Prevotella intermedia
From MicrobeWiki, the student-edited microbiology resource
A Microbial Biorealm page on the genus Prevotella intermedia
Contents |
Classification
Higher order taxa
Domain:Bacteria
Kingdom: Bacteroidetes/Chlorobi group
Phylum: Bacteroidetes
Class: Bacteroidetes
Order: Bacteroidales
Family: Prevotellaceae
Genus: Prevotella (1).
Species
Prevotella intermedia
This microbe is also known as Prevotella intermedius, Bacteroides intermedius, and Bacteroides melaninogenicus subsp. intermedius (2).
Description and significance
Prevotella intermedia is a gram-negative, black-pigmented periodontal pathogen (6). Their possession of black pigments is the reason why these organisms are also known as Bacteroides melaninogenicus subsp. intermedius. These rod-shaped microbes are strict oral anaerobes, but a short oxygen exposure will not be sufficient to kill them (5). These organisms live in the periodontal pockets in between the teeth where they co-exist with other microbes, forming an oral microbiota (3).
Prevotella intermedia has a variety of known strains, Prevotella intermedia 17 being the most common one. This strain is isolated from human periodontal pockets. Prevotella intermedia 27 on the other hand are clinical isolates from periapical lesions. Lastly, Prevotella intermedia ATCC 25611 is the type strain (6).
Determining the genome sequence of Prevotella intermedia is crucial as these organisms are known to cause Periodontitis and acute necrotizing ulcerative gingivitis. Periodontal diseases pose greater risks than what was previously thought as recent research have linked them to coronary heart disease (6). Hence, medical treatments against these Periodontitis causing organisms are becoming increasingly valuable. And knowing the genome sequence of Prevotella intermedia is one key step in developing such treatments.
These microorganisms are usually isolated in periodontal lesions of all patients inflicted with Periodontitis, regardless of the stage of the disease (6). A common way to isolate Prevotella intermedia is to collect specimens from Periodontitis lesions. This is done by isolating the sample site with cotton rolls, removing the supragingival plaque and then inserting a sterile paper point to the depth of the periodontal pocket and retaining it there for 10 seconds. After the collection of samples, they are then processed by culturing the cells on an anaerobic chamber and then incubating them at 35 degrees Celsius for 5-7 days (5).
Genome structure
The genome sequence of Prevotella intermedia strain 17 is composed of 2,699,437 base pairs. It has a 43.7 % guanine cytosine content and a 56.3 % adenine thymine content. 97. 84 % of the genome (2816/2878 genes) represent coding regions that encode for 2816 proteins (7). This organism has circular chromosomes with a characterized plasmid (pYHBi).The presence of a megaplasmid that is 580 Kb is also being entertained by researchers; however, very little is known about the plasmid at the moment (8). Sequencing of this organism's genome was accomplished last January 30, 2004 by John Heidelberg of the J. Craig Venter Institute (7). The sequencing of this type of microbes led to an increase ability to combat their pathogenic activities.
Cell structure and metabolism
Prevotella intermedia is a gram-negative bacteria, characterized by an outer and inner membrane, along with a thin peptidoglycan layer. Plaque formation, usually induced by the lack of oral hygiene, leads to increased amounts of gingival crevicular fluid in the mouth. Prevotella intermedia growth is then stimulated by this influx of crevicular fluid because it contains nutrients such as hemin and vitamin K, which are essential for the microbe's growth. Ideal growth conditions for Prevotella intermedia also includes a slightly basic pH and a constant temperature between 34 and 36 degrees Celsius (3).
It is interesting to note that this type of bacteria increases proportion in its subgingival habitat when there is a marked increase in levels of steroid hormones, such as estrogen and progesterone, in the cell plasma and in the host's saliva. Apparently, these hormones serve as growth factors for the microbes. This observation accounts for the fact that pregnancy and puberty, events that involve increased hormone production, is often accompanied by gingivitis (4).
Prevotella intermedia secretes salivary IgA proteases which degrades salivary IgA1 and IgA2--the first line of defense of the mouth against pathogen invasion--thereby making them successful in initiating usurpation of the teeth and of the oral mucosa (3).
Ecology
Communication among oral bacteria like Prevotella intermedia and its co-inhabitants is essential for colonization and subsequent biofilm formation on the enamels of the teeth. Human oral bacteria communicate with their environment by adhering to surfaces and forming mixed-species communities. As each cell attaches to the surface, it forms new surfaces where others can adhere. Adherence is critical for survival because without it, the bacteria will be drained down with the saliva. Prevotella intermedia interact with other organisms inside the mouth like Actionomyces spp., Streptococci spp. and Veillonella spp. to name a few. These microbes have developed a concert of interaction methods such as cell to cell recognition, genetic exchange and metabolite exchange. As a matter of fact, a signaling molecule named autoinducer-2 is found in many oral bacteria. This compound is believed to participate in cell to cell recognition among bacteria. Prevotella intermedia is known to produce high levels of this molecule (9).
These oral microbes are also classified into 2 categories depending on their placement in plaques during temporal sampling. The first category belongs to the early colonizers. These early colonizers perpetrate through the teeth just a few hours after professional cleaning. They are characterized by the ability to bind to host receptors. The second category belongs to the late colonizers, which include Prevotella intermedia. F. nucleatum acts as the bridge that coaggregates the early and late colonizers (9). Again, the whole theme of interaction for survival is seen here.
Prevotella intermedia is known to synergize with Peptostreptococcus micros, making the two types of microbes successful in causing dentoalveolar infections. Subcutaneous injections of P. micros in mouse together with alive cells of P. intermedia leads to larger abscess compared to single injections of each. A significant increase in abscess size was also observed when plate-cultured cell suspension of P. micros was injected into the mouse with culture filtrate of P. intermedia. Furthermore, P. intermedia was found to enhance virulence of P. micros. The virulence of P. micros is also enhanced even though the cultured filtrate of P. intermedia was injected in separate sites of the mouse. It has been hypothesized that the fatty acids secreted by P. intermedia suppress human polymorphonuclear neutrophil functions thereby improving P. micros' virulence. On the other hand, the culture filtrate of P. micros did not affect P. intermedia's virulence but broth culture of P. micros enhanced the virulence of P. intermedia. Thus, it is concluded that while the products of P. intermedia increases virulence of the other type of microbe indirectly by altering the host's condition, the living cells of P. micros--and not its products-- directly enhances the virulence of P. intermedia (10). This synergistic behavior between the two plays an important role in the development and prognosis of dentoalveolar infection.
Pathology
Prevotella intermedia is a human pathogen, often invading the human buccal epithelial cells. Bacteria are always present in the mouth as even healthy gingival tissues possess inflammatory cells. But as bacterial plaque accumulates, these inflammatory cells increase in number causing the the gingival tissues to swell, bleed and become edematous. Streptococci are usually the initial colonizers. As a result of bleeding and tissue inflammation, nutrients needed by other microbes such as Prevotella intermedia become increasingly available, hence promoting their proliferation. The sudden domination of anaerobic, gram-negative species like Prevotella intermedia in the mouth is correlated with Periodontitis (11).
The host launches various anti-inflammatory responses against the bacteria, which can be both protective and destructive to the host's tissues. Protective responses include removal of bacteria products such as antigens, LPS and enzymes. However, the host's inflammatory response also includes the activation of matrix metalloproteases--agents responsible for collagen loss in tissues. Such collagen loss leads to attachment loss, thereby deepening the depression where gingival tissues contact the tooth surface. This further deepening creates the periodontal pocket. The loss of attachment is also responsible for converting Gingivitis to Periodontitis (11).
A common strategy of invasive bacteria like Prevotella intermedia includes triggering the host cell to be subjected to cytoskeletal re-arrangements mediated by internalizations. In Prevotella intermedia strain 17, which is the isolate from periodontal pockets, the presence of a type C fimbriae enables it to bind more avidly to epithelial cells and to agglutinate with several mammalian erythrocytes. Hence, it is hypothesized that type C fimbriae stimulates invasion by enabling the bacteria to adhere to the cell's surface,which has receptors specific for fimbriae. This binding may then induce internalizations, which are essential for host cell invasion. Prevotella intermedia strains 27 and 25611 lack type C fimbriae. Therefore, it is integral to distinguish between these strains in the quest for antidotes to Periodontitis and other related systemic conditions (6).
Periodontitis is the disruption of connective tissue attachment along with the adjacent alveolar bone (3). Some symptoms include development of new spaces between the teeth, change in the manner that the teeth fit together when biting and swelling of the gums. Since there is no single bacterial species that is solely connected with Periodontitis, a vaccine targeting a specific species is unlikely to be effective. However, Periodontitis is significantly correlated with an overgrowth of a finite number of anaerobic bacteria. So, this disease can be suppressed by lifetime mechanical debridements or by utilizing antimicrobial agents that target the participating anaerobes (11).
Application to Biotechnology
Prevotella intermedia is a periodontal pathogen, commonly found in human buccal epithelial cells. Its aggregation with other anerobic microbes in the mouth causes Periodontitis, a severe form of gum disease. Recent studies have also discovered invasion of human coronary artery endothelial cells and coronary artery smooth muscle cells by Prevotella intermedia, which explains why there appears to be a correlation between periodontal disease and coronary heart disease (12). Thus, Prevotella intermedia is only known for its disease causing ability and has no recognized benefit to society so far. Further investigation will be needed to discover efficient ways to utilize these organisms to the advantage of society.
Current Research
Because it is an oral human pathogen that causes Periodontitis, Prevotella intermedia has garnered much attention among dental researchers. These organisms became more popular when recent studies emerged linking Periodontitis to various diseases. Ogrendik et. al. investigated the relationship between Periodontitis and Rheumatoid Arthritis (RA). They conducted such investigation by determining the pathogen specific IgG levels formed against Prevotella intermedia 25611 oral bacteria in blood samples of RA patients and normal patients with the use of the ELISA method (enzyme-linked immunosorbent assay). Ogrendik's group found that IgG and IgA antibody levels in synovial fluid samples of RA patients were significantly higher against Prevotella intermedia. They concluded that this phenomenon is indicative of an active antibody response in synovial tissue and of a potential correlation between periodontal and inflammatory joint diseases. Thus, the group suggests reconsideration of the involvement of Periodontitis in RA pathogenesis (13).
In line with this, the group of Brian Dorn at the University of Florida established that specific anaerobic species like Prevotella intermedia strain 17 invades human coronary artery endothelial cells (HCAEC) and coronary artery smooth cells (CASMC). They accomplished this through the use of antibiotic protection assay and electron microscopy. Such discovery testifies to the correlation between coronary heart disease and periodontal disease. This invasion was also hypothesized to involve actin polymerization of cytoskeleton in a metabolically active cell since administration of Cythochalasin D, an actin polymerization inhibitor, inhibits most of the invasive bacteria. Dorn's group concluded by saying that bacterial invasion of HCAEC and CASMC "insults" the arterial wall, thereby raising the possibility that infection of the coronary wall by pathogens like Prevotella intermedia can be a crucial factor that contributes to coronary heart disease (12).
Research has continued to correlate Periodontitis with a spectrum of other diseases. Mealey and Rose added Diabetes to the growing number of diseases linked to Periodontitis. In their article, they discovered that Diabetes mellitus induces Periodontitis and at the same time, Periodontitis can also have negative effects on a patient's metabolic state, and is therefore involved in Diabetes. Mealey et. al. states that Diabetes is caused by a change in immune cells' functions, which causes defense mechanisms like phagocytosis to be impaired. These defects in defense facilitates the persistence of bacteria in the periodontal pockets, leading to increased destruction of the periodontal tissues. On other other hand, periodontal diseases apparently have a significant impact on the metabolic state. One evidence to this is the worsening of glycemic control if periodontal diseases are present. Mealey and Rose proposed that chronic gram negative periodontal infections may cause poor glycemic control and an increased insulin retardation. Thus, Mealey and Rose concluded that it is integral for dental and medical health providers to discern the interaction between these two diseases to provide better care for their patients (14).
References
3. Marcotte, H., and Lavoie, M. " Oral Microbial Ecology and the Role of Salivary Immunoglobulin A". Microbiology and Molecular Biology Reviews. 1998. Volume 62. p. 71-109. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=98907
4. Kornman, K., and Loesche, W. " Effects of estradiol and progesterone on Bacteroides melaninogenicus and Bacteroides gingivalis". Infection and Immunity. 1982. Volume 35. p. 256-263. http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=6119293
5. Nguyen, D., Contreras, A., Flynn, J., and Slots, J. "Proficiencies of 3 Anaerobic Culture Systems for Recovering Periodontal Pathogenic Bacteria". Journal of Clinical Microbiology. 1999. Volume 37. p. 171-174. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=84198
6. Dorn, B., Leung, K., and Progulske-Fox, A. "Invasion of Human Oral Epithelial Cells by Prevotella Intermedia". Infection and Immunity. 1998. Volume 66. p. 6054-6057. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=108773
7. http://cmr.tigr.org/tigr-scripts/CMR/GenomePage.cgi?org=gpi
9. Kolenbrander, P., Andersen, R., Blehert, D., Egland, P., Foster, J., and Palmer, R. "Communication Among Oral Bacteria". Microbiology and Molecular Biology Reviews. 2002. Volume 66. p. 486-505. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=120797
10.Araki, H., Kuriyama, K., and Karasawa, T. "The Microbial Synergy of Peptostreptococcus micros and Prevotella intermedia in a Murine Abscess Model". Oral Microbiology and Immunology. 2004. Volume 19. p. 177-181. http://www.medscape.com/medline/abstract/15107069
11. Loesche, W., and Grossman, N. "Periodontal disease as a Specific, Albeit Chronic, Infection: Diagnosis and Treatment". Clinical Microbiology Reviews. 2001. Volume 14. p. 727-752. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=89001
12. Dorn, B., Dunn, W., and Progulske-Fox, A. "Invasion of Human Coronary Artery Cells by Periodontal Pathogens". Infection and Immunity. 1999. Volume 67. p. 5792-5798. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=96956
13. Ogrendik, M., Kokino, S., Ozdemir, F., Bird, P., and Hamlet, S. "Serum Anitbodies to Oral Anaerobic Bacteria in Patients with Rheumatoid Arthritis". Medscape General Medicine. 2005. Volume 7. p. 588-591. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1681585
14. Mealey, B., and Rose, L. "Periodontal Inflammation and Diabetes Mellitus". Connections. 2007. Volume 1. p. 470-476. http://www.contemporaryoralhygieneonline.com/issues/articles/2007-01_01.asp
Edited by Angela Baja student of Rachel Larsen
Edited by KLB
