Necrotizing fasciitis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

Pathophysiology

The pathophysiology of necrotizing fasciitis is common to all types of NF but the speed of development and associated clinical features differs depending on the causative organisms.

• The transmission of pathogens occurs through the following routes

• External trauma
• Direct spread from a perforated viscus (particularly colon, rectum, or anus)
• Urogenital organ

• Following transmission, the bacteria uses the entry site to invade the fascial planes which causes the wide spread necrosis of superficial fascia, subcutaneous fat, nerves, arteries and veins.

Pathogenesis

The pathogenesis of necrotizing fasciitis is the result of bacterial and host factors.

Bacterial Factors

Type 1 NF

• The exact pathogenesis of type 1 necrotizing fasciitis is not fully understood.
• It is thought that type 1 NF is caused by polymicrobial species that work together to enhance the spread of infection (Synergistic).

Type 2 NF

• Group A streptococcus is the most common causative agent of type 2 NF.
• The pathogenesis of type 2 NF is the result of virulence factors of streptococcus which includes

• Adherence of bacteria to host tissue

• Protein F (fibronectin binding protein)
• Lipoteichoic acid
• M protein that mediate attachment of pathogen to host cells.

• Inhibition of phagocytosis

• Hyaluronic acid capsule
• M protein

• Extracellular exotoxins

• Streptokinase
• Streptolysin O and S
• Streptodornase (DNase B)
• Hyaluronidase
• Streptococcal pyrogenic exotoxins (Spe)

• Superantigen

• These virulence factors are variably used by bacteria throughout each stage of infection (initiation, local replication and dissemination), which requires the highly coordinated regulation of virulence gene expression.

Host factors

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“Flesh-eating bacteria” is a misnomer, as the bacteria do not actually eat the tissue. They cause the destruction of skin and muscle by releasing toxins (virulence factors). These include streptococcal pyogenic exotoxins and other virulence factors. S. pyogenes produces an exotoxin known as a superantigen. This toxin is capable of activating T-cells non-specifically. This causes the over-production of cytokines that over-stimulate macrophages. The macrophages cause the actual tissue damage by releasing oxygen free radicals that are normally intended to destroy bacteria but are capable of damaging nearly any macromolecule they contact in the body.