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Teo Jia Ling Tricia; Bench E; 31/08/2016

Classification

Higher order taxa

Bacteria – Bacteria – Firmicutes – Negativicutes – Selenomonadales – Veillonellaceae – Veillonella

Species

Veillonella parvula
Strain ATCC 10790

Description and significance

It is a non-motile, non-spore forming, anaerobic gram-negative coccus. It can grow in pairs or in chains and grow to about 0.3 to 0.5m in size ^[1].

It was first described by Veillon and Zuber in 1898 as “Staphylococcus parvulus” ^[2] before being renamed as Veillonella parvula by Prévot in 1933 ^[3] and early experiments were conducted on V. parvula oral isolates ^[4]. It is commonly found in the human oral cavity, especially in subgingival dental plaque, gastrointestinal tract and vagina, as part of the microflora ^[1][4][5]. It is involved in establishing early microbial colonies in dental plaque formation, along with Streptococcus and other species ^[6][7] and can make up 10% of the early colonizing bacteria on the enamel ^[8]. However, it can also be associated with dental and other infections ^[1][9].

It plays an important role in microbial food chain by metabolizing end products of carbohydrate-fermenting bacteria, such as lactic acid bacteria, allowing it to symbiotically establish itself in anaerobic environments ^[10][11]. Despite its prevalence in the human body, studies on this bacterium has been extremely limited due to its difficulty in manipulation. Thus, it is still not well understood ^[12].

12 species have been described under the same genus ^[12], of which 6 species have been suggested to facilitate the development of oral biofilms ^[13]. V. parvula is the most abundant in the human oral cavity and gastrointestinal tract ^[12].

Genome structure

V. parvula is the only fully assembled genome in the Veillonella genus and comprises of 2,132,142 bp genome size circular chromosome, with 38.6% GC content. It encodes 1, 920 genes, of which 73.6% are functional, 61 RNAs and 1,859 proteins ^[1].

Cell structure and metabolism

V. parvula has a distinctive lipopolysaccharide (LPS) on its outer membrane. Its cell wall also consists of cadaverine and putrescine, which are essential for growth ^[14] and it is non-motile (1).

Biofilms develop when initial colonizers, streptococci and actinomyces bind to host-derived receptors in the saliva film-coated tooth enamel. This allows subsequent binding of Veillonella and other bacteria via coadhesion. Coaggregation, involving binding and cell-to-cell recognition between genetically distinct microbial species, subsequently follows, resulting in plaque formation. Saliva is a complex nutrient source. Development of plaque is thought to involve spatial organization of different bacteria and interactions between species, which in combination, is able to metabolize latent nutrients into usable ones to be further processed by other species ^[11].

V. parvula is involved in plaque development as it is able to interact metabolically with streptococci. Consumption of sucrose is then converted to glucose or fructose by streptococci. Most glucose is converted to lactate which is utilized by Veillonella, converting it into propionate, acetate and carbon dioxide for energy. This sets up a metabolic food chain in the dental plaque. It is also able to utilize other fermented organic acids such as pyruvate, malate and fumarate. V. parvula is unable to utilize carbohydrates and amino acids for energy ^[10][11].

Some sucrose is converted by streptococcal extracellular glucosyltransferase into dextran, which allows Veillonella to adhere and establish itself on tooth surfaces. Fructose, a product of dextran synthesis, can then be incorporated into Veillonella lipopolysaccharide (LPS), contributing to the production of endotoxic LPS ^[10].

Ecology

V. parvula is an anaerobe, found in subgingival plaque ^[15]. Development of thick plaque provides favourable anaerobic conditions, thus V. parvula is mostly distributed in deeper plaque layers. It is found to increase in numbers in presence of gingival infection ^[10].

In the development of biofilm and plaque, V. parvula associates with other oral microbes to establish itself in the oral microbial ecosystem via coadhesion and coaggregation. Coaggregation is mediated by binding of lectin-like adhesins to receptor polysaccharide on streptococci ^[5][11].

Pathology

Generally considered to be of low virulence. However, a study by Lupens et al. depicted the ability of V. parvula to enhance the pathogenicity of other bacterium, when co-cultured together, and its implication on polymicrobial diseases such as caries and periodontitis. It was shown that co-culture of Streptococcus mutans and V. parvula in a biofilm changes the physiology of S. mutans and enhances its antimicrobial property ^[16]. In rare cases, V. parvula can also cause deep neck infections, chronic maxillary sinusitis and bacteraemia, meningitis, endocarditis, tonsillitis, discitis, prosthetic joint infection ^[1][17].

Presence of LPS on V. parvula cell wall was shown to significantly elevate IL-6 production in immune cells in a Toll-like receptor 4 (TLR4)-dependent process, resulting in inflammatory and immune response which occur during infections ^[17].

Risk factors of V. parvula infections include individuals with periodontal disease, immune deficiency, premature birth and use of intravenous drugs ^[17].

Bacteria is resistant to vancomycin, tetracycline, aminoglycosides and ciprofloxacin (9), but infection can typically be treated with penicillin, cephalosporin, clindamycin, metronidazole, chloramphenicol ^[18].

Application to biotechnology

Studies on Veillonella species have been limited to physiological characterizations due to its complexity in genetic manipulability. This makes it one of the least understood organism, in terms of biology and pathogenic potential, in the human microbiome, despite its prevalence in the human body ^[12].

Liu et al. reported to have done the first genetic transformation in V. atypica, using a shutter vector, paving the way for future use of V. atypica as a genetic system for Veillonella studies ^[19].

The lactic acid metabolism property of V. parvula can potentially be exploited in the farming industry. Ruminal acidosis has been a significant concern in the farming industry, which causes death and weight loss in sheep and cattle. Rumen lactic acidosis occurs when the ruminant consumes large amounts of feeds high in ruminal fermentable carbohydrates, which they are unaccustomed to. This leads to the production of lactic acid in the rumen, reducing the efficiency of rumen flora and fermentation ^[20]. A previous study by Kung et al. showed that the use of another lactate-utilizing bacteria, Megasphaera elsdenii, is able to reduce lactate levels in vitro. This finding could possibly be translated in vivo ^[21]. V. parvula can thus potentially be an alternate form of ruminal acidosis treatment and prevention in the future.

Current research

V. parvula is a major hydrogen sulphide (H2S) producer, making it a major cause of bad breath. However, little research was done on physiological properties affecting of H2S production by V. parvula. A recent study by Washio et al., investigated the effects of cell growth stages and environmental factors, such as pH and presence of lactate, on H2S production. H2S is produced from L-Cysteine, found in saliva due to epithelial cell desquamation. Keratin, a major protein in desquamated epithelial cell, may serve as a source of L-Cysteine for H2S production by V. parvula. It was reported that H2S production is influenced by changes in pH and lactate, which is likely to be influenced by the production of lactic acid by streptococci ^[22].

Another recent study on the distribution and frequency of Veillonella species on tongue biofilms of Thai children showed that Veillonella species were more frequently detected in individuals with poor oral hygiene and thus may be a marker for oral hygiene status ^[23].

References

1. Gronow, S., Welnitz, S., Lapidus, A., Nolan, M., Ivanova, N., Glavina Del Rio, T., et al. (2010) Complete genome sequence of Veillonella parvula type strain (Te3). Stand Genomic Sci 2: 57–65.

2. Veillon, A., and Zuber, M. (1898) Recherches sur quelques microbes strictement anaérobies et leur rôle en pathologie. Arch Med Exp 1898 10: 517–545.

3. Prévot, A. (1933) Études de systématique bactérienne. I: Lois générale. II: Cocci anaérobies. Ann Sci Nat Bot 15: 23–260.

4. Rogosa, M. (1964) The Genus Veillonella. J Bacteriol 87: 162–170.

5. Chalmers, N.I., Palmer, R.J., Cisar, J.O., and Kolenbrander, P.E. (2008) Characterization of a Streptococcus sp.-Veillonella sp. community micromanipulated from dental plaque. J Bacteriol 190: 8145–8154.

6. Diaz, P.I., Chalmers, N.I., Rickard, A.H., Kong, C., Milburn, C.L., Palmer, R.J., et al. (2006) Molecular characterization of subject-specific oral microflora during initial colonization of enamel. Appl Environ Microbiol 72: 2837–48

7. Li, J., Helmerhorst, E.J., Leone, C.W., Troxler, R.F., Yaskell, T., Haffajee, A.D., et al. (2004) Identification of early microbial colonizers in human dental biofilm. J Appl Microbiol 97: 1311–1318.

8. Vesth, T., Ozen, A., Andersen, S.C., Kaas, R.S., Lukjancenko, O., Bohlin, J., et al. (2013) Veillonella , Firmicutes : Microbes disguised as Gram negatives. 431–448.

9. Marriott, D., Stark, D., and Harkness, J. (2007) Veillonella parvula discitis and secondary bacteremia: a rare infection complicating endoscopy and colonoscopy? J Clin Microbiol 45: 672–4

10. Delwiche, E. a, Pestka, J.J., and Tortorello, M.L. (1985) The veillonellae: gram-negative cocci with a unique physiology. Annu Rev Microbiol 39: 175–93.

11. Periasamy, S., and Kolenbrander, P.E. (2010) Central role of the early colonizer Veillonella sp. in establishing multispecies biofilm communities with initial, middle, and late colonizers of enamel. J Bacteriol 192: 2965–2972.

12. Liu, J., Merritt, J., and Qi, F. (2011) Genetic transformation of Veillonella parvula. FEMS Microbiol Lett 322: 138–144

13. Mashima, et al.pdf Mashima, I., Fujita, M., and Nakatsuka, Y. (2015) The Distribution and Frequency of Oral Veillonella spp. Associated with Chronic Periodontitis. Int J Curr Microbiol … 4: 150–160.

14. Kanio, Y., and Nakamura, K. (1987) Putrescine and cadaverine are constituents of peptidoglycan in Veillonella alcalescens and Veillonella parvula. J Bacteriol 169: 2881–2884.

15. Palmer, R.J., Diaz, P.I., and Kolenbrander, P.E. (2006) Rapid succession within the Veillonella population of a developing human oral biofilm in situ. J Bacteriol 188: 4117–4124.

16. Sbi, L., Kara, D., Bandounas, L., Mj, J., Fra, W., Bruning, O., and Tm, B. (2008) Effect of Veillonella parvula on the antimicrobial resistance and gene expression of Streptococcus mutans grown in a dual-species biofilm. 183–189.

17. Matera, G., Muto, V., Vinci, M., Zicca, E., Abdollahi-Roodsaz, S., Veerdonk, F.L. Van De, et al. (2009) Receptor recognition of and immune intracellular pathways for Veillonella parvula lipopolysaccharide. Clin Vaccine Immunol 16: 1804–1809.

18. Fisher, R.G., and Denison, M.R. (1996) Veillonella parvula bacteremia without an underlying source. J Clin Microbiol 34: 3235–3236.

19. Liu, J., Xie, Z., Merritt, J., and Qi, F. (2012) Establishment of a tractable genetic transformation system in Veillonella spp. Appl Environ Microbiol 78: 3488–3491.

20. Lean, I., Annison, F., Bramley, E., Browning, G., Cusack, P., Farquharson, B., et al. (2007) Ruminal Acidosis – understandings, prevention and treatment.

21. Hession, A., and Kung, L. (2014) Vitro Lactate Accumulation in Ruminal Fermentations by Inoculation with Megasphaera. J Anim Sci 1995: 250–256.

22. Washio, J., Shimada, Y., Yamada, M., Sakamaki, R., and Takahashi, N. (2014) Effects of pH and lactate on hydrogen sulfide production by oral Veillonella spp. Appl Environ Microbiol 80: 4184–4188.

23. Mashima, I., Theodorea, C., Thaweboon, B., Thaweboon, S., and Nakazawa, F. (2016) Identification of Veillonella Species in the Tongue Biofilm by Using a Novel One-Step Polymerase Chain Reaction Method. PLoS One 11.

This page is written by Tricia Teo for the MICR3004 course, Semester 2, 2016