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Streptococcus pyogenes

Cell Wall: Gram Positive Shape: Cocci
Biochemistry: Catalase Negative Metabolism: Microaerophilic
Streptococcal subclassification: Group A, beta-hemolytic
Virulence Factors
  • M protein
    • A component of the S. pyogenes cell wall that protects organism from phagocytosis. Antibodies to M Protein generated by the Humoral Immunity are protective, leading to bacterial opsonization, and thus form the basis of immunity. However, over 80 M protein serotypes exist and antibodies generated to one serotype does not protect against infection by another.
  • Streptolysin O and Streptolysin S
    • Streptolysins are enzymes that contribute to lysis of red and white blood cells (gives beta-hemolytic S. pyogenes its hemolytic ability). Streptolysin O is inactivated by oxygen (Oxygen Labile) while Streptolysin S is not (Oxygen Stabile). Antibodies to Streptolysin O are generated by the humoral immunity and can be quantified as Anti-streptolysin O Antibodies (i.e. ASO titer). Antibodies are not generated to Streptolysin S.
  • Pyrogenic and Erythrogenic Exotoxins
    • These exotoxins are only produced by some strains of S. pyogenes which have undergone transduction with a particular phage. Release of pyrogenic exotoxin can result in Toxic Shock Syndrome. Release of erythrogenic exotoxin can result in scarlet fever as described below.
Clinical Consequences
  • Overview
    • S. pyogenes causes pathology either through local pyogenic infections, release of exotoxins, or by initiating a dysregulated immune response that targets host tissues and thus Autoimmune Disease.
  • Local Pyogenic Infections
    • Pharynx: S. Pyogenes is the cause of classic "Strep Throat" or pharyngitis which manifests as erythematous tonsils covered with a purulent exudate in conjunction with lymphadenopathy in the neck as well as fever. Penicillins can be used for treatment of streptococcal pharyngitis.
    • Skin: Can manifest as folliculutis,cellulitis, to impetigo. Skin infetions by S. pyogenes cannot be distinguished easily from those caused by S. aureus; therefore, dicloxacillin which covers both organisms is often used.
    • Necrotizing Fasciitis: Only caused by certain strains with particular M proteins. Organisms are introduced through traumatic breaks in the skin and rapidly move through fascial planes leaving a path of necrosis. Manifests as rapid swelling of the skin which at first appears reddish but evolves to a purple/blackish color. Fluid-filled bullae often arise. Treatment involves: 1) Surgical removal of infected fascia, 2) Antibiotic: Penicillin G, 3) Inhibition of exotoxin release using clindamycin which blocks bacterial protein translation.
  • Exotoxin Release
    • Scarlet Fever: Caused by certain strains of S. pyogenes which carry erythrogenic exotoxin. Manifests as a pharyngitis accompanied by a characteristic skin rash and high fever. The scarlet-red rash, composed of tiny papules, characteristically begins in the upper trunk and spreads to the extremities whilst sparing the palms and soles.
    • Streptococcal Toxic Shock Syndrome: Caused by certain strains of S. pyogenes which carry pyrogenic exotoxin.
  • Induction of Dysregulated Immune Response
  • Thankfully, S. pyogenes is still highly sensitive to penicillins. See above particular pathologies for specific treatments. Generally, if only S. pyogenes is suspected Penicillin G is sufficient; however, if S. pyogenes or Staphylococcus aureus could both be the cause then a penicillinase-resistant penicillin such as dicloxacillin should be used. If exotoxin release plays a major role in pathology then, in addition to Penicillin G, a translation-inhibiting antibiotic like clindamycin is added.