User:S4415589
Name: Jovin Choo Jia Ying
Bench: E
Date: 31 August 2016
[1]
Porphyromonas gingivalis
Classification
Higher order taxa
Bacteria – Bacteria – Bacteroidetes – Bacteroide – Bacteroidales – Porphyromonadaceae – Porphyromonas
Species
Species name: Porphyromonas gingivalis
Type strains: 381, 2561, ATCC 33277, BCRC 14417, CCRC 14417, CCUG 25893, CCUG 25928, CIP 103683, Coykendall 2561, DSM 20709, JCM 12257, KCTC 5121, KDI, NCTC 11834, Slots 2561, SU63, W50, W83
(consult LPSN http://www.bacterio.net/index.html for this information)
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 [1], [2]
Porphyromonas gingivalis is found in 86% of subgingival plaque samples from patients suffering from chronic periodontitis. P. gingivalis is a non-motile, asaccharolytic, obligate anaerobe, gram negative, rod shaped bacterium. It is known to form black-pigmented colonies after being culture for 6-10 days on blood agar due to accumulation of heme. It requires iron for its growth. P. gingivalis was previously named Bacteroides gingivalis before reclassification into a new genus. It is a secondary colonizer of dental plaque which adheres to primary colonizer such as Streptococcus gordonii and P. intermedia.
As P. gingivalis is a prime etiological agent that causes severe forms of periodontitis, understanding the mechanism of the pathogenesis will allow for development of treatment for periodontal disease and hopefully eradicate Porphyromonas gingivalis.
Genome structure
Select a strain for which genome information (e.g. size, plasmids, distinct genes, etc.) is available.
W83 is a virulent strain of P. gingivalis with genome size of 2,343,479 bp and an average GC content of 48%. Its found to have 4 ribosomal operons, 2 structural RNA gene and 53 tRNA genes. A total of 1990 ORFs were identified. As iron is a major requirement for P. gingivalis, multiple systems relating to iron uptake such as iron chelate ABC uptake system, TonB-dependent iron receptors and FeoB ferrous iron uptake systems have been discovered. Clusters of gene (PG1582-86) responsible for ensuring tolerance to oxygen in the oral cavity have also been isolated. Genes encoding for adherence factors such as hemagglutinin (PG0411, 1326, 1674, 1427, 1548, 2198) and capsule were also identified in this strain (PG0106-0120, PG0435-0437, PG1140-49 and PG1560-1565).
Cell structure and metabolism
Cell wall
Like any other Gram-negative bacteria, P. gingivalis has both outer (OM) and inner membrane (IM) separated by the periplasm, which contains the peptidoglycan layer. The IM is made up of a phospholipid bilayer with various integral IM proteins while OM is made up of an asymmetrical bilayer with phospholipids in the inner learflet and lipopolysaccharides (LPS) on the outer. The OM is hypothesized to be high associated with the formation and maintenance of biofilms within periodontal microflora, mediated by OM proteins. As the OM is the most exposed area of the cell, OM proteins such as LptO, RagA, RagB and OmpA-like proteins are also important providing adherence to host cells and secreting gingipains.
Biofilm formation
Biofim formation is employed by the bacteria to protect it against environmental stresses. In P. gingivalis, it has been discovered that the polyphosphate kinase activity, encoded by the ppk gene is a requirment for biofilm formation. Stress-associated protein uspA is influenced by the production of intracellular polyphosphate and is postulated to play a role in the formation of biofilms.
The formation of dental plaque is made up of biofilm formation of different species of microflora exisiting in commensal harmony with the host. P. gingivalis forms biofilms with Streptococcus gordonii through LuxS-dependent signalling, which is able to mediate interspecies communication in mixed species biofilms. Initial adherence between S. gordonii Ssp surface protein and P. gingivalis minor fimbriae is required prior biofilm formation.
Motility
P. gingivalis species are non-motile.
Metabolic functions
P. gingivalis possesses a limited capacity to uptake and metabolize organic nutrients. Metabolic reconstruction analysis has shown that P. gingivalis poorly utlizes glucose and does not use carbohydrates to support its growth. This could be due to the environment it localizes in – sugar availability is low in deep periodontal pockets. Instead, P. gingivalis prefers peptides as its carbon and nitrogen source. The bacteria also possess hexose aminidases that degrades complex amino sugars from host cell, which renders the host cell more susceptible to be degraded by bacterial proteases. Iron aquisition is also important for survival and growth of P. gingivalis.
Ecology
Aerobe/anaerobe, habitat (location in the oral cavity, potential other environments) and microbe/host interactions.
P. gingivalis is an obligate anaerobe. It’s major habitat is found to be in the subgingival sulcus of the human oral cavity with preference to reside in deep periodontal pockets. Higher number of bacteria can be found in locations with periodontitis and in lower or non-detectable sites with subgingivalis health or plaque-associated gingivitis.
P. gingivalis have been isolated and cultured from supragingival plaque, oral mucosal surfaces, dorsum of the tongue, saliva as well as the pharynx. P. gingivalis is not found in any other microbiota of any body site.
Microbe/Host interactions
Bacterial adherence begins in the oral cavity before prolierating in the dental plaque. Fimbriae, proteases, hemagglutinins and LPS partitipate in the adherence of P. gingivalis to host cells. Fimbriae are able to bind to multiple sites such as epithelial cells, fibroblasts, salivary components, hemoglobin and several extracellular matrix proteins of the human host. Coaggregation with other plaque-forming bacteria also assists in colonization of P. gingivalis. P. gingivalis invades by the membrane ruffling mechanism of host cells and is internalized through vacuoles. Activation of human epithelial cells, spleen cells and peripheral blood monocytes by P. gingivalis fimbriae results in the release of IL1, IL6, IL8 and TNF A.
Pathology
Do these microorganisms cause disease in the oral cavity or elsewhere?
Application to biotechnology
Bioengineering, biotechnologically relevant enzyme/compound production, drug targets,…
Current research
Summarise some of the most recent discoveries regarding this species.
References
References examples
- ↑ MICR3004
This page is written by Jovin Choo Jia Ying for the MICR3004 course, Semester 2, 2016
