Higher order taxa
Eubacteria; Firmicutes; Bacilli; Lactobacillales; Streptococcaceae
Streptococcus, S. sanguinis
Also known as: Streptococcus sanguis
Description and Significance
Streptococcus sanguinis is a Gram-positive, nonmotile, non-spore forming cocci found in healthy human mouths. This microbe is mostly found in dental plaque, which can then colonize dental cavities. It is also often found in the bloodstream which allows it to inhabit the heart valves causing bacterial endocarditis, a serious heart disease that can possibly lead to death (4).
The genome of Streptococcus sanguinis was determined via whole-gene shotgun sequencing. It has a circular structure of DNA that consists of 2,388,435 bp. The size of the sequence is significantly larger than the genome of other members in the Streptococcus family. S. sanguinis has relatively higher percentage (43.4%) of Guanine and Cytosine base pairing than that of others which requires higher energy to break the Hydrogen bond during the process of replication; it allows to differentiate this organism from other streptococci. The genome of this bacteria can encode 2,274 proteins, 61 tRNAs, and four rRNA operons(7). Its genome can also encode a sigma factor 70, known as "housekeeping" sigma factor which transcribes genes in a growing cell to keep them alive.
Cell Structure and Metabolism
S. sanguinis is a coccus shaped Gram-positive bacteria that has a thick cell wall consisting of peptidoglycan (also called murein which is unique to bacteria and is responsible for its shape and rigidity) as well as teichoic acids (Schaechter 2006). This organism has a very well-built system for energy production despite an incomplete TCA cycle(Kreb Cycle or Citric acid cycle). It contains many enzymes that enhance metabolic pathways including biosynthesis, pentose phosphate pathway, gluconeogenesis, fermentation of sugars and carbohydrates, and so on. Such enzymes used for gluconeogenesis allow the bacterium to convert amino acids into fructose-6-phosphate, an important metabolic precursor used to make peptidoglycan(cell wall) and an initial substrate required for pentose phosphate pathway. Many of these enzymes were found in other streptococci and some are not present(7).
"S. sanguinis directly binds to oral surfaces and serves as a tether for the attachment of a variety of other oral microorganisms which colonize the tooth surface, form dental plaque, and contribute to the etiology of both caries and periodontal disease"(7). A study shows that SrtA gene in S. sanguinis participates in anchoring adhesin proteins on the bacterial surface, however, it is mainly effective on its adhesion to epithelial cells. Oral streptococci colonize the smooth surface of teeth using hydrophobic interactions. Based on the results of experiments, which suggest that decreases in hydrophobicity are due to a lack of SrtA gene, it was indicated that SrtA gene may have a role of "adhesion to teeth, restorable dental materials, and epithelial cells in the oral cavity" (8).
As a key agent to infective endocarditis, S. sanguinis can attach to the bloodstream and damage heart valves. Specifically, "fibrin and platelets are deposited at the site of endothelial cell trauma, forming a sterile vegetation where bacteria may adhere and colonize" in the presence of bacteria in the bloodstream. Endocarditis can proceed through entrance of oral streptocci to the bloodstream during dental procedures or even during normal daily activities such as eating (2).
Ecology and Application to Biochemistry
S. sanguinis is commonly found in oral cavities and the bloodstream. Environment factors such as cell density, nutritional availability, and pH can influence the interaction between streptococci: S. sanguinis and S. mutans. Such interactions can be brought through chemicals that are produced from bacteria. Hydrogen peroxide is produced by S. sanguinis and its presence can decrease the growth of S. mutans. In a nutrient-rich environment, hydrogen peroxide production is turned off and energy required for the production of hydrogen peroxide is instead used for cell growth. On the other hand, if there are not enough nutrients or the pH of the environment is low, hydrogen peroxide production is turned on allowing competition against S. mutans. Thus, the environment regulates the competition and coexistance of S. sanguis and S. mutans (10).
Studies were done to understand the relationship between S. sanguinis and other oral bacteria such as mutans streptococci. Specifically, a study was done to analyze colonization of bacterium,its proportion, and the role of saliva during formation of dental plaque within mother-infant pairs. The study concluded that the tooth emergence increases as the proportion of saliva in mouth increases. Also, they discovered that S. sanguinis and mutans streptococci have an inverse relationship that when mutans streptococci colonize teeth, less S. sanguinis is present. Results suggest different ways of controlling dental caries (1).
A study was done to determine the role of immunoglobulin G in relation to cardiovascular disease caused by bacteria, specifically, S. sanguis. It was concluded that platelet activation depends on a immunoglobulin G (IgG) and its binding to strains of S. sanguis. In this study, four strains from S. sanguis and one S. gordonii strain was used and results showed that three strains from S. sanguis showed significant number of IgG binding while the rest of the strains showed low binding. Thus, the platelet aggregation is regulated by the extent of IgG binding response to the presence of S. sanguis (9).
A study was also done to find the effects of procaine and tetracaine, both anesthetics, on S. sanguis. At the conclusion of the study, they found that procaine and tetracaine have a specific effect on S. sanguis, depending on when a cell goes through transient physiological change, known as competence. Procaine and tetracaine effect S. sanguinis similiarily, in that onset occurs during the precompetence stage and decreases as it goes through the postcompetence stage. Thus, the anesthetics have an inhibitory effect on S. sanguis competence; when procaine or tetracaine bind to the appropriate ligands on the surface of the cell, DNA-mediate gene transfer does not take place(6).
1. P. W. Caufield, A. P. Dasanayake, Y. Li, Y. Pan, J. Hsu, and J. M. Hardin. "Natural History of Streptococcus sanguinis in the Oral Cavity of Infants: Evidence for a Discrete Window of Infectivity." Infection and Immunity. 2000., vol.68, no.7 (4018-4023).
2. S. Paik, L. Senty, S. Das, J. C. Noe, C. L. Munro, and T. Kitten. "Indentification of Virulence Determinants for Endocarditis in Streptococcus sanguinis by Signature-Tagged Mutagenesis". Infection and Immunity. 2005., vol.73, no.9 (6064-6074).
3. Schaechter, Moselio, John L. Ingraham, and Frederick C. Neidhardt. Microbe. ASM Press. Washington. 2006.
7. P. Xu, J. M. Alves, T. Kitte, A. Brown, Z. Chen, L. S. Ozaki, P. Manque, X. Ge, M. S. Serrano, D. Puiu, S. Hendricks, Y. Wang, M. D. Chaplin, D. Akan, S. Paik, D. L. Peterson, F. L. Macrina, and G. A. Buck. "Genome of the Opportunistic Pathogen Streptococcus sanguinis." J. Bacteriol. 2007. vol.189, no.8 (3166-3175)
A. McNicol, R. Zhu, R. Pesun, C. Pampolina, E. C. Jackson, G. H. W. Bowden, and T. Zelinski. 2006. "A role for immunoglobulin G in donor-specific Streptococcus sanguis-induced platelet aggregation". Thrombosis and Haemostasis vol.95 no.2 (288-93)
Edited by Sung Oh, student of Rachel Larsen and Kit Pogliano