Streptococcus sanguinis

Classification

Higher order taxa

Eubacteria; Firmicutes; Bacilli; Lactobacillales; Streptococcaceae

Genus species

Streptococcus, S. sanguinis

Also known as: Streptococcus sanguis

NCBI: Taxonomy

Description and Significance

Streptococcus sanguinis is a Gram-positive, nonmotile, nonsporeforming, catalase-negative cocci that occur in pairs or chains living in healthy human mouth. This microbe is mostly found in dental plaque, which can then colonize dental cavities. It is also often found in bloodstream where it inhabits in the heart valves, and it has a key role of causing bacterial endocarditis, which can be a serious heart disease and possibly lead to death.[1]

Photo of S. sanguinis was obtained from Virginia Commonwealth University

Genome Structure

The genome of Streptococcus sanguinis was determined via whole-gene shotgun sequencing and observed that it has a circular structure of DNA that is consist of 2,388,435 bp. The size of the sequence is significantly larger than the genome of other members of Streptococcus sequenced. 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(Xu et al. 2007[2]). It's genome can also encode a sigma factor 70, known as "housekeeping" sigma factor which transcribe genes in a growing cell to keep them alive. "Genome Sequence"

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 the 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 enhances metabolic pathways including biosynthesis, pentose phosphate pathway, gluconeogenesis, fermentation of sugars and carbohydrates, and so on. Such enzymes used for gluconeogenesis allows 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.

Pathology

"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"(Xu et al. 2007). 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 colonzie the smooth surface of teeth using hydrophobic interactions, with such hydrophobic bonding. Based on the results of experiments, which suggest that decrease in hydrophobicity is 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 celss in the oral cavity". [3]

As a key agent to infective endocarditis, S. sanguinis can attach to 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 bloodstream. Endocarditis can be proceded through entrance of oral streptocci to bloodstream during dental procedures or even during normal daily activities such as, eating.

Current Studies

Studies were done to understand the relationship between S. sanguinis and other oral bacteria such as mutans streptococci. Specifically, study was done to analyze colonization of bacterium,its proportion, and the role of saliva during formation of dental plaque within mother-infant pairs. 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 tooth, less S. sanguinis is present. Results suggest different ways of controlling dental caries.[4]

Reference

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. 2007. "Genome of the Opportunistic Pathogen Streptococcus sanguinis." Journal of Bacteriology, vol.189, no.8 (3166-3175)

P. W. Caufield, A. P. Dasanayake, Y. Li, Y. Pan, J. Hsu, and J. M. Hardin. 2000. "Natural History of Streptococcus sanguinis in the Oral Cavity of Infants: Evidence for a Discrete Window of Infectivity." Infection and Immunity, vol.68, no.7 (4018-4023)

Virginia Commonwealth University Streptococcus sanguinis Genome Sequencing Project . "Background on Streptococcus sanguinis." 2007.

Virginia Commonwealth University Streptococcus sanguinis Genome Sequencing Project . "Sequence Data." 2007.

"Wikipedia Streptococcus sanguinis"

Schaechter, Moselio, John L. Ingraham, and Frederick C. Neidhardt. Microbe. ASM Press. Washington. 2006

Edited by Sung Oh, student of Rachel Larsen and Kit Pogliano