Streptococcus pyogenes
| Categorization | |
|---|---|
| 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
- Rheumatic Fever (see page)
- Acute Proliferative Glomerulonephritis (AKA Post-streptococcal glomerulonephritis. See page)
| Treatment |
|---|
- 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.