Difference between revisions of "Veillonella parvula"

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Kristoffer Hua
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{{Uncurated}}
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{{Biorealm Genus}}
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==Classification==
  
Bench C
 
 
21/09/2016
 
<ref>MICR3004</ref>
 
==Classification==
 
 
===Higher order taxa===
 
===Higher order taxa===
  
Bacteria – Proteobacteria – Betaproteobacteria – Neisseriales– Neisseriaceae – Kingella
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Bacteria; Firmicutes; Clostridia; Clostridiales; Veillonellaceae
  
 
===Species===
 
===Species===
[[Image:K_oralis_gramstain.png‎|frame|right|150px|Gram stain of <i>Kingella oralis</i> isolated from oral cavity of infected cat.<sup>[[#References|[9]]]</sup>]]
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[[Image:veipa.jpg‎|frame|right|150px|Te3 strain of ''V. parvula'' as show by scanning electron microscope [6]]]  
<i>Kingella oralis</i>
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''Veillonella parvula''
  
Type strain: UB-38, ATCC 51147, CCUG 30450, CIP 103803.
 
 
==Description and significance==
 
==Description and significance==
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''Veillonella parvula'' is a gram negative, strict anaerobic, non-spore-forming coccus-shaped bacterium. It is found in the gut of humans and dental plaque. While considered non-pathogenic, it has been linked with rare cases of meningitis, osteomyelitis, and periodontal disease [7]. It cannot metabolize carbohydrates, but instead uses organic acids like lactate.
  
<i>Kingella oralis</i> is a gram negative, bacilli-shaped facultative anaerobe.<sup>[[#References|[1]]]</sup> This organism is found to have high prevalence in human dental plaque, mucosal surfaces and in saliva.<sup>[[#References|[2]]]</sup> Contrary to the other members of the <i>Kingella</i> genus, <i>K. oralis</i> is a common colonizer in the human oral cavity that has little involvement in diseases. Associations of this bacteria and periodontitis have been recognized. This is because in some periodontitis infection sites, high prevalence is evident. However, correlations to the severity are not clearly distinguished. <sup>[[#References|[3]]]</sup>
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Perhaps the most significant role of ''V. parvula'' is its involvement in biofilms. It is able to coaggregate with other organisms, namely ''Streptococcus mutans'', to the dental plaque. The two organisms have a mutualistic relationship with each other; ''V. parvula'' cannot adhere to the surface of teeth by itself, and so attaches to ''S. mutans''. It can use the lactate product formed by ''S. mutans'' for its metabolism, in the process forming a less corrosive acid. In this particular case, the biofilm has been found to be more resistant to antimicrobials than either of the singular species [1].
  
Studies in culture indicate that it is a non-motile organism; however the cells are capable of forming spreading colonies on agar.<sup>[[#References|[1]]]</sup> Similarities in phenotypic traits and oral distribution with <i>Eikenella corrodens</i> make it difficult to detect <i>K. oralis</i> with rapid diagnostic assays. <sup>[[#References|[3]]]</sup>
 
 
==Genome structure==
 
==Genome structure==
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The genome is a single circular chromosome comprised of 2,132,142 base pairs with a GC content of 38.6%. 1920 genes have been documented, 1859 of which code for proteins, and 61 associated with RNA [6].
  
Like most bacteria, <i>K. oralis</i> has a circular genome which contains 2,406,670 base pairs with a GC content of 54.3%. A total of 2371 genes have been recognized, 2315 encoding for proteins and 56 associated with RNA.<sup>[[#References|[4]]]</sup>
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==Cell and colony structure==
==Cell structure and metabolism==
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The cells of ''V. parvula'' are coccus shaped, non-motile, roughly 0.4 µm in diameter, and predominantly occur in chains [6]. Like other gram negative bacteria, ''V. parvula'' has an outer layer of lipopolysaccharide which is a known virulence factor [4]. Putrescine and cadaverine are major constituents of ''V. parvula’s'' peptidoglycan and it cannot live without them [2]. Also present are plasmalogens, ether phospholipids found mainly in mammals and other anaerobic bacteria which may be connected to regulation of membrane fluidity.
  
The cells of <i>K. oralis</i> are depicted as non-motile agar-corroding rods in sizes of 0.6-0.7 µm x 1-3 µm with rounded ends that can occur in chains or pairs.<sup>[[#References|[2]]]</sup> As a gram negative bacterium, <i>K. oralis</i> comprises of the typical structural compositions (lipopolysaccharides, porins, lipoproteins and peptidoglycans).
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==Metabolism==
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''V. parvula'' cannot ferment carbohydrates. It uses organic acid by-products of carbohydrate processing organisms for its metabolism. Their main source of energy and metabolites is from the conversion of lactate into propionate and acetate as shown in the following stoichiometric equation: [3]
 +
 
 +
8 lactate > 5 propionate + 3 acetate + 3 CO2 + H2
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 +
Oddly, despite a missing hexokinase necessary for the beginning steps of glycolysis, ''V. parvula'' still has a functioning pyruvate kinase. It is possible the pyruvate kinase is involved in gluconeogenesis when deactivated by ATP [5].
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 +
''V. parvula'' can also use the enzyme methylmalonyl-CoA decarboxylase to metabolize succinate in the presence of lactate. The resulting free energy can be used to power a sodium ion pump [7].
  
Typically, members of the <i>Kingella</i> genus ferment glucose and are nutritionally demanding, oxidase-positive and catalase-negative bacterium. <i>Kingella</i> cells produce acid from glucose and other carbohydrates. <sup>[[#References|[5]]]</sup> Unlike <i>Kingella Kingae</i>, <i>K. oralis</i> cannot produce acid from maltose or reduce nitrite and nitrate in its metabolic process. <sup>[[#References|[2]]]</sup>
 
 
==Ecology==
 
==Ecology==
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''V. parvula'' is found in the gut and oral cavity of humans. In the oral cavity, the microbe is able to form biofilms with other organisms with similar niches [1]. ''V. parvula'' gets a large majority of its lactate from the organisms it coaggregates with.
  
Colonisation of the oral cavity and the upper respiratory tract and its survivability is determined by a few factors. As a mesophile, the organism can persist in temperatures between 20°C and 45°C.<sup>[[#References|[4]]]</sup> Interbacterial adhesion between genetically distinct bacteria such as streptococci and actinomyces species allow for efficient usage of nutrients and protection. <sup>[[#References|[6]]]</sup>
 
 
==Pathology==
 
==Pathology==
 
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''V. parvula'' is usually not considered a pathogen. However, it has been implicated with rare cases of meningitis, osteomyelitis, and periodontal disease [8]. The lipopolysaccharide has been found as a major virulence factor in some of these diseases [4]. Other more pathogenic microbes such as ''S. mutans'' use the biofilm formed with ''V. parvula'' as a virulence factor for periodontal disease [1], and therefore ''V. parvula'' could be indirectly involved with the pathogenesis of other microbes ''V. parvula'' is susceptible to penicillin [6].
<i>K. oralis</i> is a pathogenic microorganism as it has been indicated to be associated with periodontitis in humans. As the dominant species of the subgingival microbiota in periodontitis sites, the capacity to cause disease is highlighted. <sup>[[#References|[3]]]</sup> Furthermore, a case study in 2010 has indicated that it has the capacity to infect felines and perhaps other animals. <sup>[[#References|[9]]]</sup>
 
 
 
Species belonging to the <i>Kingella</i> genus express multiple virulence factors. A type IV pili is used for enhancing adhesion to epithelial and synovial cells for colonisation. <i>K. oralis</i> forms spreading/corroding colonies with high density pilation by regulating a major pilus subunit, pilA1 through expressing high levels of σ54. Although it may have a direct link to periodontitis, it is less virulent than <i>K. kingae</i> which produces RTX Toxin, a potent cytotoxin. <sup>[[#References|[7]]]</sup>
 
  
 
==References==
 
==References==
1.[https://books.google.com.au/books?id=VloMBAAAQBAJ&pg=PA374&lpg=PA374&dq=kingella+oralis+pathogen&source=bl&ots=6d1gdrdRXo&sig=pO3I-5S_YPZfwJvXReDmfkf2lbo&hl=en&sa=X&ved=0ahUKEwi5y-jWrp3PAhUEOj4KHUt2AWYQ6AEIRjAF#v=onepage&q=kingella%20oralis&f=false Mahon, C.R., Lehman, D.C., Jr, G.M., 2014. Textbook of Diagnostic Microbiology. Elsevier Health Sciences.]
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1. Luppens SB, et. al. 2008. Effect of Veillonella parvula on the antimicrobial resistance and gene expression of Streptococcus mutans grown in a dual-species biofilm, Oral Microbial Immunology, 23(3):183-9
  
2.[https://books.google.com.au/books?id=nnGhc44bypAC&pg=PA745&lpg=PA745&dq=periodontitis+Kingella+oralis&source=bl&ots=gLd_ElB4eb&sig=iZjjOYYzATjvzSly-NTK5Awj69o&hl=en&sa=X&ved=0ahUKEwjLlMCtu53PAhWJWT4KHViWAUQQ6AEIQTAF#v=onepage&q=periodontitis%20Kingella%20oralis&f=false Liu, D., 2011. Molecular Detection of Human Bacterial Pathogens. CRC Press.]
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2. Y Kamio and K Nakamura. 1987. Putrescrine and cadaverine are consitiuients of peptidoglycan in Veillonella alcalescens and Veillonella parvula, Journal of Bacteriology, 169(6):2881
  
3.[http://onlinelibrary.wiley.com/doi/10.1111/j.1399-302X.1996.tb00206.x/abstract Chen, C., 1996. Distribution of a newly described species, Kingella oralis, in the human oral cavity. Oral Microbiology and Immunology <b>11</b>: 425–427. ]
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3. Stephen K. C. Ng and Ian R. Hamilton. 1971. Lactate metabolism by Veillonella parvula, Journal of Bacteriology, 105(3):999
  
4.[http://www.ncbi.nlm.nih.gov/genome/?term=Kingella%20oralis National Center for Biotechnology Information, Kingella oralis overview, viewed 19-09-2016]
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4. H Nygren, G Dahlén and L A Nilsson. 1979. Human complement activation by lipopolysaccharides from Bacteroides oralis, Fusobacterium nucleatum and Veillonella parvula, Infection and Immunity, 26(2):391
  
5.[https://books.google.com.au/books?id=l56-WMdyqzcC&pg=PA284&lpg=PA284&dq=Kingella+fastidious&source=bl&ots=FZ17b5O3de&sig=5eSrsWmqTP3R-XmUowIciOBuAtQ&hl=en&sa=X&ved=0ahUKEwirtKX7wJ_PAhVIPD4KHZQcDfQQ6AEIZTAJ#v=onepage&q=Kingella%20fastidious&f=false Engelkirk, P.G., Duben-Engelkirk, J.L., 2008. Laboratory Diagnosis of Infectious Diseases: Essentials of Diagnostic Microbiology. Lippincott Williams & Wilkins.]
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5. S K Ng and I R Hamilton. 1975. Purification and regulatory properties of pyruvate kinase from Veillonella parvula, Journal of Bacteriology, 122(3):1274.
  
6.[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4249035/ Ruhl, S., Eidt, A., Melzl, H., Reischl, U., Cisar, J.O., 2014. Probing of Microbial Biofilm Communities for Coadhesion Partners. Appl Environ Microbiol <b>80</b>: 6583–6590.]
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6. Sabine Gronow, et al. 2010. Complete genome sequence of Veillonella parvula type strain (Te3T), Stand Genomic Sci., 2(1): 57-65.
  
7.[http://jb.asm.org/content/189/2/430.full.pdf Kehl-Fie, T. E., Geme, J.W., 2007 Identification and Characterization of an RTX Toxin in the Emerging Pathogen Kingella kingae. J. Bacteriol. <b>189</b>:430-436]
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7. J B Huder and P Dimroth. 1993. Sequence of the sodium ion pump methylmalonyl-CoA decarboxylase from Veillonella parvula, The Journal of Biological Chemistry, vol. 268, No. 33.
  
8.[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4284298/ Yagupsky, P., 2015. Kingella kingae: Carriage, Transmission, and Disease. Clin Microbiol Rev <b>28</b>: 54–79.]
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8. Maqsood A. Bhatti and Michael O. Frank. Veillonella parvula Meningitis: Case Report and Review of Veillonella Infections, Clinical Infectious Diseases, 31(3): 839-840
  
9.[http://www.vetpol.org.pl/prawo-projekty-legislacja/doc_download/727-04-artykul Adaszek, Ł., et al. (2010). "A case of Kingella oralis infection in the cat." Życie Weterynaryjne <b>85</b>(7): 604-606]
 
  
<references/>
 
  
This page is written by Kristoffer Hua for the MICR3004 course, Semester 2, 2016
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Edited by Steve Severn of Dr. Lisa R. Moore, University of Southern Maine, Department of Biological Sciences, http://www.usm.maine.edu/bio

Latest revision as of 08:26, 22 September 2016

This student page has not been curated.

A Microbial Biorealm page on the genus Veillonella parvula

Classification

Higher order taxa

Bacteria; Firmicutes; Clostridia; Clostridiales; Veillonellaceae

Species

Te3 strain of V. parvula as show by scanning electron microscope [6]

Veillonella parvula

Description and significance

Veillonella parvula is a gram negative, strict anaerobic, non-spore-forming coccus-shaped bacterium. It is found in the gut of humans and dental plaque. While considered non-pathogenic, it has been linked with rare cases of meningitis, osteomyelitis, and periodontal disease [7]. It cannot metabolize carbohydrates, but instead uses organic acids like lactate.

Perhaps the most significant role of V. parvula is its involvement in biofilms. It is able to coaggregate with other organisms, namely Streptococcus mutans, to the dental plaque. The two organisms have a mutualistic relationship with each other; V. parvula cannot adhere to the surface of teeth by itself, and so attaches to S. mutans. It can use the lactate product formed by S. mutans for its metabolism, in the process forming a less corrosive acid. In this particular case, the biofilm has been found to be more resistant to antimicrobials than either of the singular species [1].

Genome structure

The genome is a single circular chromosome comprised of 2,132,142 base pairs with a GC content of 38.6%. 1920 genes have been documented, 1859 of which code for proteins, and 61 associated with RNA [6].

Cell and colony structure

The cells of V. parvula are coccus shaped, non-motile, roughly 0.4 µm in diameter, and predominantly occur in chains [6]. Like other gram negative bacteria, V. parvula has an outer layer of lipopolysaccharide which is a known virulence factor [4]. Putrescine and cadaverine are major constituents of V. parvula’s peptidoglycan and it cannot live without them [2]. Also present are plasmalogens, ether phospholipids found mainly in mammals and other anaerobic bacteria which may be connected to regulation of membrane fluidity.

Metabolism

V. parvula cannot ferment carbohydrates. It uses organic acid by-products of carbohydrate processing organisms for its metabolism. Their main source of energy and metabolites is from the conversion of lactate into propionate and acetate as shown in the following stoichiometric equation: [3]

8 lactate > 5 propionate + 3 acetate + 3 CO2 + H2

Oddly, despite a missing hexokinase necessary for the beginning steps of glycolysis, V. parvula still has a functioning pyruvate kinase. It is possible the pyruvate kinase is involved in gluconeogenesis when deactivated by ATP [5].

V. parvula can also use the enzyme methylmalonyl-CoA decarboxylase to metabolize succinate in the presence of lactate. The resulting free energy can be used to power a sodium ion pump [7].

Ecology

V. parvula is found in the gut and oral cavity of humans. In the oral cavity, the microbe is able to form biofilms with other organisms with similar niches [1]. V. parvula gets a large majority of its lactate from the organisms it coaggregates with.

Pathology

V. parvula is usually not considered a pathogen. However, it has been implicated with rare cases of meningitis, osteomyelitis, and periodontal disease [8]. The lipopolysaccharide has been found as a major virulence factor in some of these diseases [4]. Other more pathogenic microbes such as S. mutans use the biofilm formed with V. parvula as a virulence factor for periodontal disease [1], and therefore V. parvula could be indirectly involved with the pathogenesis of other microbes V. parvula is susceptible to penicillin [6].

References

1. Luppens SB, et. al. 2008. Effect of Veillonella parvula on the antimicrobial resistance and gene expression of Streptococcus mutans grown in a dual-species biofilm, Oral Microbial Immunology, 23(3):183-9

2. Y Kamio and K Nakamura. 1987. Putrescrine and cadaverine are consitiuients of peptidoglycan in Veillonella alcalescens and Veillonella parvula, Journal of Bacteriology, 169(6):2881

3. Stephen K. C. Ng and Ian R. Hamilton. 1971. Lactate metabolism by Veillonella parvula, Journal of Bacteriology, 105(3):999

4. H Nygren, G Dahlén and L A Nilsson. 1979. Human complement activation by lipopolysaccharides from Bacteroides oralis, Fusobacterium nucleatum and Veillonella parvula, Infection and Immunity, 26(2):391

5. S K Ng and I R Hamilton. 1975. Purification and regulatory properties of pyruvate kinase from Veillonella parvula, Journal of Bacteriology, 122(3):1274.

6. Sabine Gronow, et al. 2010. Complete genome sequence of Veillonella parvula type strain (Te3T), Stand Genomic Sci., 2(1): 57-65.

7. J B Huder and P Dimroth. 1993. Sequence of the sodium ion pump methylmalonyl-CoA decarboxylase from Veillonella parvula, The Journal of Biological Chemistry, vol. 268, No. 33.

8. Maqsood A. Bhatti and Michael O. Frank. Veillonella parvula Meningitis: Case Report and Review of Veillonella Infections, Clinical Infectious Diseases, 31(3): 839-840


Edited by Steve Severn of Dr. Lisa R. Moore, University of Southern Maine, Department of Biological Sciences, http://www.usm.maine.edu/bio