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Emily Mantilla Bench B 31/08/2016

Classification

Higher order taxa

Prokaryote – Bacteria – Firmicutes – Negativicutes – Veillonellales – Veillonellaceae – Veillonella

Species

Veillonella parvula

Identified strains:

• Veillonella parvula AC2_8_11_AN_NA_2
• Veillonella parvula ACS-068-V-Sch12
• Veillonella parvula ATCC 17745
• Veillonella parvula DSM 2008
• Veillonella parvula HSIVP1

Description and significance

V. parvula is one of the six species belonging to the genus Veillonella which are gram-negative cocci and obligate anaerobes ^[1],^[2]. It is a nonfermentative organism that lives optimally at 37 C and a PH range 6.5-8.0 thus it is commonly found in the human oral, intestinal and vaginal microflora. The NCBI genome record for strain DSM 2008 reports a collection date before 1898 in France, isolated from the intestinal tract ^[2]. It has been identified as a causal pathogen of endocarditis, bacterimia and opportunistic infection ^[2]. Several studies have confirmed that it has an important role in the formation of dental plaque biofilm favouring the association of other peridontal pathogens and contributing as causal agents of systemic diseases. The high prevalence of this pathogen in patients that have poor oral health has prompted to understand the role of V. parvula in health and disease as well as its contribution to the human microbiome.

Genome structure

There is complete genome available from the NCBI for "V. parvula DSM 2008" (RefSeq NC_013520.1). The genome has a size of 2.13 Mb with 1,893 genes, 9 pseudo-genes and 3 frameshift genes. The GC content is 38.6% and encodes 1,822 proteins. There are 12 rRNA, 48 tRNA and 2 other RNA ^[3].

Cell structure and metabolism

V. parvula is coccus shaped and does not have a peptidoglycan layer, therefore it is gram-negative organism ^[3]. This bacterial species is particularly good at colonizing and surviving the acid environment of the mouth in part due to its metabolism. Some RNA-sequencing studies have identified a histidine biosynthesis pathway particularly upregulated suggesting that high levels of intra-cellullar histidine assist with an increased intra-cellullar buffering capacity, facilitating the adaptation to the acidic environment ^[2]. It is generally appreciated that V. parvula depends on the production of lactate by other bacterial species, such as Streptococcus, forming stable symbiotic relationships as in biofilms. The increased gene expression for lactate degradation indicates that V. parvula prefers short-chain organic acids as its main energy source including pyruvate and oxaloacetate ^[4],^[5]. Additionally, it has been found that theVeillonella genus has a metabolic activity that produces hydrogen sulfide (H2S) from L-cysteine involving cystathionine beta-synthase and cystathionine gamma-lyase enzymes ^[5]. An increase in the concentration of lactate, such as after consuming food, causes an increase in the production of H2S leading to characteristic malodors in the mouth.

Ecology

V.parvula is a dominant species in the oral microbiome along V. atypica and V.dispar. This pathogen has been isolated from the periodontal pocket and has a role in dental plaque biofilm formation in the human oral cavity. V. parvula requires lactate as a nutrient source so it is commonly found in association with other lactic-acid-producing species thus contributing to the cause of dental caries. Therefore it is established as the predominant species in subjects that have poor oral hygiene compared to those with moderate or good hygiene ^[1]. Moreover, it is found in the subgingival biofilm of patients with chronic periodontitis ^[3].

Pathology

V.parvula has not only been associated with periodontal and endovascular infections but also with more serious cases including, osteomyelitis, meningitis, prosthetic joint infection, and pleuropulmonary infection ^[7],^[8]. Thus, constituting rare events in which V. parvula has been identified as the sole causal organism ^[7]. The isolation of this organism has been possible in most of the cases but it still remains unclear about the cellular and molecular mechanisms leading to pathogenesis and the correspondent immune response ^[8]. Several studies have identified the LPS endotoxin as the virulence factor responsible for triggering inflammatory response during infection by inducing cytokine production ^[8]. However, it was found that the cytokine levels produced by V. parvula LPS are lower than those induced by E. coli LPS ^[8]. These findings correspond with the observed clinical symptoms on both types of infections. For instance, V. parvula infection has less complicated biological effects than E.coli infection which can cause acute inflammatory reaction and even death ^[8]. On study has discovered that oral V. parvula LPS is recognized by the toll-like receptor 4 (TLR4) and activates the p38 MAP kinase triggering an inflammatory response pathway in peripheral blood mononuclear cells ^[8]. In this way, the model indicates how periodontal lesion casue TLR4 activation leading to the inflammatoru response characteristic of periodontitis ^[8].

Application to biotechnology

Bioengineering, biotechnologically relevant enzyme/compound production, drug targets,…

Current research

Summarise some of the most recent discoveries regarding this species.

References

1. Mashima, I., Theodorea, C.F., Thaweboon, B., Thweboon, S., Nakazawa, F. (2016) Identification of Veillonella Species in the Tongue Biofilm bu using a Novel One-Step Polymerase Chain Reaction Methods. PlOs one 11(6): e0157516.

2. Mashima, I., Fujita, M., Nakatsuka, Y., Furuichi, Y., Herastuti,S., et al (2015) The Distribution and Frequency of Oral Veillonella spp. Associated with Chronic Periodontitis. Int J Curr Microbiol App Sci 4(3): 150-160

3. NCBI Prokaryote Genome Annotation, Veillonella parvula DSM 2008

4. Do, T., Sheehy, E. C., Mulli, T., Hughes, F., Beighton, D. (2015). Transcriptomic analysis of three Veillonella spp. present in carious dentine and in the saliva of caries-free individuals. Front Cell Infect Microbiol, 5:25. doi: 10.3389/fcimb.2015.00025

5. Washio, J., Shimada, Y., Yamada, M., Sakamaki, R., Takahashi, N., (2014) Effects of pH and lactate on hydrogen sulfide production by oral Veillonella spp. Appl Environ Microbiol 80(14): 4184–8. doi:10.1128/AEM.00606-14

6. [Boo TW, Cryan B, O’Donnell A, Fahy G (2005) Prosthetic valve endocarditis caused by Veillonella parvula. J Infect 50: 81–3. doi:10.1016/j.jinf.2003.11.008.]

7. Brook I (2008) Infective endocarditis caused by anaerobic bacteria. Arch Cardiovasc Dis 101: 665–76. doi:10.1016/j.acvd.2008.08.008.

8. Matera G, Muto V, Vinci M, Zicca E, Abdollahi-Roodsaz S, et al. (2009) Receptor recognition of and immune intracellular pathways for Veillonella parvula lipopolysaccharide. Clin Vaccine Immunol 16(12): 1804–9. doi:10.1128/CVI.00310-09.

n. Sundqvist, G., (1992) Associations between microbial species in dental root canal infections. Oral Microbiol Immunol 7(5):257–262. pmid:1494447 doi: 10.1111/j.1399-302x.1992.tb00584.x

This page is written by Emily Mantilla for the MICR3004 course, Semester 2, 2016