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]

Overview

“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.

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, deep fascia, subcutaneous fat, nerves, arteries, and veins.
• Superficial skin and deeper muscles are typically spared.
• In late stages, lesions develop liquefaction necrosis at all tissue levels.

Pathogenesis

The pathogenesis of necrotizing fasciitis is the result of bacterial and host 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).
• Synergistic NF is comparatively slow process evolving over days.
• It usually develops in the area where gut flora breaches the mucosa, entering the tissue planes.

Type 2 NF

• Group A streptococcus is the most common causative agent of type 2 NF.
• Type 2 NF is initially insidious but progress more rapidly.
• The disease may appear spontaneously with no obvious focus. Hematogenous infection from many foci such as ascending vaginitis, primary peritonitis reaches the fascial layer or seeds vimentin exposed by muscle damage.
• irect inoculation of GAS through wounds or associated surgery is less common.
• The pathogenesis of type 2 NF is the result of the following process:

• Inhibition of phagocytosis of bacteria by hyaluronic acid capsule and M protein
• Adherence of bacteria to host cell through adherence factors such as M protein, protein F and lipoteichoic acid
• Release of exotoxins (streptococcal pyogenic exotoxins and superantigens) into blood cascading release of cytokines
• Activation of inflammatory process which begins to kill bacteria along with injury to the surrounding healthy cells
• The inflamed cells release more cytokines that stimulate more inflammatory cells

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  Virulence Factors of Group A Streptococcus

• 

  Inhibition of phagocytosis

• 

  Adherance to host cell and release of exotoxins

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  Activation of host immune response

Gross pathology

On gross pathology the characteristic findings of necrotizing fasciitis include:

• Subcutaneous emphysema
• Edema
• Erythema
• Bulae
• Skin sloughing
• Dull grey discoloration

• 

  Beginning of necrotizing fasciitis

• 

  Necrotizing fasciitis of left leg

Microscopic histopathological analysis

On microscopic histopathological analysis, the characteristic findings of necrotizing fasciitis are

• Early stages

• Obliterative vasculitis with microangiopathic thrombosis
• Acute inflammation of subcutaneous tissue
• Superficial hyaline necrosis along with edema and inflammation of the dermis and subcutaneous fat
• Dense neutrophil-predominant inflammatory infiltrate

• Late stages

• Noninflammatory intravascular coagulation and hemorrhage
• Myonecrosis

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