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Name  
Name Ashley de Klerk
Bench ID
Bench C
Date
Date 13 Aug 2016
<ref>MICR3004</ref>
<ref>MICR3004</ref>


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===Higher order taxa===
===Higher order taxa===
Kingdom Domain Phylum Class Order Family Genus
Cellular organisms Bacteria Firmicutes Negativicute Veillonellales Veillonellaceae Veillonella
 
===Species===
===Species===
Species name and type strain (consult LPSN http://www.bacterio.net/index.html for this information)
Species name: ''Veillonella parvula'' <sup>[[#References|[1]]]</sup>
 
Type strain: DSM 2008 <sup>[[#References|[1]]]</sup>


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


Give a general description of the species (e.g. where/when was it first discovered, where is it commonly found, has it been cultured, functional role, type of bacterium [Gram+/-], morphology, etc.) and explain why it is important to study this microorganism. Examples of citations <sup>[[#References|[1]]]</sup>, <sup>[[#References|[2]]]</sup>
The French scientists Veillon and Zuber first discovered ''Veillonella parvula'' in 1898 <sup>[[#References|[2]]]</sup>. V. ''parvula'' is an anaerobic bacterium that has a gram negative cell wall <sup>[[#References|[2]]]</sup>. It is in the form of cocci, usually grown in pairs and it is commonly found in both the supra- and subgingival plaque, as well as the gastrointestinal tract <sup>[[#References|[3]]]</sup>. V. ''parvula'' is one of few bacterial species that is able to be cultured. It does not play a functional role within the human body but has been 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 bacterial pathogens <sup>[[#References|[4]]]</sup>.


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


Select a strain for which genome information (e.g. size, plasmids, distinct genes, etc.) is available.  
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 and the remaining 27% of genes were annotated as hypothetical proteins <sup>[[#References|[3]]]</sup>.


==Cell structure and metabolism==
==Cell structure and metabolism==


Cell wall, biofilm formation, motility, metabolic functions.  
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 <sup>[[#References|[5]]]</sup>. 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 a 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 <sup>[[#References|[6]]]</sup>.
 
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 <sup>[[#References|[7]]]</sup>. They utilize the metabolic end products of co-existing carbohydrate-fermenting bacteria <sup>[[#References|[8]]]</sup>. 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.


==Ecology==
==Ecology==


Aerobe/anaerobe, habitat (location in the oral cavity, potential other environments) and microbe/host interactions.
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 <sup>[[#References|[3]]]</sup>.


==Pathology==
==Pathology==


Do these microorganisms cause disease in the oral cavity or elsewhere?
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 <sup>[[#References|[2]]]</sup>. 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 damaged areas of 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 <sup>[[#References|[2]]]</sup>.


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


Bioengineering, biotechnologically relevant enzyme/compound production, drug targets,
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 it is susceptible to cephalotin (1.6 μg/ml), penicillin G (0.4 μg/ml) and clindamycin (0.1 μg/ml) <sup>[[#References|[9]]]</sup>.


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


Summarise some of the most recent discoveries regarding this species.
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 <sup>[[#References|[4]]]</sup>. 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'' is rarely thet direct cause of disease, it may be facilitating the pathogenicity of other bacterial pathogens <sup>[[#References|[4]]]</sup>.


==References==
==References==
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References examples
References examples


1. [http://onlinelibrary.wiley.com/doi/10.1046/j.1462-2920.1999.00007.x/full Sahm, K., MacGregor, B.J., Jørgensen, B.B., and Stahl, D.A. (1999) Sulphate reduction and vertical distribution of sulphate-reducing bacteria quantified by rRNA slotblot hybridization in a coastal marine sediment. Environ Microbiol <b>1</b>: 65-74.]
1.[http://www.bacterio.net/veillonella.html LPSN]
 
2. [http://femsre.oxfordjournals.org/content/38/5/996?r=1&l=ri&fst=0 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. [http://standardsingenomics.org/content/2/1/57/ 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. [http://iai.asm.org/content/83/1/417.short 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. [http://aem.asm.org.ezproxy.library.uq.edu.au/content/54/8/1957 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.[http://journals.lww.com/revmedmicrobiol/Abstract/1997/12001/Salient_structural_features_in_the_chemical.2.aspx 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. [http://onlinelibrary.wiley.com.ezproxy.library.uq.edu.au/doi/10.1111/j.1749-6632.1985.tb18426.x/abstract Dimroth, P. (1985) Biotin-dependent Decarboxylases As Energy Transducing Systems. Annals of the New York Academy of Sciences 447:72-85.]
 
8.[http://www.sciencedirect.com.ezproxy.library.uq.edu.au/science/article/pii/0003996970900312 Gibbons, R.J., Nygaard, M. (1970) Interbacterial aggregation of plaque bacteria. Archives of Oral Biology 15:1397,IN1339-1400,IN1339.]


2. [http://www.homd.org Human Oral Microbiome]
9. [http://aac.asm.org.ezproxy.library.uq.edu.au/content/1/2/148 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.]


<references/>
<references/>


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

Latest revision as of 02:19, 23 September 2016

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

Classification

Higher order taxa

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

Species

Species name: Veillonella parvula [1]

Type strain: DSM 2008 [1]

Description and significance

The French scientists Veillon and Zuber first discovered Veillonella parvula in 1898 [2]. V. parvula is an anaerobic bacterium that has a gram negative cell wall [2]. It is in the form of cocci, usually grown in pairs and it is commonly found in both the supra- and subgingival plaque, as well as the gastrointestinal tract [3]. V. parvula is one of few bacterial species that is able to be cultured. It does not play a functional role within the human body but has been 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 bacterial pathogens [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 and the remaining 27% of genes 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 a 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 bacteria [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.

Ecology

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].

Pathology

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 damaged areas of 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 it 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 is rarely thet direct cause of disease, it may be facilitating the pathogenicity of other bacterial pathogens [4].

References

References examples

1.LPSN

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