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[Current views on the pathomorphology and pathogenesis of dysentery]
Abstract:
According to the literature and the authors' data in patients who died of dysentery Shigellae are found seldom because of postmortem shedding of superficial colonic epithelium infected by them. Shigella adhesion and invasion into the colonocytes are regularly found in the colon biopsies. As shown recently in experiments, Shigella outer membrane proteins forming "contact haemolysin" ("virulence plasmid" product) are responsible for their invasion. In the small intestine this cytotoxin is destroyed by trypsin, therefore Shigella invasion takes place in the large intestine where it also lyses vacuole membranes around the bacteria in colonocytes. Widespread cytopathic alterations of the epithelium with a damage to ribosome and protein synthesis, disturbance of vascular permeability and fluid hypersecretion in the small intestine result from Shiga-like enterotoxin-cytotoxin. Extent of the inflammatory leukocyte response depends on the degree of Shigella invasion and multiplication and the destruction of the epithelium. Damages to the endothelium and blood coagulation system resulting occasionally in the infectious-toxic shock, are associated with Shigella destruction by leukocytes and absorption of lipopolysaccharide endotoxin released by them. Interepithelial lymphocytes especially those containing lysosome-like granules (similar to the blood "natural killers") play an important role in the response to Shigella.
Insights
Shigella bacteria invade the large intestine using outer membrane proteins, causing epithelial damage and fluid secretion. Leukocyte responses and endotoxin absorption can lead to severe complications like toxic shock.
Area of Science:
- Microbiology
- Pathology
- Immunology
Background:
- Shigella bacteria are a common cause of dysentery.
- Postmortem shedding of colonic epithelium complicates Shigella detection in deceased patients.
- Shigella adhesion and invasion into colonocytes are key pathogenic events.
Purpose of the Study:
- To elucidate the mechanisms of Shigella invasion and pathogenesis in the human colon.
- To understand the role of Shigella virulence factors in epithelial damage and host response.
- To investigate the contribution of the host immune system to Shigella infection.
Main Methods:
- Analysis of colon biopsies from patients with dysentery.
- Experimental studies on Shigella outer membrane proteins and their cytotoxic effects.
- Investigation of the host's inflammatory and immune responses to Shigella infection.
Main Results:
- Shigella invasion is mediated by outer membrane proteins forming "contact haemolysin", primarily in the large intestine.
- Shiga-like enterotoxin-cytotoxin causes widespread epithelial damage, disrupts protein synthesis, and induces fluid hypersecretion.
- Leukocyte response, endotoxin absorption, and damage to the endothelium can lead to infectious-toxic shock.
- Interepithelial lymphocytes, including natural killer-like cells, play a significant role in the host response.
Conclusions:
- Shigella employs specific virulence factors for invasion and pathogenesis, leading to significant epithelial damage.
- The host immune response, involving leukocytes and lymphocytes, is crucial in combating Shigella infection but can also contribute to severe pathology.
- Understanding these mechanisms is vital for developing effective treatments for Shigella-induced dysentery.