The Potential Role of Persister Cells in Urinary Tract Infections.

PURPOSE OF REVIEW: This review explores the role of persister cells in urinary tract infections (UTIs). UTIs are one of the most common bacterial infections, affecting millions of people worldwide. Persister cells are a subpopulation of bacteria with dormant metabolic activity which allows survival in the presence of antibiotics. RECENT FINDINGS: This review summarizes recent research on the pathogenesis of persister cell formation in UTIs, the impact of persister cells on the effectiveness of antibiotics, the challenges they pose for treatment, and the need for new strategies to target these cells. Furthermore, this review examines the current state of research on the identification and characterization of persister cells in UTIs, as well as the future directions for investigations in this field. This review highlights the importance of understanding the role of persister cells in UTIs and the potential impact of targeting these cells in the development of new treatments.

Pathophysiologic Insights into the Transition from Asymptomatic Bacteriuria to Urinary Tract Infection.

PURPOSE OF REVIEW: Asymptomatic bacteriuria (ASB) can be found in the general population but it is more common in catheterized patients. Some patients develop urinary tract infections (UTI) and others stay asymptomatic throughout time. The scientific community lacks a pathophysiologic explanation of why asymptomatic bacteriuria stays asymptomatic most of the time, and why and how it sometimes transitions to UTI. In an attempt to bridge this gap in knowledge, a summary of the current literature is conducted on the pathophysiologic differences between ASB and UTI, beyond their clinical differences. RECENT FINDINGS: ASB and UTI cannot be differentiated just by their phylogroup or number of virulence factors. The difference may be in their metabolism gene expression. The literature lacks a pathophysiological explanation of the transition from ASB to UTI, and recent discoveries suggest that metabolic gene expression may hold the key.