Streptococcus Pyogenes

Group A, beta-hemolytic strep

 

Structure and physiology

Capsule (outermost layer)

• Hyaluronic acid -> nonimmunogenic

 

Cell wall

• Fimbriae (pilus-like structure)
  * contain M-protein (major virulence factor) and lipoteichoic acid (LTA)
  * LTA and M-protein facilitate adhesion to epithelia
  M-protein -> highly variable N-terminal exposed, antiphagocytic, also antigenic.
• Group A-specific C-carbohydrate (definition of group A)
• Protein F - faciliate attachment to fibronectin

 

Extracellular products

• Streptococcal pyrogenic exotoxins (SPEs) - type A, B, and C.
• Cytolytic toxins and other exoenzymes
  * Streptolysin O (oxygen-labile) - damages cells including PMNs
  * Streptolysin S (oxygen-stable) - damages erythrocytes, leukocytes, and platelets
  * Streptokinase (fibrinolysin) - converts plasminogen to plasmin
     -> thrombolysis
  * Streptodornases (DNAses) - breakdown DNAs in necrotic tissue
     -> aids spread of infection
  * C5a peptidase - inactivates complement C5a
     -> interferes with chemotaxis of WBC
  * Hyaluronidase - hydrolyses structural carbohydrate hyaluronic acid
     -> aids spread of infection

 

Epidemiology

Spread by respiratory droplets or skin contact. Person to person.

Does not survive well in the environment.

Reservior - infected patient or healthy carriers (on skin, mucous membrane (esp nasopharyngeal)

 

Pathogenesis

1. Attachment to mucosa, aided by protein F, lipoteichoic acid, protein M
2. Colonisation OR...
3. Phagocytosis inhibited by hyaluronic acid capsule and M protein
4. Fast spread by reduced viscosity of pus via streptokinase, streptodornase, hyaluronidase
5. Hemotogenous spread

 

Clinical significance

1. Cellulitis

Major cause, probably more than staph aureus

 

2. Acute pharyngitis or pharyngotonsilitis

Most common bacterial cause, esp in 2 to 20 y.o.

Most cases are mild, compared to other etiology

2.1. Strep throat

Severe, purulent inflammation of posterior oropharynx and tonsillar area

2.2. Scarlet fever

Sunburn-like rash

 

3. Impetigo

Caused by staph aureus and strep pyogenes

Most commonly on lower legs

Treated with topical agent (mupirocin) and/or penicillin or first-generation cephalosporin

 

4. Erysipelas

All age gropus.

Fiery red, advancing erythema, esp on face or lower limbs.

 

5. Puerperal sepsis

Purulent vaginal discharge plus systemically unwell

 

6. Invasive group A streptococcal (GAS) disease

Cellulitis or necrotising fasciitis/myositis (cellulitis with necrosis)

+ toxic-shock-like syndrome (fever, hypotension, multi-organ involvement, sunburn-like rash)

 

7. Acute rheumatic fever

Due to cross-reaction between the strep antigen (esp M protein) and antigens of the heart and joint tissues.

2 to 3 weeks after pharyngitis

Rheumatic fever is preventable with 10 days of antibiotics (and the reason for it)

 

8. Acute glomerulonephritis

1 week after pharyngitis or impetigo

Deposit of antigen-antibody complex on the glomerular basement membrane.

No evidence that antibiotic treatments prevent acute GN.

 

Laboratory identification

Colony morphology - small, opalescent, surrounded by large zone of beta hemolysis.

Serology - antibody to streptolysin-O (ASO test)

Serology - anti-DNAse B titers (ADB test) for strep skin infections.

 

Treatment

First line - Penicillin G

Second line - clarithromycin, azithromycin (for penicillin allergy patients)

Drainage and debridement for necrotizing fasciitis/myositis

 

Prevention

Prolonged prophylactic antibiotic therapy indicated after just one episode of rheumatic fever

 

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Things to revise/add later:

Bibliography: LWW microbiology

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