection <b>39</b>:177–179.]
 
10. [http://www.ncbi.nlm.nih.gov/pubmed/26379996 Ozan F, Öncel ES, Duygulu F, Çelik İ, Altay T. 2015. Prosthetic hip joint infection caused by Rothia dentocariosa. Int J Clin Exp Med <b>8</b>:11628–31.]
 
11. [http://www.ncbi.nlm.nih.gov/pubmed/15876953 Ohashi M, Yoshikawa T, Akimoto S, Fujita A, Hayakawa S, Takahashi M, Arakawa Y, Asano Y. 2005. Severe acute tonsillitis caused by Rothia dentocariosa in a healthy child. Pediatr Infect Dis J <b>24</b>:466–7.]
 
12. [http://www.ncbi.nlm.nih.gov/pubmed/11915880 Elving GJ, van der Mei HC, Busscher HJ, van Weissenbruch R, Albers FWJ. 2002. Comparison of the microbial composition of voice prosthesis biofilms from patients requiring frequent versus infrequent replacement. Ann Otol Rhinol Laryngol <b>111</b>:200–3.]


1. [http://onlinelibrary.wiley.com/doi/10.1046/j.1462-2920.1999.00007.x/full Sahm, K., MacGregor, B.J., Jørgensen, B.B., and Stahl, D.A. (1999) Sulphate reduction and vertical distribution of sulphate-reducing bacteria quantified by rRNA slotblot hybridization in a coastal marine sediment. Environ Microbiol <b>1</b>: 65-74.]
13. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3177827/ Zamakhchari M, Wei G, Dewhirst F, Lee J, Schuppan D, Oppenheim FG, Helmerhorst EJ. 2011. Identification of rothia bacteria as gluten-degrading natural colonizers of the upper gastro-intestinal tract. PLoS One <b>6</b>.]


2. [http://www.homd.org Human Oral Microbiome]
14. [http://www.ncbi.nlm.nih.gov/pubmed/24265267 Kataoka H, Taniguchi M, Fukamachi H, Arimoto T, Morisaki H, Kuwata H. 2014. Rothia dentocariosa induces TNF-alpha production in a TLR2-dependent manner. Pathog Dis <b>71</b>:65–68.]


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This page is written by<your name> for the MICR3004 course, Semester 2, 2016
This page is written by Clarence Sim for the MICR3004 course, Semester 2, 2016

Latest revision as of 06:58, 23 September 2016

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

1. Georg LK, Brown JM. 1967. Rothia, gen. nov. an aerobic genus of the family Actinomycetaceae. Int J Syst Bacteriol 17:79–88.

2. Brown JM, Georg LK, Waters LC. 1969. Laboratory identification of Rothia dentocariosa and its occurrence in human clinical materials. Appl Microbiol 17:150–6.

3. Lesher RJ, Gerencser MA, Gerenscer VF. 1974. Morphological, Biochemical, and Serological Characterization of Rothia dentocariosa. Int J Syst Bacteriol 24:154–159.

4. Rothia dentocariosa (ID 1968) - Genome - NCBI

5. Ruhl S, Eidt A, Melzl H, Reischl U, Cisar JO. 2014. Probing of Microbial Biofilm Communities for Coadhesion Partners. Appl Environ Microbiol 80:6583–6590.

6. Zhou Y, Yang J, Zhang L, Zhou X, Cisar JO, Palmer RJ. 2016. Differential Utilization of Basic Proline-Rich Glycoproteins during Growth of Oral Bacteria in Saliva. Appl Environ Microbiol 82:5249–5258.

7. Schaumann S, Staufenbiel I, Scherer R, Schilhabel M, Winkel A, Stumpp SN, Eberhard J, Stiesch M. 2014. Pyrosequencing of supra- and subgingival biofilms from inflamed peri-implant and periodontal sites. BMC Oral Health 14:157.

8. Heller D, Helmerhorst EJ, Gower AC, Siqueira WL, Paster BJ, Oppenheim FG. 2016. Molecular Characterization of the Microbial Diversity in the Early, In Vivo -Formed, Dental Biofilm. Appl Environ Microbiol 82:AEM.03984-15.

9. Shakoor S, Fasih N, Jabeen K, Jamil B. 2011. Rothia dentocariosa endocarditis with mitral valve prolapse: case report and brief review. Infection 39:177–179.

10. Ozan F, Öncel ES, Duygulu F, Çelik İ, Altay T. 2015. Prosthetic hip joint infection caused by Rothia dentocariosa. Int J Clin Exp Med 8:11628–31.

11. Ohashi M, Yoshikawa T, Akimoto S, Fujita A, Hayakawa S, Takahashi M, Arakawa Y, Asano Y. 2005. Severe acute tonsillitis caused by Rothia dentocariosa in a healthy child. Pediatr Infect Dis J 24:466–7.

12. Elving GJ, van der Mei HC, Busscher HJ, van Weissenbruch R, Albers FWJ. 2002. Comparison of the microbial composition of voice prosthesis biofilms from patients requiring frequent versus infrequent replacement. Ann Otol Rhinol Laryngol 111:200–3.

13. Zamakhchari M, Wei G, Dewhirst F, Lee J, Schuppan D, Oppenheim FG, Helmerhorst EJ. 2011. Identification of rothia bacteria as gluten-degrading natural colonizers of the upper gastro-intestinal tract. PLoS One 6.

14. Kataoka H, Taniguchi M, Fukamachi H, Arimoto T, Morisaki H, Kuwata H. 2014. Rothia dentocariosa induces TNF-alpha production in a TLR2-dependent manner. Pathog Dis 71:65–68.


This page is written by Clarence Sim for the MICR3004 course, Semester 2, 2016