Staphylococcus aureus: Virulence and Toxin

Staphylococcus aureus: Virulence and Toxin


VIRULENCE FACTOR:

  • Cell wall associated structures
Techoic acid
  • Adhesion
  • Protection against complement mediated opsonization.
  • Antitechoic acid antibodies found in the patients with active endocarditisndue to S. aureus’
Peptidoglycan

 

  • Inhibits inflammatory response
  • Activates complement system
  • Induce release of cytokines
  • Endotoxin like activity

 

Capsule
  • Adhere to host cell
  • Resist phagocytosis

 

Clumping factor (bound coagulase)

 

  • Cause organism to clump in presence of plasma

 

ProteinA

 

  • Binds to Fc moiety of IgG, exerting antiopsomin
  • Strongly antiphagocytic effect
  • Responsible for Coagglutination

 

Extracellular Enzymes

Free Coagulase
  • Clots plasma by acting along with CRF present in plasma, binding to prothrombin and converting fibrinogen to fibrin
  • Detected by tube coagulase test
  •  8 types. 
  • Most human strain form – A coagulase
staphylokinaseDNAase

 

  • Degrades fibrin clots

 

Hyaluronidase serokinase
  • Hydrolyze the acidic mucopolyysaccharides  present in matrix of connective tissues

 

Nuclease

 

  • heat stable nuclease (DNAse)
Lipases
  • Helps in infecting skin and subcutaneous tissue
Protease
  • Helps spread infection

TOXINS Cytolytic Toxins

α-Hemolysin
  • Protein inactive at 70oC
  • Reactivated paradoxically at 100″C.
  • Less active against human erythrocytes.
  • Leukocidal
  • Cytotoxic
  • Dermonecrotic
  • Neutotoxic
  • Lethal.
β- Hemolysin
  • Hot cold phenomenon
  • Sphingomyelinase
  • Hemolytic for sheep cells. 
δ  – Hemolysin
  • Detergent like effect on cell membranes,
  • Plays role in S. aureus diarrhea
  • disease
γ – Hemolysin 
  • Bicomponent protein. 
Leukocidin (Panton valentine Toxin
  • Bi component toxin
  • Associated with farunculosis
  • Important virulence factor in MRSA infection.
  • Kills WBCS by producing holes in their CM

Enterotoxin

  • Act on ANS to cause illness
  • Preformed
  • Types:A, B, C 1-3, D, E and H
  • Heat stable toxin
  • Responsible for staphylococcal food poisoning which occur 2-5 hrs after consuming meat and fish or milk products.

Source:

  • Usually food handler which is carrier.
  • Mechnism: Type A toxin is responsible for most cases.
    • Toxin acts directly on autonomic nervous system (Vagal stimulation) andvomiting center.

TSST

  • Produce fever, skin rashes,diarrhoea,conjunctivitis,and death to shock
  • TSST-1 = Enterotoxin F = Pyrogenic Exotoxin C is responsible for most cases.
  • TSST-1 binds to MHC class II molecules, yieldingT-Cell stimulation.
  • Staph. Enterotoxin and TSST are super antigen 
  • Leading to an excessive and non regulated immune response.

Exfoliating toxin/Epidermotolytic Toxin / ET / Exfoliatin

  • Breaks intracellular bridges in the stratum granulosum of epidermis
  • Causes its separation from underlying tissue
  • Resulting in a blistering and exfoliating disease of skin
  • Cause staphylococcal scalded skin syndrome (SSS).
  • Severe form is called Rittels disease in neonate arrd toxic epidermal neuolysis in elderly.
  • Milder form are pemphigus neonatorum and bullous impetigo.

Two type:

  • ETA (chromosomal gene product, heat stable)
  • ETB (plasmidnmediated, heat labile). 
  • Possess serine protease activity which triggers exfoliation.

Exam Important

  • About 30% of general population are healthy nasal carriers
  • Epidermolysis and TSS toxin are superantigens
  • Toxic shock syndrome is Staphylococcus infection is due to superantigen, Leucocidin and Hemolysin
  • Staphylokinase enzyme produced by Staphylococcus aureus that dissolves fibrin clots 
  • Toxins of Staphylococcus are Enterotoxin 
  • Staphylococcus aureus remains in the skin for longer period because of Hyaluronidase 
  • Methicillin resistance is chromosome mediated

 

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