A Beginner’s Guide to S. Pyogenes

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Hippocrates was the first to describe Fournier’s Gangrene or Necrotizing Fasciitis, caused by my selected pathogen Streptococcus pyogenes, in the Fifth Century BCE. He cited that several individuals had contracted a disease that “was a trivial accident…flesh, [tendons, nerves], and bones fell away in large quantities…there were many deaths.” (Cocanour, 2017). S. pyogenes, as a string of cocci, first described by Austrian surgeon Theodor Billroth as being associated with infections of wounds in 1874. (Billroth, 1874) Louis Pasteur isolated the bacteria from women with puerperal fever, the leading cause of death in women and infants at the time. S. pyogenes infamously causes scarlet fever, this disease causes redness in skin, sore throat and ulcerous tonsils. Scarlet fever was first recognized in the 1500s by Sicilian anatomist Giovanni Filippo Ingrassias who described the occurrence as “the whole body appeared to be on fire.” This description differentiated the rash from those caused by measles. (Ingrassia, 1553). During the time, Europe was suffering several epidemics of scarlet fever. French physician Jean Cottyar of Poitiers was first to officially describe the disease and publish soreness of the throat as a symptom in 1578 (Rolleston, 1928). Puerperal fever, or childbed fever, was a common cause of death in the 1700s. (Ferretti, 2016).  Hungarian physician Ignac Semmelweis observed S. pyogenes, then he called ‘cadaver particle’, being transmitted by surgeons into obstetric wards from diseased bodies in 1842. Though he had no scientific explanation for this progress, mortality rates shrunk when sterilization practices were implemented in hospitals. It wasn’t until Louis Pasteur attributed the microbe to the disease in 1879. Epidemics of scarlet fever were prominent as well in the 17th and 18th century, S. pyogenes was found as the culprit of the disease in 1924 when George and Gladys Dick identified the presence of a toxin produced by the bacteria that causes the symptoms of scarlet fever (Dick G. F., 1924).

Streptococcus pyogenes is an aerotolerant Gram-positive bacterium. The cells non-motile cells do not sporulate and arrange themselves in a chain formation. These bacteria are particular about their growing environment, they should be kept at 37 degrees Celsius and have 5-10% CO2. The growth medium used to grow S. pyogenes is made of neo peptone extracts, glucose for carbon, and a mixture of nutrients from beef heart infusion (Gera, 2013). This combination stems from the fact that S. pyogenes creates lactic acid from fermenting glucose, the broth was first implemented for S. pyogenes in 1932. The incubation period of S. pyogenes is one to three days under ideal conditions (Todd EW, 1932). There isn’t an ideal UV radiation for growing S. pyogenes, however, they can be killed using a 120 μW/cm2 bulb germicidal lamp (Scott, 2012).

Being aerotolerant, Streptococcus pyogenes goes through glycolysis via the Embden-Meyerhof-Parnas (EMP) pathway, following a series of steps involving twelve enzymes. This pathway resembles the typical glycolysis with the addition of steps from the Entner-Doudoroff (ED) pathway contributing glyceraldehyde and pyruvate. When glucose content is low, such as in the mouth or on the surface of skin, the cells are forced into a pathway using complex carbohydrates that are not glucose, this is considered a salvage pathway. When glucose is in excess, S. pyogenes undergoes steps called the phosphoenolpyruvate (PEP)-dependent phosphotransferase (PTS) system (Calderón-Santiago M, 2019). This system begins when the gene in control of catabolizing polypeptides into glucose are repressed and the cell begins to metabolize the sugars and carbon rapidly, this event is called carbon catabolite repression (CCR) (Pancholi, 2016).

Works Cited

Billroth, T. (1874). Untersuchungen über die Vegetationsformen von Coccobacteria septica und der Antheil, welchen sie an der Entstehung und Verbreitung der accidentellen Wundkrankheiten haben. Retrieved from NIH.gov: https://www.ncbi.nlm.nih.gov/books/NBK333430/#

Calderón-Santiago M. (2019, January). Human sweat metabolomics for lung cancer screening. Retrieved from PubMed – NCBI: https://www.ncbi.nlm.nih.gov/pubmed/25935675

Cocanour, C. S. (2017). Management and Novel Adjuncts of Necrotizing Soft Tissue Infections. Retrieved from Surgical Infections: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5393412/

Dick G. F., D. G. (1924). The etiology of scarlet fever. Journal of the American Medical Association. , 301-302.

Ferretti, J. a. (2016, Febuary 10). Streptococcus pyogenes : Basic Biology to Clinical Manifestations . Retrieved from University of Oklahoma Health Sciences Center: https://www.ncbi.nlm.nih.gov/books/NBK333430/#

Gera, K. &. (2013). Laboratory Growth and Maintenance ofStreptococcus pyogenes(The Group A Streptococcus, GAS). . Current Protocols In Microbiology, 10-19.

Ingrassia, G. F. (1553). De tumoribus praeter naturum. Naples.

Pancholi, V. &. (2016). Streptococcus pyogenes Metabolism. Retrieved from University Of Oklahoma Health Sciences Center: https://www.ncbi.nlm.nih.gov/books/NBK333417/

Rolleston, J. (1928). The History Of Scarlet Fever. The British Medical Journal, 2, 92.

Scott, J. N. (2012). Phage-Like Streptococcus pyogenes Chromosomal Islands (SpyCI) and Mutator Phenotypes: Control by Growth State and Rescue by a SpyCI-Encoded Promoter. . Frontiers In Microbiology.

Todd EW, H. L. (1932). A new culture medium for the production of antigenic streptococcal haemolysin. .Journal of Pathology and Bacteriology.

 

 

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