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The pathogenesis of urinary tract infections associated with Escherichia coli, Staphylococcus saprophyticus and S.
L A McTaggart1, R C Rigby, T S Elliott
1Department of Clinical Microbiology, Queen Elizabeth Hospital, Edgbaston, Birmingham.
Abstract:
A model was developed in mice to study the pathogenesis of urinary tract infections caused by Staphylococcus saprophyticus strains LM-1 and LM-2, Escherichia coli SP444 and S. epidermidis E001. Murine urinary bladders were inoculated with 10(8) bacteria via a temporary urinary catheter and samples of urine and bladder were removed at days 1, 3, 5 and 10 after inoculation. They were examined both bacteriologically and by electronmicroscopy. Severe disruption of the urothelium was present immediately and the urothelium had become oedematous and ulcerated with increased urothelial exfoliation. Disruption of the urothelium was similar with all the four pathogens studied. The three strains of coagulase-negative staphylococci preferentially attached to the urothelial cell tight junctions and were not associated with polymorphonuclear leucocytes. In comparison, E. coli SP444 was randomly attached over the entire urothelium and was often in association with macrophages. Phagocytosis of E. coli by superficial urothelial cells also occurred.
Insights
This study reveals how different bacteria cause urinary tract infections in mice. Staphylococcus strains target cell junctions, while E. coli attaches randomly, showing varied pathogenesis.
Area of Science:
- Microbiology
- Pathogenesis Research
- Urology
Background:
- Urinary tract infections (UTIs) are common, with various bacteria implicated.
- Understanding pathogen-host interactions is crucial for developing effective treatments.
- Coagulase-negative staphylococci and Escherichia coli are significant UTI pathogens.
Purpose of the Study:
- To investigate the pathogenesis of UTIs caused by Staphylococcus saprophyticus, Staphylococcus epidermidis, and Escherichia coli in a murine model.
- To compare the adherence patterns and host responses induced by these distinct bacterial uropathogens.
Main Methods:
- Development of a murine model for UTI by inoculating bladders with Staphylococcus saprophyticus, S. epidermidis, and E. coli.
- Bacteriological and electron microscopy analysis of urine and bladder tissues at multiple time points post-inoculation.
- Assessment of urothelial damage, bacterial attachment sites, and host immune cell association.
Main Results:
- All four bacterial strains induced severe urothelial disruption, characterized by edema, ulceration, and exfoliation.
- Coagulase-negative staphylococci preferentially adhered to urothelial tight junctions, with minimal association with polymorphonuclear leukocytes.
- E. coli exhibited random attachment across the urothelium, often interacting with macrophages, and was phagocytosed by superficial urothelial cells.
Conclusions:
- Distinct adherence mechanisms and host interaction patterns exist between coagulase-negative staphylococci and E. coli during UTI pathogenesis.
- The murine model effectively demonstrates differential urothelial responses to various bacterial uropathogens.
- Findings provide insights into the early stages of UTI development and potential therapeutic targets.