Toxins and other virulence factors

TOXINS AND VIRULENCE FACTORS
  • Streptococci form several exotoxins and enzymes, which contribute to its virulence.

Extra cellular toxins

Hemolysins

  • Streptolysins O and S are produced by groups A, C and G.

Streptolysin O

  • It is so called because it is oxygen labile. It is an antigenic protein and is active in the reduced form.
  • On blood agar, its activity is seen only in pour plates and not in surface cultures. It is also heat labile.
  • It is lethal on I/V inj. into animals and has a specific cardiotoxic activity. It is a general cytotoxin.
  • Red cells of all animal species except mouse are lysed. Streptolysin O is antigenic and antistreptolysin regularly appears in sera following Streptococcal infection.
  • Estimation of this antibody (ASO) titre is a standard serological procedure for the retrospective diagnosis of infection with S.pyogenes.

Streptolysin S

  • It is an oxygen stable haemolysin and so is responsible for the beta haemolysis seen around streptococcal colonies on the surface of blood agar plates.
  • It is called Streptolysin S since it is soluble in serum. Addition of serum to broth increased the yield of haemolysin.
  • It is protein but not antigenic. It has been shown experimentally to be nephrotoxic. Erythrogenic toxin (Streptococcal pyogenic exotoxins/ Dick toxin)
  • Four erythrogenic toxins are known and most strains of S. pyogenes produce one or more. They are pyogenic and enhance susceptibility to lethal shock by endotoxin.
  • The toxin is thermostable and antigenic. The intradermal injection in rats leads to development of erythema.
  • This reaction is called as “Dick test” or Schultz-charlton reaction and it is useful for diagnosis of scarlet fever.

Enzymes

  • Streptokinase (Fibrinolysin): Filtrates of streptococci gp, A, E & G produces fibrinolysin. This toxin promotes the lysis of fibrin clots by activating a plasminogen.
  • Fibrinolysin plays a biological role in streptococcal infections by breaking down the fibrin barrier around the lesions and facilitating the spread of infection.
  • Deoxyribonucleases (Streptodornase): These cause depolymerisation of DNA, pyogenic exudates contains large amount of DNA, derived from the nuclei of necrotic cells.
  • Streptodornase helps to liquefy the thick pus and may be responsible for the thin serous character of streptococcal exudates.
  • Four antigenically distinct streptodornase, A, B, C & D have been recognized.
  • Hyaluronidase: This enzyme breaks down the hyaluronic acid of the tissues. This might favour the spread of infection along intercellular spaces.
  • Streptococci possess a hyaluronic acid capsule and also elaborate a hyaluronidase- a seemingly self-destructive process. This is produced by group A, C, G and B Streptococci.
  • Proteinase: This is another instance of an apparently self-destructive enzyme, since it is capable of breaking down the M protein, streptokinase and hyaluroindase.
  • The enzyme is, however, produced only under special conditions such as an acidic pH (5.5 –6.5). Such conditions may be produced by tissue destruction, as in abscesses.
  • Most strains of S. pyogenes form proteinase.
  • Neuraminidase: This activity is detected in streptococci groups A, B, C, G and L. This enzyme is a virulence factor for pathogens surviving on mucosal surface.
    In addition to this M types of S.pyogenes produce NADase and other many strains also produce esterase, amylase and N-acetyl glucosaminidase.

Serum opacity factor

  • When group A. streptococci is grown in horse serum it produces an opalescence of the serum. This opacity factor is a protein.
  • This is a lipoproteinase and opalescence is a result of an agglomeration of the bacterial antigen.
Last modified: Monday, 4 June 2012, 4:11 AM