Necrotizing fasciitis pathophysiology: Difference between revisions
| Line 42: | Line 42: | ||
“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 [[toxin]]s (virulence factors). These include streptococcal pyogenic exotoxins and [[Streptococcus pyogenes|other virulence factors]]. ''S. pyogenes'' produces an exotoxin known as a [[superantigen]]. This toxin is capable of activating [[T-cell]]s non-specifically. This causes the over-production of [[cytokines]] that over-stimulate [[macrophage]]s. 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. | “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 [[toxin]]s (virulence factors). These include streptococcal pyogenic exotoxins and [[Streptococcus pyogenes|other virulence factors]]. ''S. pyogenes'' produces an exotoxin known as a [[superantigen]]. This toxin is capable of activating [[T-cell]]s non-specifically. This causes the over-production of [[cytokines]] that over-stimulate [[macrophage]]s. 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. | ||
===Gross pathology=== | |||
On gross pathology the characteristic findings of necrotizing fasciitis include:<ref name=necrotizing fasciitis>Librae pathology (2015) https://librepathology.org/wiki/Necrotizing_fasciitis Accessed on September 2,2016</ref> | |||
*Subcutaneous emphysema | |||
*Edema | |||
*Erythema | |||
*Bulae | |||
*Skin sloughing | |||
==References== | ==References== | ||
Revision as of 18:01, 2 September 2016
|
Necrotizing fasciitis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Necrotizing fasciitis pathophysiology On the Web |
|
American Roentgen Ray Society Images of Necrotizing fasciitis pathophysiology |
|
Risk calculators and risk factors for Necrotizing fasciitis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]
Overview
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 the following process:
- Inhibition of phagocytosis of bacteria by hyaluronic acid capsule and M protein
- Adherance of bacteria to host cell through adherence factors such as M protein, protein F and lipoteichoic acid
- Release of exotoxins (streptococcal pyogenic exotoxins and superantigen) into blood cascading release of cytokines
- Activation of inflammatory process which begins to kill bacteria along with injury to surrounding healthy cells
- The inflamed cells release more cytokines that stimulate more inflammatory cells
-
Virulence Factors of Group A Streptococcus
-
Inhibition of phagocytosis
-
Adherance to host cell and release of exotoxins
-
Activation of host immune response
“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.
Gross pathology
On gross pathology the characteristic findings of necrotizing fasciitis include:
- Subcutaneous emphysema
- Edema
- Erythema
- Bulae
- Skin sloughing