Virulence factor

A virulence factor is a property of a micro- organism that determines its pathogenic effect. It can be a structural element as well as a metabolite of a microorganism.

Adhesins

Fimbriae adhesins or membrane proteins which allow bacteria to adhere to target cells. Here react the adhesins with the homologous host cell receptors.

Antiphagozytosefaktoren

Antiphagozytosefaktoren prevent phagocytosis. This means that the bacterium is not received and destroyed by phagocytic cells of the immune system. Various components of bacteria may be effective antiphagozytär:

  • Capsule: The bacteria capsule is made of sugar or amino acid compounds. To encapsulated, pathogenic bacteria, for example, pneumococci.
  • M protein of group A streptococci: A streptococci have a surface protein, but which may be inactivated by antibodies.
  • Protein A of Staphylococcus aureus: The Protein A binds the IgG defense, " upside ", namely the Fc end, ensuring that it can not act ( antiopsonierende effect )
  • Leukozidine: Leukozidine are bacterial metabolites, which have a damaging effect on phagocytes ( " phagocytes " ) have. For example, Staphylococcus aureus has Leukozidine.
  • Coagulase: This protein is secreted by, for example, Staphylococcus aureus. Coagulase and prothrombin together Koagulothrombin which converts the bound fibrinogen to fibrin. Fibrin forms a slimy layer of protection to the bacteria.
  • Clumping factor A of Staphylococcus aureus is a surface protein which binds fibrinogen.

Invasion factors

Invasion factors allow pathogens to spread in the tissue. These include, for example:

  • Streptokinase: for example, in group A streptococci. Streptokinase activated plasmin resulting in the fibrinolysis, ie the dissolution of fibrin.
  • Hyaluronidase: hyaluronidase acts on hyaluronic acid of the connective tissue, and is also called " spreading factor". This virulence factor is, for example at A streptococci, pneumococci, staphylococci, and Clostridium perfringens.
  • Scourge: flagella enable the active mobility of the bacteria
  • Protease: resolution of proteins (protein )
  • DNAse: Resolution of DNA
  • Lipase resolution of lipids ( fats)

Endotoxins

Endotoxins are toxins (toxins ) from the outer membrane of gram-negative bacteria. The only known endotoxin, the lipid A, which occurs at the outer membrane of all gram-negative bacteria in the lipopolysaccharide (LPS). Lipid A is released upon death of the bacterium and then exerts its toxic effects:

  • Interleukin 1 is released from macrophages, resulting in a febrile response
  • TNF (tumor necrosis factor α ) is released. This results in a dilation of the vessels ( vasodilation ) which can lead to septic shock.
  • Lipid- A binds to B -cell receptors, resulting in maturation of the B- lymphocytes
  • The complement via the alternative pathway is activated
  • Influencing of the kinin system, blood coagulation

In the course of sepsis (blood poisoning) with gram-negative pathogens may lead to an endotoxin poisoning after antibiotic therapy, as much endotoxin is released by the massive dying of the pathogens. This can lead to shock.

Exotoxins

Exotoxins are toxins that are secreted by living bacteria. Often they are only formed by bacteria that are infected by a bacteriophage. Different modes of action of exotoxins are:

  • Lipase: Lipase Through the membrane of the target cells is enzymatically partially degraded, such as α - toxin of Clostridium perfringens
  • Pore-forming toxins: Through transmembrane pore formation, the membrane is perforated
  • Neurotoxins: These toxins damage the nerves or the transmission of neurotransmitters Tetanus toxin of Clostridium tetani
  • Botulinum toxin of Clostridium botulinum
Pilus Group A streptococcal infection Immunoglobulin G B cell Hemostasis Cholera Diphtheria toxin Transcription (genetics)#Elongation
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