Streptococcus Pyogens

INTRODUCTION:
  • Aerotolerant and an extracellular bacterium, made up of non-motile and non-sporing cocci.
  • Group A streptococci when grown on blood agar typically produces small zones of beta-hemolysis, a complete destruction of red blood cells and can make colonies greater than 5 mm in size
  • Cultured on blood agar plates incubation period of 1 to 3 days
  • Catalase-negative and Gram-positive
  • Not soluble in 10% bile, Ferment trehalose but not ribose,Hydrolyse PYR & Ferment trehalose but not ribose
  • Antibiotic used for sensitivity in identification of streptococcus pyogenes is Bacitracin
METHOD OF TRANSMISSION:
  • Respiratory droplets
  • Hand contact with nasal discharge and skin contact with impetigo lesions
  • The pathogen can also be found in its carrier state (anus, vagina, skin, pharynx)
  • Can also be spread from cattle to humans through raw milk and contaminated foods (salads, milk, eggs)
BACTERIOLOGY
  • SEROTYPING
  • Serotyping S. pyogenes is based on its M protein & their surface T-antigen.
  • Four of the 20 T-antigens have been revealed to be pili.
  • Over 220 M serotypes and about 20 T serotypes are known.
VIRULENCE FACTOR:
  • Carbohydrate-based bacterial capsule composed of hyaluronic acid surrounds the bacterium, protecting it from phagocytosis by neutrophils.
  • Capsule and several factors embedded in the cell wall, including M protein, lipoteichoic acid, and protein F (SfbI) facilitate attachment to various host cells.
  • M protein also inhibits opsonization by the alternative complement pathway by binding to host complement regulators.
  • The M protein found on some serotypes is also able to prevent opsonization by binding to fibrinogen.
  • Virulent strains produce 'matt' (finely granular) colony & Avirulent strains produce 'glossy' colonies.
LYSOGENY:
  • All strains of S. pyogenes are polylysogenized.
  • In general, the genome of S. pyogenes strains isolated during disease are >90% identical, they differ by the phage they carry.
Name Description
Streptolysin O An exotoxin, one of the bases of the organism's beta-hemolytic property, streptolysin O causes an immune response and detection of antibodies to it; antistreptolysin O (ASO) can be clinically used to confirm a recent infection.
Streptolysin S An exotoxin, one of the bases of the organism's beta-hemolytic property, streptolysin O causes an immune response and detection of antibodies to it; antistreptolysin O (ASO) can be clinically used to confirm a recent infection.
Streptococcal pyrogenic exotoxin A (SpeA) A cardiotoxic exotoxin, another beta-hemolytic component, not immunogenic and O2 stable: A potent cell poison affecting many types of cell including neutrophils, platelets, and subcellular organelles.
Streptococcal pyrogenic exotoxin C (SpeC) Superantigens secreted by many strains of S. pyogenes: This pyrogenic exotoxin is responsible for the rash of scarlet fever and many of the symptoms of streptococcal toxic shock syndrome, also known as toxic shock like syndrome(TSLS).
Streptokinase Enzymatically activates plasminogen, a proteolytic enzyme, into plasmin, which in turn digests fibrin and other proteins
Hyaluronidase Hyaluronidase is widely assumed to facilitate the spread of the bacteria through tissues by breaking down hyaluronic acid, an important component of connective tissue. However, very few isolates of S. pyogenes are capable of secreting active hyaluronidase due to mutations in the gene that encode the enzyme. Moreover, the few isolates capable of secreting hyaluronidase do not appear to need it to spread through tissues or to cause skin lesions. Thus, the true role of hyaluronidase in pathogenesis, if any, remains unknown.
Streptodornase Most strains of S. pyogenes secrete up to four different DNases, which are sometimes called streptodornase. The DNases protect the bacteria from being trapped in neutrophil extracellular traps (NETs) by digesting the NETs' web of DNA, to which are bound neutrophil serine proteases that can kill the bacteria.
C5a peptidase C5a peptidase cleaves a potent neutrophil chemotaxin called C5a, which is produced by the complement system.C5a peptidase is necessary to minimize the influx of neutrophils early in infection as the bacteria are attempting to colonize the host's tissue. C5a peptidase, although required to degrade the neutrophil chemotaxin C5a in the early stages of infection, is not required for S. pyogenes to prevent the influx of neutrophils as the bacteria spread through the fascia.
Streptococcal chemokine protease The affected tissue of patients with severe cases of necrotizing fasciitis are devoid of neutrophils.The serine protease ScpC, which is released by S. pyogenes, is responsible for preventing the migration of neutrophils to the spreading infection. ScpC degrades the chemokine IL-8, which would otherwise attract neutrophils to the site of infection.
DISEASES:
  • Infections typically begin in the throat or skin. The most striking sign is a strawberry-like rash
  1. Pharyngitis (strep throat)
  2. Localized skin infection (impetigo)
  3. Erysipelas and cellulitis
  4. Necrotizing fasciitis
  5. Scarlet fever
  6. Streptococcal toxic shock syndrome
  7. Autoimmune-mediated complications( rheumatic fever and acute postinfectious glomerulonephritis).
Exam Question
  •  Produce numerous exotoxins and exoenzymes
  • S.pyogens is Gram-positive cocci
  • S.pyogens is Catalase negative Cellulitis is commonly Caused by S. pyogens
  • Streptococcus pyogenes Causes necrotizing fascitis
  • Streptococcus pyogenes is Beta hemolytic
  • M. protein, Pyrotoxin, Streptolysin O is virulence factor of s. pyogens
  • Streptococcus pyogenes causes rheumatic heart disease
  • Antibiotic used for sensitivity in identification of streptococcus pyogenes is Bacitracin
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