Related Experiment Video
Updated: Jun 13, 2026

Establishment and Characterization of UTI and CAUTI in a Mouse Model
Published on: June 23, 2015
[Urinary tract infections and antibiotic resistance]
1Pharmazeutische Biologie und Mikrobiologie, Department Chemie, Universität Hamburg, Bundesstrasse 45, 20146, Hamburg, Deutschland. heisig@chemie.uni-hamburg.de
Abstract:
Urinary tract infections (UTI) usually are monoinfections caused by the endogenous microflora including gram-negatives, such as Escherichia coli, or gram-positives, like enterococci. This allows for an empiric treatment of uncomplicated UTIs and a short duration of therapy to minimize the probability for the development of resistance. Resistance often is based upon mutations altering the drug target (sulfonamides, trimethoprim, fluoroquinolones, fosfomycin) or acquisition of resistance genes (beta-lactams). The latter can be collocated with other resistance genes on mobile genetic elements mediating multiple drug resistance. Such elements are part of the chromosome of the Escherichia coli clonal group A (cgA). The prevalence of resistance to nitrofurantoin and fosfomycin is below 6%, while that of sulfonamide/trimethoprim varies between 15 and 50% all over Europe. Resistance to fluoroquinolones and amoxycillin approximates 15 and over 30%, respectively. A value of >20% for the empiric treatment of uncomplicated UTIs is associated with a significantly increased duration of therapy suggesting alternative antibiotic regimens.
Related Concept Videos
Mechanism of Antibiotic Resistance in MRSA
Urinary Tract Infection III: Diagnostic Studies and Interprofessional Care
Urine Studies II: Urine Culture and Sensitivity Test
Antibiotic Selection
Development of Antibiotic Resistance
Urinary Tract Infection II: Pathophysiology

