Prevotella intermedia: Difference between revisions
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=6. Ecology= | =6. Ecology= | ||
P. intermedia generally requires the organic compounds hemin and menadione to grow. | |||
Despite having specific growth requirements, Prevotella is found in diverse areas of the human body. These regions range from the human oral cavity to human feces (5). Because of intraspecies differences that exist among the Prevotella genus, it is capable of thriving in diverse environments (5). P. intermedia is an opportunistic pathogen, therefore it thrives in diseased sites of the human body and has varying levels of pathogenicity. Consequently, healthy areas have lower levels of degradative enzyme activity. P. intermedia strains contain virulence factors that allow them to accommodate needs in these environments (5). | |||
=7. Pathology= | =7. Pathology= | ||
How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms. | How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms. |
Revision as of 19:11, 11 December 2017
1. Classification
a. Higher order taxa
Bacteria; Bacteroidetes; Bacteroidetes; Bacteroidales; Prevotellaceae; Prevotella intermedia (1)
2. Description and significance
Prevotella intermedia is a bacteria that previously went by the Genus name of Bacteroides. With advancements in DNA sequencing, researchers discovered that many bacteria previously classified as Bacteroides would be more appropriately fit for a new genus, Prevotella, due to their bile-sensitive characteristics. The genus Bacteroides was re-classified to contain bacteria that are bile-resistant gram-negative bacilli (2). One of only two stains of the entire Prevotella genus, among all species, that has had its entire DNA genome sequenced is P. intermedia (3). As with other pathogenic species of Prevotella, P. intermedia has been researched for its various pathogenic effects in humans. It is commonly studied for its role in the oral cavity, and more specifically, periodontal disease. P. intermedia is seen as the main cause of many periodontal diseases and is often hard to eliminate in infected areas, due to its ability to form biofilms. It antibiotic-resistant capabilities have serious implications for human health (4). P. intermedia’s pathogenic impacts on human health are not yet fully understood.
3. Genome structure
Prevotella intermedia 17, a strain from the human periodontal pocket, was the first published genome sequence of Prevotella. Genes involved in P. intermedia’s cell envelope structure are highly conserved among multiple strains, including Prevotella intermedia 17. AdpB, a binding protein on the cell surface which is thought to be involved in the microbe’s adhesion capabilities, is highly conserved and found in all strains of P. intermedia (5). In the process of analyzing different strains of P. intermedia, scientists have found that only about 3% of the whole genome typically accounts for alignment between two strains. Despite the small percentage of alignment in nucleotide sequences, scientists found a 49Kb region where gene content is conserved and shared among the different genomes. Prevotella, as a genus, is reported to have roughly 165-170 core genes P. intermedia’s set of core genes allows it to thrive in diverse environments (5).
4. Cell structure
Prevotella intermedia is an anaerobic, gram-negative, rod-shaped bacterium (6). P. intermedia is also classified as a black pigmented bacteria because of its formation of shiny and smooth colonies which appear either a grey, light brown, or black color on blood agar plates (7). P. intermedia has been found to possess exopolysaccharides which are composed of neutral sugars and mannose and are a major component of biofilm formation. These exopolysaccharides provide P. intermedia the ability to evade the innate human immune system (8).
5. Metabolic processes
P. intermedia is known as a periodontopathic bacteria whose metabolic activity often results in an accelerated development of oral biofilm-mediated diseases. P. intermedia metabolites are known to initiate and promote oral disease, both directly and indirectly (9). This bacterium is non-acid producing and utilizes amino acids and peptides as metabolic substrates. Fluoride is added into toothpastes in order to inhibit these metabolic substrates that result in disease (9). P. intermedia is known to metabolize glucose, allowing it to readily exist in the human oral cavity. Glucose metabolism utilizes the EMP pathway and hexokinase, which tends to increase the anaerobic properties of the organism. P. intermedia also favors catabolizing nitrogenous compounds for energy sources (10).
6. Ecology
P. intermedia generally requires the organic compounds hemin and menadione to grow. Despite having specific growth requirements, Prevotella is found in diverse areas of the human body. These regions range from the human oral cavity to human feces (5). Because of intraspecies differences that exist among the Prevotella genus, it is capable of thriving in diverse environments (5). P. intermedia is an opportunistic pathogen, therefore it thrives in diseased sites of the human body and has varying levels of pathogenicity. Consequently, healthy areas have lower levels of degradative enzyme activity. P. intermedia strains contain virulence factors that allow them to accommodate needs in these environments (5).
7. Pathology
How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.
7. Key microorganisms
Include this section if your Wiki page focuses on a microbial process, rather than a specific taxon/group of organisms
8. Current Research
Include information about how this microbe (or related microbes) are currently being studied and for what purpose
9. References
It is required that you add at least five primary research articles (in same format as the sample reference below) that corresponds to the info that you added to this page. [Sample reference] Faller, A., and Schleifer, K. "Modified Oxidase and Benzidine Tests for Separation of Staphylococci from Micrococci". Journal of Clinical Microbiology. 1981. Volume 13. p. 1031-1035.