Abstract

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. 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.

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