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Early colonic lesions in experimental Shigella infection in rhesus monkeys: revisited
1Department of Experimental Pathology, Walter Reed Army Institute of Research, Washington, D.C.
Abstract:
Rhesus monkeys (Macaca mulatta), given 3 x 10(8) to 5 x 10(10) Shigella flexneri 2a orally, developed signs of acute shigellosis within 24 hours. A diffuse acute colitis was well established at 48 hours. The inflammatory reaction was confined to the mucosa. The submucosa showed only edema. The shigellae were found predominantly in the columnar cells of the surface epithelium, less frequently in those of the crypt, and least frequently in the lamina propria. Shigella bacilli invaded the columnar cells from the intestinal lumen. The bacilli multiplied within epithelial cells and spread laterally to adjacent epithelial cells and penetrated the lamina propria. The bacterial invasion affected epithelial cells unevenly and resulted in the disappearance of goblet cells and pyknotic shrinkage of the surface epithelial cells. Epithelial cells had abnormal and accelerated exfoliation which resulted in multifocal epithelial defects. There was a distinct correlation between the quantity of bacilli present in tissues and the intensity of the inflammatory response. The small intestines were spared.
Insights
Oral infection with Shigella flexneri 2a in rhesus monkeys caused acute colitis. Bacterial invasion of intestinal epithelial cells led to inflammation and tissue damage, sparing the small intestine.
Area of Science:
- Microbiology
- Pathology
- Gastroenterology
Background:
- Shigellosis is a significant cause of bacterial dysentery.
- Understanding the pathogenesis of Shigella infection is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the pathological changes and bacterial distribution in rhesus monkeys following oral Shigella flexneri 2a infection.
Main Methods:
- Rhesus monkeys were orally administered varying doses of Shigella flexneri 2a.
- Clinical signs, gross pathology, and histopathology of the colon were examined at 24 and 48 hours post-infection.
Main Results:
- Oral Shigella flexneri 2a infection induced acute colitis within 24-48 hours.
- Shigella bacilli primarily invaded and multiplied within colonic epithelial cells, leading to cell damage, goblet cell loss, and epithelial defects.
- Inflammation was concentrated in the mucosa, with edema in the submucosa; the small intestine remained unaffected.
Conclusions:
- Shigella flexneri 2a directly invades and damages colonic epithelial cells, driving the inflammatory response in acute shigellosis.
- The observed pathology correlates with bacterial load, highlighting the direct impact of bacterial invasion on host tissue.