Parvimonas micra: Difference between revisions

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==Species==
==Species==
Parvimonas micra (P. micra) and type of strain includes ATCC 33270, CCUG 46357, CIP 105294, DSM 20468, GIFU 7824, JCM 12970, NCTC 11808, and VPI 5464 <sup>[[#References|[2]]]</sup>.  
''Parvimonas micra'' (P. micra) and type of strain includes ATCC 33270, CCUG 46357, CIP 105294, DSM 20468, GIFU 7824, JCM 12970, NCTC 11808, and VPI 5464 <sup>[[#References|[2]]]</sup>.  


==Description and significance==
==Description and significance==


P. micra is a gram positive cocci that forms pairs and groups of short chains, where it is not associated with the formation of spores <sup>[[#References|[3, 4]]]</sup>. The bacterium is an obligate anaerobe and was first identified and classified in 1933 as Peptostreptococcus micros <sup>[[#References|[3, 5]]]</sup>. The species was then reclassified in 1999 as Micromonas micros and again in 2006 as Parvimonas micra <sup>[[#References|[5]]]</sup>. Since its discovery, the bacterium has been deemed a commensal pathogen in the human oral cavity, where it is most abundant in the subgingival dental plaque <sup>[[#References|[3, 4, 6]]]</sup>.  
''P. micra'' is a gram positive cocci that forms pairs and groups of short chains, where it is not associated with the formation of spores <sup>[[#References|[3, 4]]]</sup>. The bacterium is an obligate anaerobe and was first identified and classified in 1933 as ''Peptostreptococcus micros'' <sup>[[#References|[3, 5]]]</sup>. The species was then reclassified in 1999 as ''Micromonas micros'' and again in 2006 as ''Parvimonas micra'' <sup>[[#References|[5]]]</sup>. Since its discovery, the bacterium has been deemed a commensal pathogen in the human oral cavity, where it is most abundant in the subgingival dental plaque <sup>[[#References|[3, 4, 6]]]</sup>.  


P. micra can be observed via culturing, where anaerobic culture vials and blood agar can be used to achieve observable colonies <sup>[[#References|[3]]]</sup>. Incubation period is suggested to be around 48 hours <sup>[[#References|[3]]]</sup>. The importance of this bacterium regarding research would be its implication in pathogen mediated diseases in humans, such as periodontitis <sup>[[#References|[7]]]</sup>.  
''P. micra'' can be observed via culturing, where anaerobic culture vials and blood agar can be used to achieve observable colonies <sup>[[#References|[3]]]</sup>. Incubation period is suggested to be around 48 hours <sup>[[#References|[3]]]</sup>. The importance of this bacterium regarding research would be its implication in pathogen mediated diseases in humans, such as periodontitis <sup>[[#References|[7]]]</sup>.  




Figure 1: Purple staining indicates the presence of P. micra, where the stain colouration is associated with gram positive bacteria <sup>[[#References|[16]]]</sup>.  
Figure 1: Purple staining indicates the presence of ''P. micra'', where the stain colouration is associated with gram positive bacteria <sup>[[#References|[16]]]</sup>.  


==Genome structure==
==Genome structure==


Genome structural analysis of P. micra based on strain A293 displayed a genome size of 1,680,794bp, where it had a G + C content of 28.3% <sup>[[#References|[4]]]</sup>. The strain contained 49 contigs, where contig size varied from 539bp to 407,487bp <sup>[[#References|[4]]]</sup>. Further genome analysis displayed that the genome comprises of 1,560 coding sequences and 46 RNAs, where 40 represents tRNAs and 6 rRNAs <sup>[[#References|[4]]]</sup>.  
Genome structural analysis of ''P. micra'' based on strain A293 displayed a genome size of 1,680,794bp, where it had a G + C content of 28.3% <sup>[[#References|[4]]]</sup>. The strain contained 49 contigs, where contig size varied from 539bp to 407,487bp <sup>[[#References|[4]]]</sup>. Further genome analysis displayed that the genome comprises of 1,560 coding sequences and 46 RNAs, where 40 represents tRNAs and 6 rRNAs <sup>[[#References|[4]]]</sup>.  


The total number of genes detected in the A293 strain was around 430 genes <sup>[[#References|[4]]]</sup>. From this, 137 genes are associated with the metabolism of proteins, 60 are involved the processing carbohydrates, 86 are essential in amino acid synthesis, 58 are key in DNA synthesis, and 89 are related to RNA synthesis <sup>[[#References|[4]]]</sup>. The 62 genes out of the 89 genes associated with RNA synthesis were identified to be involved in nucleotide formation and nucleoside synthesis, while 3 genes out of 89 genes are related with prophages, phage, plasmids, and transposable elements <sup>[[#References|[4]]]</sup>.  
The total number of genes detected in the A293 strain was around 430 genes <sup>[[#References|[4]]]</sup>. From this, 137 genes are associated with the metabolism of proteins, 60 are involved the processing carbohydrates, 86 are essential in amino acid synthesis, 58 are key in DNA synthesis, and 89 are related to RNA synthesis <sup>[[#References|[4]]]</sup>. The 62 genes out of the 89 genes associated with RNA synthesis were identified to be involved in nucleotide formation and nucleoside synthesis, while 3 genes out of 89 genes are related with prophages, phage, plasmids, and transposable elements <sup>[[#References|[4]]]</sup>.  
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==Cell structure and metabolism==
==Cell structure and metabolism==


P. micra is a gram-positive bacterium, which indicates that a large composition of its cell wall is made up of a thick layer of peptidoglycan <sup>[[#References|[3]]]</sup>. P. micra has no flagella and is associated with biofilms in the subgingival dental plaque of the human oral cavity <sup>[[#References|[7]]]</sup>. Often observed as micro-colonies in the top layer of these biofilms, its presence has pathogenic potential and can give rise to periodontitis <sup>[[#References|[7]]]</sup>. Scientific finding has suggested that P. micra resides in biofilms that have already been developed, as it has no ability to form structures associated with biofilm formation <sup>[[#References|[8]]]</sup>.  
''P. micra'' is a gram-positive bacterium, which indicates that a large composition of its cell wall is made up of a thick layer of peptidoglycan <sup>[[#References|[3]]]</sup>. ''P. micra'' has no flagella and is associated with biofilms in the subgingival dental plaque of the human oral cavity <sup>[[#References|[7]]]</sup>. Often observed as micro-colonies in the top layer of these biofilms, its presence has pathogenic potential and can give rise to periodontitis <sup>[[#References|[7]]]</sup>. Scientific finding has suggested that ''P. micra'' resides in biofilms that have already been developed, as it has no ability to form structures associated with biofilm formation <sup>[[#References|[8]]]</sup>.  




Figure 2: Cluster of P. micra bacterial cells indicated using a yellow fluorescence, where they are detected in the top layer of the biofilm associated with the sub-gingival dental plaque <sup>[[#References|[7]]]</sup>.  
Figure 2: Cluster of ''P. micra'' bacterial cells indicated using a yellow fluorescence, where they are detected in the top layer of the biofilm associated with the sub-gingival dental plaque <sup>[[#References|[7]]]</sup>.  


==Ecology==
==Ecology==


P. micra is an obligate anaerobe that resides in the human oral cavity, where it is most abundant in the subgingival dental plaque as a commensal pathogen <sup>[[#References|[3, 4, 6]]]</sup>. In addition, P. micra is also identified to inhabit the gastrointestinal tract <sup>[[#References|[9]]]</sup>. Furthermore, it is suggested that P. micra has a potential to be a constitute of the vaginal flora; however, further research is required for verification <sup>[[#References|[3, 10]]]</sup>.  
''P. micra'' is an obligate anaerobe that resides in the human oral cavity, where it is most abundant in the subgingival dental plaque as a commensal pathogen <sup>[[#References|[3, 4, 6]]]</sup>. In addition, ''P. micra'' is also identified to inhabit the gastrointestinal tract <sup>[[#References|[9]]]</sup>. Furthermore, it is suggested that ''P. micra'' has a potential to be a constitute of the vaginal flora; however, further research is required for verification <sup>[[#References|[3, 10]]]</sup>.  


==Pathology==
==Pathology==


P. micra is regarded as one of the pathogens that causes periodontitis in humans, which is a commonly observed disease <sup>[[#References|[7, 8]]]</sup>. The pathogenesis of periodontitis involves the damage of tissue structures that support the teeth, such as the gums, the alveolar bone, and periodontal ligament, due to bacterial infection and inflammation <sup>[[#References|[11, 12]]]</sup>. In addition, the disease is associated with severe complications if treatment is not provided early and adequately, as there is potential for it to spread to surrounding tissues <sup>[[#References|[8]]]</sup>.  
''P. micra'' is regarded as one of the pathogens that causes periodontitis in humans, which is a commonly observed disease <sup>[[#References|[7, 8]]]</sup>. The pathogenesis of periodontitis involves the damage of tissue structures that support the teeth, such as the gums, the alveolar bone, and periodontal ligament, due to bacterial infection and inflammation <sup>[[#References|[11, 12]]]</sup>. In addition, the disease is associated with severe complications if treatment is not provided early and adequately, as there is potential for it to spread to surrounding tissues <sup>[[#References|[8]]]</sup>.  


Regarding pathogenesis, P. micra, is associated with the disturbance of the composition and abundance of commensal microorganisms established within biofilms that coats the subgingival dental plaque <sup>[[#References|[8]]]</sup>. Therefore, a disturbance that leads to a slight increase in the abundance of pathogenic bacterial species, especially P. micra, would increase the likelihood of an infection or a disease to occur, such as periodontitis.  
Regarding pathogenesis, ''P. micra'', is associated with the disturbance of the composition and abundance of commensal microorganisms established within biofilms that coats the subgingival dental plaque <sup>[[#References|[8]]]</sup>. Therefore, a disturbance that leads to a slight increase in the abundance of pathogenic bacterial species, especially ''P. micra'', would increase the likelihood of an infection or a disease to occur, such as periodontitis.  


P. micra has also been documented to be involved in polymicrobial infections with Aggregatibacter aphrophilus, where it causes pleural empyema <sup>[[#References|[13]]]</sup>. In addition, P. micra has been recently documented to cause endocarditis, where the bacterium was identified through molecular sequencing <sup>[[#References|[14]]]</sup>. Furthermore, P. micra has been recently identified to be associated with septic arthritis of native joints, which suggests that this bacterium could be a potential pathogen for infections associated with joints and bones <sup>[[#References|[9]]]</sup>.  
''P. micra'' has also been documented to be involved in polymicrobial infections with Aggregatibacter aphrophilus, where it causes pleural empyema <sup>[[#References|[13]]]</sup>. In addition, ''P. micra'' has been recently documented to cause endocarditis, where the bacterium was identified through molecular sequencing <sup>[[#References|[14]]]</sup>. Furthermore, ''P. micra'' has been recently identified to be associated with septic arthritis of native joints, which suggests that this bacterium could be a potential pathogen for infections associated with joints and bones <sup>[[#References|[9]]]</sup>.  


Other infections and diseases associated with P. micra includes peritonsillar abscesses, respiratory infections, pleural empyema, intracranial abscesses, paranasal sinus infections, spondylodiscitis, pericarditis, and septic embolism <sup>[[#References|[3, 14, 15]]]</sup>. The ability of P. micra to cause infection in other sites of the human body apart from the oral cavity is suggested to be due to the translocation of the bacterium from the oral cavity or from the gastrointestinal tract <sup>[[#References|[14]]]</sup>. However, further research is required to investigate the mechanisms behind this process as well as examining the genes and structures within this bacterium that are involved as virulence factors.  
Other infections and diseases associated with ''P. micra'' includes peritonsillar abscesses, respiratory infections, pleural empyema, intracranial abscesses, paranasal sinus infections, spondylodiscitis, pericarditis, and septic embolism <sup>[[#References|[3, 14, 15]]]</sup>. The ability of ''P. micra'' to cause infection in other sites of the human body apart from the oral cavity is suggested to be due to the translocation of the bacterium from the oral cavity or from the gastrointestinal tract <sup>[[#References|[14]]]</sup>. However, further research is required to investigate the mechanisms behind this process as well as examining the genes and structures within this bacterium that are involved as virulence factors.  


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


Currently, there is limited use of P. micra in biotechnology, which includes the development of antibiotics and antibacterial monomers for use in periodontitis and cavity disinfection <sup>[[#References|[16, 17]]]</sup>. This is due to P. micra having the potential to mediate infection and disease, such as periodontitis <sup>[[#References|[14]]]</sup>.  
Currently, there is limited use of ''P. micra'' in biotechnology, which includes the development of antibiotics and antibacterial monomers for use in periodontitis and cavity disinfection <sup>[[#References|[16, 17]]]</sup>. This is due to ''P. micra'' having the potential to mediate infection and disease, such as periodontitis <sup>[[#References|[14]]]</sup>.  


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


Recent findings regarding P. micra includes recently documented diseases that the bacterium can potentially cause, such as endocarditis <sup>[[#References|[12]]]</sup>. Another recent discovery include how P. micra can be involved in polymicrobial infections with Aggregatibacter aphrophilus, where it causes pleural empyema <sup>[[#References|[13]]]</sup>. Furthermore, it has been documented that P. micra could be a potential pathogen associated with joint and bone infections, where a recent case study has discovered that septic arthritis of native joints can be caused by this bacterium <sup>[[#References|[9]]]</sup>.  
Recent findings regarding ''P. micra'' includes recently documented diseases that the bacterium can potentially cause, such as endocarditis <sup>[[#References|[12]]]</sup>. Another recent discovery include how ''P. micra'' can be involved in polymicrobial infections with ''Aggregatibacter aphrophilus'', where it causes pleural empyema <sup>[[#References|[13]]]</sup>. Furthermore, it has been documented that ''P. micra'' could be a potential pathogen associated with joint and bone infections, where a recent case study has discovered that septic arthritis of native joints can be caused by this bacterium <sup>[[#References|[9]]]</sup>.  


A recent literature has displayed interaction that occurs in the subgingival dental plaque between a bacterium of candidate division TM7 and other bacterial species, such as P. micra <sup>[[#References|[18]]]</sup>. Certain bacterial species studied by the literature are associated with the potential to mediate periodontitis <sup>[[#References|[18]]]</sup>. The interaction identified included morphological change that occured in TM7 bacteria, where it changed from a cocci to a rod, when it was in close proximity with P. micra bacteria <sup>[[#References|[18]]]</sup>. This change is due to the variations in metabolic conditions and signalling within the biofilm, where further research could provide understanding about these bacterial species and their potential to mediate disease in a biofilm environment <sup>[[#References|[18]]]</sup>.  
A recent literature has displayed interaction that occurs in the subgingival dental plaque between a bacterium of candidate division TM7 and other bacterial species, such as ''P. micra'' <sup>[[#References|[18]]]</sup>. Certain bacterial species studied by the literature are associated with the potential to mediate periodontitis <sup>[[#References|[18]]]</sup>. The interaction identified included morphological change that occured in TM7 bacteria, where it changed from a cocci to a rod, when it was in close proximity with ''P. micra'' bacteria <sup>[[#References|[18]]]</sup>. This change is due to the variations in metabolic conditions and signalling within the biofilm, where further research could provide understanding about these bacterial species and their potential to mediate disease in a biofilm environment <sup>[[#References|[18]]]</sup>.  


==References==
==References==
1. [http://www.uniprot.org/taxonomy/33033 Taxonomy – Parvimonas micra]
1. [http://www.uniprot.org/taxonomy/33033 Taxonomy – Parvimonas micra]
2. [http://www.bacterio.net/parvimonas.html Genus Parvimonas]
2. [http://www.bacterio.net/parvimonas.html Genus Parvimonas]
3. [http://www.sciencedirect.com/science/article/pii/S1075996415300263 Pilmis, B., Israel, J., Monnier, A.Le., Mizrahi, A. (2015) Spondylodiscitis due to anaerobic bacteria about a case of Parvimonas micra infection. Anaerobe <b>34</b>:156-157.]
3. [http://www.sciencedirect.com/science/article/pii/S1075996415300263 Pilmis, B., Israel, J., Monnier, A.Le., Mizrahi, A. (2015) Spondylodiscitis due to anaerobic bacteria about a case of ''Parvimonas micra'' infection. Anaerobe <b>34</b>:156-157.]
4. [http://genomea.asm.org/content/1/6/e01025-13.short Ang, M.Y., Dymock, D., Tan. J.L., Thong, M.H., Tan, Q.K., Wong, G.J., Paterson, I.C., Choo, S.W. (2013) Genome Sequence of Parvimonas micra Strain A293, Isolated from an Abdominal Abscess from a Patient in the United Kingdom. Genome Announcements <b>1</b>: e01025-13.]
4. [http://genomea.asm.org/content/1/6/e01025-13.short Ang, M.Y., Dymock, D., Tan. J.L., Thong, M.H., Tan, Q.K., Wong, G.J., Paterson, I.C., Choo, S.W. (2013) Genome Sequence of ''Parvimonas micra'' Strain A293, Isolated from an Abdominal Abscess from a Patient in the United Kingdom. Genome Announcements <b>1</b>: e01025-13.]
5. [http://www.microbiologyresearch.org/docserver/fulltext/ijsem/56/11/2711.pdf?expires=1508302175&id=id&accname=guest&checksum=DF37A65CF0887B9DF80B0BD4869EE6CB Tindall, B.J., Euzeby, J.P. (2006) Proposal of Parvimonas gen. nov. and Quatrionicoccus gen. nov. as replacements for the illegitimate, prokaryotic, generic names Micromonas Murdoch and Shah 2000 and QuadricoccusMaszenan et al. 2002, respectively. International Journal of Systematic and Evolutionary Microbiology <b>56</b>: 2711-2713.]
5. [http://www.microbiologyresearch.org/docserver/fulltext/ijsem/56/11/2711.pdf?expires=1508302175&id=id&accname=guest&checksum=DF37A65CF0887B9DF80B0BD4869EE6CB Tindall, B.J., Euzeby, J.P. (2006) Proposal of Parvimonas gen. nov. and Quatrionicoccus gen. nov. as replacements for the illegitimate, prokaryotic, generic names Micromonas Murdoch and Shah 2000 and QuadricoccusMaszenan et al. 2002, respectively. International Journal of Systematic and Evolutionary Microbiology <b>56</b>: 2711-2713.]
6. [https://www.futuremedicine.com/doi/full/10.2217/fmb.12.71 Kumar, P.S. (2012) Smoking and the subgingival ecosystem: a pathogen-enriched community. Future Microbiology <b>7</b>: 917-919.]  
6. [https://www.futuremedicine.com/doi/full/10.2217/fmb.12.71 Kumar, P.S. (2012) Smoking and the subgingival ecosystem: a pathogen-enriched community. Future Microbiology <b>7</b>: 917-919.]  
7. [http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0009321 Zijnge, V., Van Leeuwen, B.M., Degener, J.E., Abbas, F., Thurnheer, T., Gmür, R., Harmsen, H.J.M. (2010) Oral Biofilm Architecture on Natural Teeth. PLoS ONE <b>5</b>: e9321.]
7. [http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0009321 Zijnge, V., Van Leeuwen, B.M., Degener, J.E., Abbas, F., Thurnheer, T., Gmür, R., Harmsen, H.J.M. (2010) Oral Biofilm Architecture on Natural Teeth. PLoS ONE <b>5</b>: e9321.]
8. [http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0013135 Standar, K., Kreikemeyer, B., Redanz, S., Münter, W.L., Laue, M., Podbielski, A. (2010) Setup of an In Vitro Test System for Basic Studies on Biofilm Behavior of Mixed-Species Cultures with Dental and Periodontal Pathogens. PLoS ONE <b>5</b>: e13135.]
8. [http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0013135 Standar, K., Kreikemeyer, B., Redanz, S., Münter, W.L., Laue, M., Podbielski, A. (2010) Setup of an In Vitro Test System for Basic Studies on Biofilm Behavior of Mixed-Species Cultures with Dental and Periodontal Pathogens. PLoS ONE <b>5</b>: e13135.]
9. [http://www.sciencedirect.com/science/article/pii/S1075996416300087 Baghban, A., Gupta, S. (2016) Parvimonas micra: A rare cause of native joint septic arthritis. Anaerobe <b>39</b>: 26-27.]  
9. [http://www.sciencedirect.com/science/article/pii/S1075996416300087 Baghban, A., Gupta, S. (2016) ''Parvimonas micra'': A rare cause of native joint septic arthritis. Anaerobe <b>39</b>: 26-27.]  
10. [https://link.springer.com/article/10.1007%2FBF02148708?LI=true Neut, C., Lesieur, V., Romond, C., Beerens, H. (1985) Analysis of Gram-Positive Anaerobic Cocci in Oral, Fecal and Vaginal Flora. European Journal of Clinical Microbiology <b>8</b>: 435-437.]  
10. [https://link.springer.com/article/10.1007%2FBF02148708?LI=true Neut, C., Lesieur, V., Romond, C., Beerens, H. (1985) Analysis of Gram-Positive Anaerobic Cocci in Oral, Fecal and Vaginal Flora. European Journal of Clinical Microbiology <b>8</b>: 435-437.]  
11. [https://bmcoralhealth.biomedcentral.com/articles/10.1186/1472-6831-14-13 Al-hebshi, N.N., Shuga-Aldin, H.M., Al-Sharabi, A.K., Ghandour, I. (2014) Subgingival periodontal pathogens associated with chronic periodontitis in Yemenis. BMC Oral Health <b>14</b> :13.]  
11. [https://bmcoralhealth.biomedcentral.com/articles/10.1186/1472-6831-14-13 Al-hebshi, N.N., Shuga-Aldin, H.M., Al-Sharabi, A.K., Ghandour, I. (2014) Subgingival periodontal pathogens associated with chronic periodontitis in Yemenis. BMC Oral Health <b>14</b> :13.]  
12. [http://journals.lww.com/eurojgh/Abstract/2013/02000/Subgingival_microflora_in_inflammatory_bowel.17.aspx Brito, F.T.P., Zaltman, C.G., Carvalho, A.M.S., Fischer, R.M.S., Persson, R.M.S., Gustafsson, A.M.S., Figueredo, C.M.S. (2013) Subgingival microflora in inflammatory bowel disease patients with untreated periodontitis. European Journal of Gastroenterology & Hepatology <b>25</b>: 239-245.]  
12. [http://journals.lww.com/eurojgh/Abstract/2013/02000/Subgingival_microflora_in_inflammatory_bowel.17.aspx Brito, F.T.P., Zaltman, C.G., Carvalho, A.M.S., Fischer, R.M.S., Persson, R.M.S., Gustafsson, A.M.S., Figueredo, C.M.S. (2013) Subgingival microflora in inflammatory bowel disease patients with untreated periodontitis. European Journal of Gastroenterology & Hepatology <b>25</b>: 239-245.]  
13. [https://www.ncbi.nlm.nih.gov/pubmed/25138795 Rodriguez-Segade, S., Velasco, D., Marcos, P.J. (2015) Empyema due to Aggregatibacter aphrophilus and Parvimonas micra Coinfection. Archivos de bronconeumología <b>51</b>: 254-255.]  
13. [https://www.ncbi.nlm.nih.gov/pubmed/25138795 Rodriguez-Segade, S., Velasco, D., Marcos, P.J. (2015) Empyema due to ''Aggregatibacter aphrophilus'' and ''Parvimonas micra'' Coinfection. Archivos de bronconeumología <b>51</b>: 254-255.]  
14. [http://www.sciencedirect.com/science/article/pii/S1075996415300676 Gomez, C.A., Gerber, D.A., Zambrano, E., Banaei, N., Deresinski, S., Blackburn, B.G. (2015) First case of infectious endocarditis caused by Parvimonas micra. Anaerobe <b>36</b>: 53-55.]
14. [http://www.sciencedirect.com/science/article/pii/S1075996415300676 Gomez, C.A., Gerber, D.A., Zambrano, E., Banaei, N., Deresinski, S., Blackburn, B.G. (2015) First case of infectious endocarditis caused by ''Parvimonas micra''. Anaerobe <b>36</b>: 53-55.]
15. [http://casereports.bmj.com/content/2012/bcr.01.2012.5644.abstract Taylor, G.M., Elliott, L., Sosin, M.D., Soo, S.S. (2012) Complication of etanercept treatment for rheumatoid arthritis – purulent pericarditis caused by a commensal organism. BMJ Case Reports <b>2012</b>: 1-3.]
15. [http://casereports.bmj.com/content/2012/bcr.01.2012.5644.abstract Taylor, G.M., Elliott, L., Sosin, M.D., Soo, S.S. (2012) Complication of etanercept treatment for rheumatoid arthritis – purulent pericarditis caused by a commensal organism. BMJ Case Reports <b>2012</b>: 1-3.]
16. [http://www.joponline.org/doi/abs/10.1902/jop.2011.100657 Mouratidou, A., D’Hoedt, B., Karbach, J., Al-Nawas, B. (2011) Antibiotic Susceptibility of Cocultures in Polymicrobial Infections Such
16. [http://www.joponline.org/doi/abs/10.1902/jop.2011.100657 Mouratidou, A., D’Hoedt, B., Karbach, J., Al-Nawas, B. (2011) Antibiotic Susceptibility of Cocultures in Polymicrobial Infections Such

Revision as of 04:56, 18 October 2017


Classification

Higher order taxa

Bacteria – Firmicutes – Tissierellia – Tissierellales – Peptoniphilaceae – Parvimonas [1]

Species

Parvimonas micra (P. micra) and type of strain includes ATCC 33270, CCUG 46357, CIP 105294, DSM 20468, GIFU 7824, JCM 12970, NCTC 11808, and VPI 5464 [2].

Description and significance

P. micra is a gram positive cocci that forms pairs and groups of short chains, where it is not associated with the formation of spores [3, 4]. The bacterium is an obligate anaerobe and was first identified and classified in 1933 as Peptostreptococcus micros [3, 5]. The species was then reclassified in 1999 as Micromonas micros and again in 2006 as Parvimonas micra [5]. Since its discovery, the bacterium has been deemed a commensal pathogen in the human oral cavity, where it is most abundant in the subgingival dental plaque [3, 4, 6].

P. micra can be observed via culturing, where anaerobic culture vials and blood agar can be used to achieve observable colonies [3]. Incubation period is suggested to be around 48 hours [3]. The importance of this bacterium regarding research would be its implication in pathogen mediated diseases in humans, such as periodontitis [7].


Figure 1: Purple staining indicates the presence of P. micra, where the stain colouration is associated with gram positive bacteria [16].

Genome structure

Genome structural analysis of P. micra based on strain A293 displayed a genome size of 1,680,794bp, where it had a G + C content of 28.3% [4]. The strain contained 49 contigs, where contig size varied from 539bp to 407,487bp [4]. Further genome analysis displayed that the genome comprises of 1,560 coding sequences and 46 RNAs, where 40 represents tRNAs and 6 rRNAs [4].

The total number of genes detected in the A293 strain was around 430 genes [4]. From this, 137 genes are associated with the metabolism of proteins, 60 are involved the processing carbohydrates, 86 are essential in amino acid synthesis, 58 are key in DNA synthesis, and 89 are related to RNA synthesis [4]. The 62 genes out of the 89 genes associated with RNA synthesis were identified to be involved in nucleotide formation and nucleoside synthesis, while 3 genes out of 89 genes are related with prophages, phage, plasmids, and transposable elements [4].

Cell structure and metabolism

P. micra is a gram-positive bacterium, which indicates that a large composition of its cell wall is made up of a thick layer of peptidoglycan [3]. P. micra has no flagella and is associated with biofilms in the subgingival dental plaque of the human oral cavity [7]. Often observed as micro-colonies in the top layer of these biofilms, its presence has pathogenic potential and can give rise to periodontitis [7]. Scientific finding has suggested that P. micra resides in biofilms that have already been developed, as it has no ability to form structures associated with biofilm formation [8].


Figure 2: Cluster of P. micra bacterial cells indicated using a yellow fluorescence, where they are detected in the top layer of the biofilm associated with the sub-gingival dental plaque [7].

Ecology

P. micra is an obligate anaerobe that resides in the human oral cavity, where it is most abundant in the subgingival dental plaque as a commensal pathogen [3, 4, 6]. In addition, P. micra is also identified to inhabit the gastrointestinal tract [9]. Furthermore, it is suggested that P. micra has a potential to be a constitute of the vaginal flora; however, further research is required for verification [3, 10].

Pathology

P. micra is regarded as one of the pathogens that causes periodontitis in humans, which is a commonly observed disease [7, 8]. The pathogenesis of periodontitis involves the damage of tissue structures that support the teeth, such as the gums, the alveolar bone, and periodontal ligament, due to bacterial infection and inflammation [11, 12]. In addition, the disease is associated with severe complications if treatment is not provided early and adequately, as there is potential for it to spread to surrounding tissues [8].

Regarding pathogenesis, P. micra, is associated with the disturbance of the composition and abundance of commensal microorganisms established within biofilms that coats the subgingival dental plaque [8]. Therefore, a disturbance that leads to a slight increase in the abundance of pathogenic bacterial species, especially P. micra, would increase the likelihood of an infection or a disease to occur, such as periodontitis.

P. micra has also been documented to be involved in polymicrobial infections with Aggregatibacter aphrophilus, where it causes pleural empyema [13]. In addition, P. micra has been recently documented to cause endocarditis, where the bacterium was identified through molecular sequencing [14]. Furthermore, P. micra has been recently identified to be associated with septic arthritis of native joints, which suggests that this bacterium could be a potential pathogen for infections associated with joints and bones [9].

Other infections and diseases associated with P. micra includes peritonsillar abscesses, respiratory infections, pleural empyema, intracranial abscesses, paranasal sinus infections, spondylodiscitis, pericarditis, and septic embolism [3, 14, 15]. The ability of P. micra to cause infection in other sites of the human body apart from the oral cavity is suggested to be due to the translocation of the bacterium from the oral cavity or from the gastrointestinal tract [14]. However, further research is required to investigate the mechanisms behind this process as well as examining the genes and structures within this bacterium that are involved as virulence factors.

Application to biotechnology

Currently, there is limited use of P. micra in biotechnology, which includes the development of antibiotics and antibacterial monomers for use in periodontitis and cavity disinfection [16, 17]. This is due to P. micra having the potential to mediate infection and disease, such as periodontitis [14].

Current research

Recent findings regarding P. micra includes recently documented diseases that the bacterium can potentially cause, such as endocarditis [12]. Another recent discovery include how P. micra can be involved in polymicrobial infections with Aggregatibacter aphrophilus, where it causes pleural empyema [13]. Furthermore, it has been documented that P. micra could be a potential pathogen associated with joint and bone infections, where a recent case study has discovered that septic arthritis of native joints can be caused by this bacterium [9].

A recent literature has displayed interaction that occurs in the subgingival dental plaque between a bacterium of candidate division TM7 and other bacterial species, such as P. micra [18]. Certain bacterial species studied by the literature are associated with the potential to mediate periodontitis [18]. The interaction identified included morphological change that occured in TM7 bacteria, where it changed from a cocci to a rod, when it was in close proximity with P. micra bacteria [18]. This change is due to the variations in metabolic conditions and signalling within the biofilm, where further research could provide understanding about these bacterial species and their potential to mediate disease in a biofilm environment [18].

References

1. Taxonomy – Parvimonas micra 2. Genus Parvimonas 3. Pilmis, B., Israel, J., Monnier, A.Le., Mizrahi, A. (2015) Spondylodiscitis due to anaerobic bacteria about a case of Parvimonas micra infection. Anaerobe 34:156-157. 4. Ang, M.Y., Dymock, D., Tan. J.L., Thong, M.H., Tan, Q.K., Wong, G.J., Paterson, I.C., Choo, S.W. (2013) Genome Sequence of Parvimonas micra Strain A293, Isolated from an Abdominal Abscess from a Patient in the United Kingdom. Genome Announcements 1: e01025-13. 5. Tindall, B.J., Euzeby, J.P. (2006) Proposal of Parvimonas gen. nov. and Quatrionicoccus gen. nov. as replacements for the illegitimate, prokaryotic, generic names Micromonas Murdoch and Shah 2000 and QuadricoccusMaszenan et al. 2002, respectively. International Journal of Systematic and Evolutionary Microbiology 56: 2711-2713. 6. Kumar, P.S. (2012) Smoking and the subgingival ecosystem: a pathogen-enriched community. Future Microbiology 7: 917-919. 7. Zijnge, V., Van Leeuwen, B.M., Degener, J.E., Abbas, F., Thurnheer, T., Gmür, R., Harmsen, H.J.M. (2010) Oral Biofilm Architecture on Natural Teeth. PLoS ONE 5: e9321. 8. Standar, K., Kreikemeyer, B., Redanz, S., Münter, W.L., Laue, M., Podbielski, A. (2010) Setup of an In Vitro Test System for Basic Studies on Biofilm Behavior of Mixed-Species Cultures with Dental and Periodontal Pathogens. PLoS ONE 5: e13135. 9. Baghban, A., Gupta, S. (2016) Parvimonas micra: A rare cause of native joint septic arthritis. Anaerobe 39: 26-27. 10. Neut, C., Lesieur, V., Romond, C., Beerens, H. (1985) Analysis of Gram-Positive Anaerobic Cocci in Oral, Fecal and Vaginal Flora. European Journal of Clinical Microbiology 8: 435-437. 11. Al-hebshi, N.N., Shuga-Aldin, H.M., Al-Sharabi, A.K., Ghandour, I. (2014) Subgingival periodontal pathogens associated with chronic periodontitis in Yemenis. BMC Oral Health 14 :13. 12. Brito, F.T.P., Zaltman, C.G., Carvalho, A.M.S., Fischer, R.M.S., Persson, R.M.S., Gustafsson, A.M.S., Figueredo, C.M.S. (2013) Subgingival microflora in inflammatory bowel disease patients with untreated periodontitis. European Journal of Gastroenterology & Hepatology 25: 239-245. 13. Rodriguez-Segade, S., Velasco, D., Marcos, P.J. (2015) Empyema due to Aggregatibacter aphrophilus and Parvimonas micra Coinfection. Archivos de bronconeumología 51: 254-255. 14. Gomez, C.A., Gerber, D.A., Zambrano, E., Banaei, N., Deresinski, S., Blackburn, B.G. (2015) First case of infectious endocarditis caused by Parvimonas micra. Anaerobe 36: 53-55. 15. Taylor, G.M., Elliott, L., Sosin, M.D., Soo, S.S. (2012) Complication of etanercept treatment for rheumatoid arthritis – purulent pericarditis caused by a commensal organism. BMJ Case Reports 2012: 1-3. 16. [http://www.joponline.org/doi/abs/10.1902/jop.2011.100657 Mouratidou, A., D’Hoedt, B., Karbach, J., Al-Nawas, B. (2011) Antibiotic Susceptibility of Cocultures in Polymicrobial Infections Such as Peri-Implantitis or Periodontitis: An In Vitro Model. Journal of Periodontology 82: 1360-1366.] 17. Hirose, N., Kitagawa, R., Kitagawa, H., Maezono, H., Mine, A., Hayashi, M., Haapasalo, M., Imazato, S. (2016) Development of a Cavity Disinfectant Containing Antibacterial Monomer MDPB. Journal of Dental Research 95: 1487-1493. 18. Soro, V., Dutton, L.C., Sprague, S.V., Nobbs, A.H., Ireland, A.J., Sandy, J.R., Jepson, M.A., Micaroni, M., Splatt, P.R., Dymock, D., Jenkinson, H.F. (2014) Axenic Culture of a Candidate Division TM7 Bacterium from the Human Oral Cavity and Biofilm Interactions with Other Oral Bacteria. Applied and environmental microbiology 80: 6480-6489.

This page is written by Tristan Villamor for the MICR3004 course, Semester 2, 2017