The ultrastructure of acute pyelonephritis in the monkey
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Updated: Nov 8, 2026

Intrarenal Injection of Escherichia coli in a Rat Model of Pyelonephritis
Published on: July 18, 2017
Abstract:
P-fimbriated E. coli, which have specific receptors on urothelial cells for their fimbriae, were used to produce pyelonephritis. Using both scanning and electron microscopy, it was shown that the bacteria attached to ureteral epithelium by 12 hours after inoculation. They developed into a biolayer of bacteria covering the epithelium by 48 hours, but did not invade within that time. In the kidney, adherence was seen by 6 hours in collecting proximal and distal tubules. While many bacteria were seen, tubular epithelium remained normal through 24 hours. The inflammatory response was first seen at 48 hours. Phagocytosis was accompanied by mortal damage to both phagocytes and surrounding tubules. This was followed by bacterial invasion of the interstitium.
Insights
P-fimbriated E. coli cause pyelonephritis by adhering to urothelial cells. Bacteria form a biofilm, triggering inflammation and damage, leading to interstitial invasion in kidneys and ureters.
Area of Science:
- Urology
- Microbiology
- Pathology
Background:
- P-fimbriated Escherichia coli (E. coli) possess fimbriae that bind to specific receptors on urothelial cells.
- This interaction is a key factor in the development of pyelonephritis, a kidney infection.
Purpose of the Study:
- To investigate the temporal dynamics of P-fimbriated E. coli adherence and tissue response in the ureter and kidney.
- To elucidate the early stages of pyelonephritis development at the cellular and tissue level.
Main Methods:
- Scanning and transmission electron microscopy were employed to visualize bacterial attachment and host cell interactions.
- Inoculation of P-fimbriated E. coli in a model system to induce pyelonephritis.
Main Results:
- Bacteria adhered to ureteral epithelium within 12 hours, forming a biofilm by 48 hours without invasion.
- In the kidney, bacterial adherence to tubules occurred by 6 hours, with normal epithelium for 24 hours.
- Inflammation initiated at 48 hours, leading to phagocyte and tubular damage, followed by interstitial invasion.
Conclusions:
- P-fimbriated E. coli initially colonize urothelial surfaces without immediate invasion.
- The host inflammatory response contributes to tissue damage, facilitating bacterial spread into the interstitium.
- Understanding these early events is crucial for developing targeted therapies against pyelonephritis.
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