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Name Ashley de Klerk Bench C Date 13 Aug 2016 [1]


Higher order taxa

Cellular organisms – Bacteria – Firmicutes – Negativicute – Veillonellales – Veillonellaceae – Veillonella


Species name: Veillonella parvula [1]

Type strain: DSM 2008 [1]

Description and significance

The French scientists Veillon and Zuber first discovered V. parvula in 1898 [2]. V. parvula is an anaerobic bacterium that has a gram negative cell wall [2]. It isin the form of cocci, usually grown in pairsandit is commonly found in both the supra- and subgingival plaque, as well as the gastrointestinal tract [3]. V. parvula is one of few bacteria spaecies that is able to be cultures. It does not play a functional role within the human body but has shown to cause disease on rare occasions. It is important to study V. parvula as it plays a significant role in the natural microbial food chain, and while V. parvula rarely causes disease, recent research has found that V. parvula may assist in the pathogenicity of other bacteria [4].

Genome structure

The V. parvula strains Te3T has a circular chromosome with a length of 2,132,142bp. There were 1,929 predicted genes from which 1,859 coded for proteins. It has a CG content of 38% and contains 15 pseudogenes. 73% of genes were assigned a putative function which the rest were annotated as hypothetical proteins [3].

Cell structure and metabolism

While V. parvula are non-motile and cannot adhear it surfaces itself, it is able to attach to specific surface structures present on other cells, often mediated by lectin-carbohydrate interactions [5]. These connections between different bacterial species form a biofilm which provides nutrients and protection for the bacteria.

As V. parvula has a Gram-negative cell wall it has much less peptidoglycan than gram-positive bacteria and it has a cell membrane, as well as an outer membrane. While V. parvula is gram-negative bacterium and has lipopolysaccharides, it is more closely related to gram positive species such as Sporomusa, Megasphaera or Selenomonas as they all share the unusual presence of cadaverine and putrescine in their cell wall. A characteristic feature of V. parvula is the presence of plasmalogens such as plasmenylserine and plasmenylethanolamine as major constituents of the cytoplasmic membrane. These ether lipids replace phospholipids and play an important role in the regulation of membrane fluidity [6].

V. parvula have an unusual metabolism where they use methylmalony-CoA decarboxylase to convert the free energy derived from decarboxylation reactions into an electrochemical gradient of sodium ions [7]. They utilize the metabolic end products of co-existing carbohydrate-fermenting [8]. V. parvula is unable to use glucose and other carbohydrates for fermentation and is unable to grow on succinate as a sole carbon source however it can decarboxylate succinate during fermentation of malate or lactate.


V. parvula is an anaerobic bacterium which is located in both the supra- and subgingival plaque, as well as in the gastrointestinal tract. V. parvula plays a significant role in the natural microbial food chain but does not usually interact directly with the host [3].


V. parvula does not usually cause disease as it is an opportunistic pathogen however, in rare cases it has been found to cause endocarditis, meningitis and osteomyelitis [2]. Endocarditis is an infection of the heart which occurs when V. parvula makes its way into the blood stream and to the heart where it attaches to damages areas in the heart. Meningitis occurs when V. parvula passes through the blood brain barrier and is then able to infect areas in the brain and spinal cord. Osteomyelitis occurs when V. parvula travels through the blood stream and infects bone [2].

Application to biotechnology

V. parvula has not been involved in any bioengineering or biotechnology research, however it has developed resistance against some antibiotics. V. parvula shows resistance to erythromycin (>25 μg/ml), kanamycin (>25 μg/ml), tetracycline (>25 μg/ml) and gentamicin (>25 μg/ml) and V. parvula is susceptible to cephalotin (1.6 μg/ml), penicillin G (0.4 μg/ml) and clindamycin (0.1 μg/ml) [9].

Current research

Current research involves the pathogenicity of duel-species biofilms compared to mono-species biofilms. For example, a study investigated the influences of the most dominant Cystic Fibrosis pathogen Pseudomonas aeruginosa and V. parvula during a biofilm associated infection process [4]. It found that the presents of V. parvula supports the growth of P. aeruginosa at the site of infection. In addition, significantly higher levels of P. aeruginosa was recovered from tissue that was coinfected with both bacterial species compared to tissue that was monoinfected with P. aeruginosa. This suggests that while V. parvula rarely causes disease it may be facilitating the virulence of other pathogens [4].


References examples


2. Rajilic-Stojanovic, M., de Vos, W.M. (2014) The first 1000 cultured species of the human gastrointestinal microbiota. FEMS Microbiol Rev 38:996-1047.

3. Gronow, S., Welnitz, S., Lapidus, A.L., Nolan, M., Ivanova, N., Glavina Del Rio, T., Copeland, A., Chen, F., Tice, H., Pitluck, S., Cheng, J-F., Saunders, E.H., Rohde, M., Goker, M., Bristow, J., Eisen, J., Markowitz, V., Hugenholtz, P., Kyrpides, N.C., Klenk, H-P., Lucas, S. (2010) Complete genome sequence of Veillonella parvula type strain (Te3T). Standards in Genomic Sciences 2.

4. Pustelny, C., Komor, U., Pawar, V., Lorenz, A., Bielecka, A., Moter, A., Gocht, B., Eckweiler, D., Musken, M., Grothe, C., Lunsdorf, H., Weiss, S., Haussler, S. (2015) Contribution of Veillonella parvula to Pseudomonas aeruginosa-mediated pathogenicity in a murine tumor model system. Infection and immunity 83:417.

5. Hughes, C.V., Kolenbrander, P.E., Andersen, R.N., Moore, L.V. (1988) Coaggregation properties of human oral Veillonella spp.: relationship to colonization site and oral ecology. Applied and Environmental Microbiology 54:1957.

6.Olsen, I. (1997) Salient structural features in the chemical composition of oral anaerobes, with particular emphasis on plasmalogens and sphingolipids. Rev Med Microbiol 8:S3-S6.

7. Dimroth, P. (1985) Biotin-dependent Decarboxylases As Energy Transducing Systems. Annals of the New York Academy of Sciences 447:72-85.

8.Gibbons, R.J., Nygaard, M. (1970) Interbacterial aggregation of plaque bacteria. Archives of Oral Biology 15:1397,IN1339-1400,IN1339.

9. Martin, W.J., Gardner, M., Washington, J.A. II. (1972) In Vitro Antimicrobial Susceptibility of Anaerobic Bacteria Isolated from Clinical Specimens. Antimicrobial Agents and Chemotherapy 1:148.

  1. MICR3004

This page is written by Ashley de Klerk (43614404) for the MICR3004 course, Semester 2, 2016