Necrotizing inflammation

Necrotizing inflammation is understood to be, on the one hand, a (mostly) bacterial infection of vital tissue, in which bacterial toxins cause necrosis and tissue damage, or, on the other hand - in the case of agranulocytosis of the host, necrosis in which the cellular inflammatory infiltrate is disproportionately low in relation to the tissue damage.

Thus, in necrotizing inflammation, the structural damage (necrosis) is in the foreground of the pathological process.

Necrotizing inflammations are dreaded complications in bone marrow aplasia, e.g. after cytostatic therapy. In the phase of agranulocytosis, areactive inflammations can occur - areactive - because the cellular (granulocytic) reaction is missing. In these cases, infections with otherwise apathogenic or low-virulent germs (bacteria/fungi) may also occur.

In the intestine, neutropenic colitis can develop and thus lead to infection by various bacteria or fungi. Intestinal bacteria up to the endogenous Clostridia infection can occur.

In rare cases, hepatitis A can also lead to a fulminant infection with subtotal organ destruction. Massive, subtotal lymph node destruction is found in the complicated course of an Epstein-Barr virus infection. Pathogenetically, severe courses of acute transplant rejection after organ transplantation also belong to these forms of inflammation.

Clinical forms of necrotizing inflammation:

• Ulcer formation in various tissues (formation of circumscribed necroses on the surfaces of the skin and mucous membranes): e.g. duodenal ulcer, ulcerative colitis, Crohn's disease.
• Abscessing inflammation: necrosis due to tissue fusion caused by granulocytic enzymes at the base of a purulent inflammation (e.g. boils).
• Necrotizing inflammation due to ischemia. E.g. foot and lower leg necrosis, pulmonary gangrene (e.g. in superinfected lung infarction).

The spectrum of causes includes chemical and physical noxae (trauma, pressure, acids, alkalis, burns, radiation damage), pathogens (viruses, bacteria, fungi, parasites), perfusion disorders, enzymes and immune reactions.

In the case of necrotizing inflammation as a result of superinfection by putrefactive agents, the affected tissue decays torpidly (i.e. like decaying wood) and smells badly (damp gangrene).

1. Grundmann (2018) Inflammation patterns. Short textbook pathology p. 156-157 Elsevier Munich
2. Gelding D et al (2016) Programmed necrosis in inflammation: Toward identification of the effector molecules. Science 352:aaf2154.