User talk:KunzA
A Microbial Biorealm page on the genus KunzA
Classification
Higher order taxa
Domain;Eubacteria Phylum;Firmicutes Class;Cocci Order;Lactobacillales Family;Streptococcaceae Genus;Streptococcus Species;S. pyogenes
Species
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NCBI: Taxonomy |
Genus: Streptococcus Species: S. pyogenes
Description and significance
Streptococcus pyogenes is a Gram positive, cocci organism (as can be seen in the results of a Gram stain in the image above) meaning that it has a thick homogenous sheath of a peptidoglycan layer and no outer membrane (Murphy 2004)(Talaro 2012). The cell wall is made up of four components, protein, polysaccharide, peptidoglycan, and teichoic acid (Hardie 1974). This peptidoglycan layer adds rigidity to the cell wall creating an overall cell-wall thickness of 20nm (Hardie 1974). The cell size of this bacteria are between 0.5-1.0µm and are spherical in shape (Hardie 1974). These cocci can grow in chains from moderate to short length and can also be seen in pairs (Hardie 1974). The most favorable growth environment for S. pyogenes is at the temperature 37°C (Hardie 1974). It cannot grow at 10°C or 45°C, at a pH of 9.6, when 6.5% NaCl is present, or with 40% bile (Hardie 1974). They are nonmotile and nonsporeforming (Todar 2008-2012),
This species of bacteria is responsible for a majority of the infectious of the genus Streptococcus and is one of the most common human pathogens. It is a pathogen that affects only humans and based on current research and studies, new diseases and syndromes (such as Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus) are being linked to this bacteria due to its successful means of avoiding immune responses by the body. Nearly 5-15% of individuals carry forms of S. pyogenes with them without any signs of disease, housing it in the respiratory tract (Todar 2008-2012). This increases the possibility of transmission, which can lead to numerous severe infections; some that may even become deadly.
Genome structure
There has been a completed genome sequence for an M1 strain of this bacertial species, S. pyogenes strain SF370 (Ferretti 2001). The genome sequencing revealed that there were nearly 1752 protein-encoding genes present in this strand, and of these only two thirds had a determined function (Hardie 1974). Of these two thirds, there were 46 genes that encoded for virulence factors that showed the different pathogenic capabilities of the organism (Hardie 1974). About six genes were found that were “superantigen-like” (Hardie 1974). The 370 genomes is a chromosome that is circular in shape as opposed to linear and contains 1,852,442 base pairs (Ferretti 2001).
Cell structure and metabolism
The surface structure of Streptococcus pyogenes is one of the most studied cellular surface structures of any bacterial species and is therefore, highly understood. S. pyogenes is a Gram positive organism, indicating that it has one cell wall layer of thick peptidoglycan, which provides a rigid structure for the bacteria (Hardie 1974). This cell wall is made up of four chemical components: protein, polysaccharide, peptidoglycan, and teichoic acid and the overall cell wall thickness is about 20nm (Hardie 1974). Within this layer, “C” polysaccharide, the cell wall polysaccharide, is linked to the peptidoglycan layer by bridges that contain phosphate (Hardie 1974). Antigenic components are located in the cell wall and these antigens are linked to this layer with covalent bonds (Hardie 1974). On the outer layer of the cell wall are fringe/fimbrae and also situated on the cell surface are the M proteins, which are protein fibrils that are heat-stable and trypsin sensitive (Hardie 1974). An alpha-helical coiled-coil structure is at the N terminus of this protein, a non-helical region followed by a coiled-coil region makes up the structure from the most distal point of the protein to the point that it reaches the cell wall, and the region most distal to the cell surface is hypervariable, immunogenic, and is the source of specificity when looking at this organisms (Hardie 1974). The T protein is not as well known in terms of its function, but it is also a protein located on the surface of the of the cell and is relatively stable and trypsin-resistant (Hardie 1974). It is found in almost all Group A Streptococcus species. This protein is constructed of 537 amino acids with the N terminus having a signal peptide and C terminus having close to identical characteristics of the membrane anchor region of surface proteins (Hardie 1974).
Streptococcus pyogenes has a fermentative energy metabolism and when introduced to a glucose broth it reaches a final pH value of 4.8-6.0 (Hardie 1974). It is catalase negative and a facultative anaerobe (Todar 2008-2012). This species of bacteria also requires medium enriched with blood in order to have substantial amounts of growth (Todar 2008-2012). Although acid is produced from many sources, S. pyogenes does not hydrolyze hippurate and does not produce acetoin or urease (Hardie 1974).
Ecology
This is strictly a human pathogen and colonization occurs in the throat or skin of individuals. Streptococcus pyogenes is known for having many forms of virulence determinants, which allow for it to cause a greater range and number of diseases that are able to then infect many different tissues within their human hosts. (Todar 2008-2012)
Pathology
Streptococcus pyogenes is exclusively a human pathogen that colonizes in the throat or skin and is responsible for a majority of the diseases that are a result of streptococcal infections (Hardie 1974). It is very successful in this due to the exotoxins and exoenzymes that are produced from this species and its many subtypes (Murphy 2004). S. pygoenes is able to avoid phagocytosis. This is able to occur due to the hyaluronic acid capsule that surrounds the bacteria cell (Hardie 1974). This results in the activation of only a weak response to the immune system due to the capsules antigenic similarity with the host, which allows it to avoid being engulfed by the body’s immune response (Hardie 1974). M proteins also allow the bacteria cells to avoid phagocytosis and are a primary virulence mechanism for surviving in a host (Hardie 1974). These proteins make up the fimbrae that are found on the out cell wall and are able to bind plasma fibrinogen to them which is able to disguise receptors on the bacterial cell (Haride 1974).
Another way in which it finds success as a pathogen is through the reslease of exotoxins (erythrogenic toxin, the streptolysin O and S), which cause red blood cell death due to the decrease of oxygen in the interstitial fluid (Murphy 2004). Streptolysins O and S in particular have the ability to break down host cells and tissue and cause cell lysis of red blood cells, and inhibit regular cell function (Hardie 1974).
Enzymes may also be released by S. pyogenes that allow it to escape a body’s immune system and/or cause destruction to the barriers that try to block spreading (Murphy 2004). Hyaluronidase breaks down tissue barriers by removing the bonds that are made up of Hyaluronic acid that otherwise hold the cells in the tissues together (Murphy 2004). Streptokinase allows S. pyogenes to spread rapidly from its initial infection site by changing the barriers set up by the immune system in the form of fibrogen clots causing these clots to then dissolve away (Murphy 2004). This enzyme has been associated with acute post-streptococcal glomerulonephritis (Hardie 1974).
Streptococcus pyogenes have always been associated with severe infections that often lead to death. In the middle of the 20th century there was a large decline in the number of cases marked by the presence of S. pyogenes but within the last 15 years these cases have risen once again (Stevens 2012). The current affects of this bacterial infection are the following diseases and syndromes: pharyngitis (strep throat), cellulitis, scarlet feverm, impetigo, streptococcal “toxic shock” sydrome, and necrotizing fasciitis (Hardie 1974). Conditions that can occur after an infection are as follows: glomerulonephriis, streptococcal reactive arthritis, acute rheumatic fever, and rheumatic heart disease (Hardie 1974). The most recent links to this bacteria have been seen in the diagnosis of movement and attention-deficit disorders, tics, and Tourette’s syndrome (Hardie 1974).
At this time, penicillin is a successful treatment of Group A streptococcal disease, of which S. pyogenes is apart of (Todar 2008-2012). No vaccines have been developed at this time (Todar 2008-2012).
Current Research and or Application to Biotechnology
1. A recent article in Scientific America, by Karen Schrock, found that Tourettes-like symptoms could be linked to the rare disease known as PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus). Other symptoms caused by this disease are Obsessive-Compulsive Disorder (OCD) and Tics. PANDAS is normally the result of a severe case of strep throat and is associated with the bacteria species S. pyogenes. How this bacterial infection located in the throat can cause such extreme alterations in behavior is due to the fact that the body’s natural production of antibodies begins to attach the cells of the body, in this case associated with the brain, due to their near resemblance to the antigens of the Streptococcal bacteria (“PANDAS” 2010). This can result in many of these neurological symptoms. (Schrock 2012) The Hyaluronic Acid Capsule is one of the reasons that S. pyogenes is able to go unnoticed by the host antibodies due to the chemical similarities between hyaluronic acid and host connective tissue (Todar 2008-2012).
2. A recent studied showed that contact and complement systems interfere with the growth of S. pyogenes in human blood. This study from the Journal of Biological Chemistry showed that the presence of the protein SIC, which is secreted by S. pyogenes, causes the activity of antibacterial peptides to be blocked due to its interference with the contact system. This then allows for the survival and growth of S. pyogenes where the activation of these systems would normally generate antibacterial peptide fragments that would kill S. pyogenes and other bacterial pathogens. The authors specifically found that the growth of S. pyogenes was enhanced in human plasma under the circumstances that the following contact components were not present: FXII, PK, or HK. This suggests that SIC can then contribute to the survival of bacteria. (Frick 2010)
3. Another recent study found that Manuka honey could inhibit the development of S. pyogenes. Manuka honey is known to have antimicrobial activity that can affect a large array of bacterial species. The study investigated the effects on this form of inhibitor on S. pyogenes through the use of planktonic and biofilm cultures. Bacterial destroying agents were found on both cultures and the biofilm culture required slightly higher amounts of the manuka honey in order to obtain these results. The honey was able to kill and disassociate the bacterial cells from the biofilm. They also found that the honey prevented S. pyogenes from binding to the protein fibronectin located in human tissue. This indicated that this unique product could be used as an antibacterial on topical surfaces that contain the infectious bacteria of S. pyogenes. The study is perhaps an enormous break through due the silent epidemic of bacterial resistance that continues to grow. (Maddocks 2012)
References
Ferretti, Joseph F., et al. "Complete Genome Sequence of an M1 Strain of Streptococcus Pyogenes." PNAS (2001). PNAS. 26 Jan. 2001. <http://www.pnas.org/content/98/8/4658.long>.
Frick, Inga-Maria, Oonagh Shannon, Per Åkesson, Matthias Mörgelin, Mattias Collin, Artur Schmidtchen, and Lars Björck. "Antibacterial Activity of the Contact and Complement Systems Is Blocked by SIC, a Protein Secreted by Streptococcus Pyogenes." The Journal of Biological Chemistry (2011): 1331-1340. PubMed Central. 2010. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3020741/?tool=pubmed>.
Hardie, Jeremy M., Whiley, Robert A.. Family VI: Streptococcaceae. In R. E. Buchanan & N. E. Gibbons (Eds.), Bergey's manual of determinative bacteriology (8th ed.). Baltimore, MD: Williams & Wilkins. 1974. 490-515.
Maddocks, S. E., M. S. Lopez, R. S. Rowlands, and R. A. Cooper. "Manuka Honey Inhibits the Development of Streptococcus Pyogenes Biofilms and Causes Reduced Expression of Two Fibronectin Binding Proteins." Microbiology. 2012. <http://mic.sgmjournals.org/content/early/2012/01/31/mic.0.053959-0.abstract>.
Murphy, Todd. "Streptococcus and Associated Pathology." Ivy Tech State College: Microbiology. 2004. <http://faculty.ivytech.edu/~twmurphy/text_pg/strep.htm>.
"PANDAS." Behavioural Neurotherapy Clinic. 2010. Web. 14 Mar. 2012. <http://www.adhd.com.au/PANDAS.htm>.
Schrock, Karen. "Could an Infection Cause Tourette's-Like Symptoms in Teenage Girls?" Scientific American. 2012. <http://www.scientificamerican.com/article.cfm?id=could-infection-cause-tourettes-like-symptoms-teenage-girls>.
Stevens, Dennis L. "Streptococcus Pyogenes (Group A β-hemolytic Streptococcus)." Streptococcus Pyogenes (Group A β-hemolytic Streptococcus). 2012. Web. 10 May 2012. <http://www.antimicrobe.org/b239.asp>.
Talaro, Kathleen Park., and Barry Chess. "A Survey of Prokaryotic Cells and Microorganisms." Foundations in Microbiology. 8th ed. New York, NY: McGraw-Hill, 2012. 89-122.
Todar, Kenneth. "Streptococcus Pyogenes and Streptococcal Disease." Todar's Online Textbook of Bateriology. 2008-2012. <http://textbookofbacteriology.net/streptococcus.html>.
Edited by student of Dr. Lynn M Bedard, DePauw University http://www.depauw.edu
