Abstract
The role of uropathogenic Escherichia coli (UPEC) in colonization and infection of female patients with anatomical and functional abnormalities of the urinary system is elusive. In this study, the phenotype, genotype and the phylogeny of UPEC strains isolated from the urine of pediatric female patients with cystitis of normal and abnormal urinary tract were determined. Multiplex PCR results demonstrated that 86% of the strains isolated from female patients with normal urinary tract (NUT), belonged to the phylo-groups B2 and D. Their prevalence decreased to 23% in strains isolated from patients with abnormal urinary tract (AUT). More of the isolates from AUT patients produced a biofilm on polystyrene and polyvinyl chloride (PVC), adhered to epithelial cells, and encoded pap and sfa genes than strains isolated from female patients with NUT. In contrast, a higher number of hemolysin-producing strains with serogroups associated with UPEC were isolated from patients with NUT. In summary, the results suggest that cystitis in female patients with NUT is associated with ExPEC, whereas cystitis in female patients with AUT is associated with pathogenic intestinal E. coli strains that have acquired the ability to colonize the bladder.
Highlights
IntroductionUrinary tract infection (UTI) is the most common infection in children [1]
After respiratory infection, urinary tract infection (UTI) is the most common infection in children [1]
The type 1 fimbria is associated to the bacterial process of colonization and invasion of the host cells, while P and S fimbriae enhance the establishment of E. coli infection in the urinary tract and significantly lower the number of colony forming-units (CFU) necessary to cause UTI [6]
Summary
Urinary tract infection (UTI) is the most common infection in children [1]. It is considered a benign infection in healthy adults, UTI may raise the risk of pyelonephritis, fetal mortality and renal complications in pediatric patients. Several bacterial species can cause urinary tract infection, the main etiological agents responsible for community-acquired UTI worldwide, and a large portion of nosocomial UTIs, are uropathogenic E. coli [2,3]. The type 1 fimbria is associated to the bacterial process of colonization and invasion of the host cells, while P and S fimbriae enhance the establishment of E. coli infection in the urinary tract and significantly lower the number of colony forming-units (CFU) necessary to cause UTI [6]
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