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Streptococcus pyogenes (group A strep)

Micro > Bacteriology > Gram-positive bacteria > Gram-Positive Cocci > Streptococci
Streptococcus Pyogenes (Group A)

Physiology and Structure
  • Gram+ cocci (grow in pairs and long chains)
  • catalase     negative --> β-hemolytic --> bacitracin sensitive --> S.     pyogenes
  • Facultative anaerobe
  • Group-specific carbohydrate (A antigen) and     type-specific antigens (M and T proteins) in cell wall

Epidemiology
  • Asymptomatic colonization in upper resp tract;     transient skin colonization
  • Can survive on dry surfaces for long periods
  • Person-person spread
    •  
    • Respiratory droplets
    •  
    • Breaks in skin after direct contact with infected      person or fomite
  • Persons at risk
    •  
    • School Aged Children (pharyngitis)
    •  
    • Patients with extensive soft-tissue infections and      bacteremia (streprococcal TSS)
    •  
    • Children ages 2-5 w poor persona hygeine (pyoderma)
    •  
    • Young children, older adults w preexisting RTI/SSTI      caused by S. pyogenes (erysipelas, cellulitis)
    •  
    • Children w severe streptococcal disease (rheumatic      fever, glomerulonephritis)
  • Ubiquitous
  • Seasonal incidences
    •  
    • Pharyngitis and assoc rheum fever/glomerulonephritis      Ã  cold months
    •  
    • Pyoderma and associated glomerulonephritis more      commonly seen in the warm months (or tropical regions of the world)
Virulence
  • Defensins
    •  
    • Hyaluronic Acid Capsule
    •  
    • C5a peptidase      (degrades C5a)
  • Adhesins
    •  
    • Lipoteichoic acid
    •  
    • M protein (inhibits      phagocytosis - primary cause of antigenic shift and drift)
  • Invasins
    •  
    • Streptokinase      (lyses blood clots; helps bact spread through tissue)
  • Toxins
    •  
    • Pyrogenic exotoxins A, B, C
    •  
    • Hemolysins (streptolysin S, O)
Pathogenesis and Diseases
  • Infections (PYOGENIC)
    •  
    • Pharyngitis (Strep      Throat)
    •  
          
      • Respiratory droplet/food       transmissionà  adhere to pharyngeal       epithelial via pili à  colonizeà  inflammationà sore throat and enlarged       cervical lymph nodes à several possible outcomes
      •   
             
        • Spontaneous recovery
        •    
        • Bacterial spread à bacteremia, meningitis,        otitis
        •    
        • Toxin release àscarlet fever, TSS
        •    
        • Anti-strep Ab reactions à glomerulonephritis,        Rheumatic fever
        •   
         
       
    • Skin infections      
    •  
          
      • Trauma inoculates bact in       skin à colonize à  inflammation à impetigo (honeycomb       crust and pustular lesions)à       deeper lesions cause erysipelase à       leads to  two possible outcomes
      •   
             
        • Spontaneous recovery
        •    
        • Anti-strep Ab reactions àglomerulonephritis
        •   
         
  • Toxin-mediated diseases (PYOGENIC)
    •  
    • Scarlet fever      
    •  
          
      • S. pyogenes pharyngitis à systemic release of       pyrogenic exotoxins A, B, C à       fever, ‘sandpaper’ rash (begins on trunk and spreads outward), ‘strawberry       tongue’ (first 2 days) à desquamation of palms and       soles after rash subsides
      •  
       
    • Toxic Septic Shock
    •  
          
      • S. pyogenes skin infection (e.g.       cellulitis) leads to a systemic release of pyrogenic exotoxin A       (superantigen) - then polyclonal T cell activation resulting in acute       fever, shock, MODS
      •  
       
    • Necrotizing fasciitis
    •  
          
      • Trauma/surgery inoculates       bacteria in fascia surrounding muscles- release of exotoxin B       (protease)- rapid necrosis along fascial plane (sparing muscles)
      •  
  • Immune-mediated diseases
    •  
    • Glomerulonephritis
    •  
          
      • S. pyogenes skin infection/pharyngitis leads       to the production of anti-strep Ab this then forms an immune complex which       deposits on glomerular Basement Membrane - glomerular inflammation       occurs – and it can be 2 weeks later, have hematuria, HTN and       periorbital edema this may leads to complete recovery likely
      •  
       
    • Rheumatic fever      
    •  
          
      • Untreated S. pyogenes       pharyngitis leads to the production of anti-strep Ab – this generates an       autoimmune cross-reaction of anti-strep Ab with epitopes on joints and       heart muscle -2 weeks later and inflammation response results in various       tissues (e.g. mitral valve) – can result in permanent       endocardial damage that may present as a murmur / valvular dysfunction years later!
      •  

Diagnosis
  • Infections and toxin-mediated diseases
    •  
    • gram stain of clinical specimen: GP cocci in chains
    •  
    • Throat/skin cultures (beta-hemolytic,      bacitracin-sensitive)
    •  
    • ASO+      (anti-streptolysin O Ab present)
  • Immune-mediated diseases
    •  
    • ASO+      
    •  
    • Renal/cardiac studies
    •  
    • Jones criteria’ for Rheumatic fever
Treatment, Control, Prevention
  • Infections
    •  
    • Penicillin G
    •  
    • Clindamycin is useful in severe invasive disease as protein synthesis inhibitor, thus blocking toxin production
  • Immune-mediated disease
    •  
    • Symptomatic
    •  
    • Give prophylactic Penicillin to pts with hx of      Rheumatic fever before procedures (e.g. dental) that can cause      bacteremias leading to endocarditis
Related concepts

1. Scarlet Fever
2. Pharyngitis
3. Strep Throat




 
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