Asymptomatic bacteriuria (ASB) is a common finding in many populations, including healthy women and persons with underlying urologic abnormalities. The 2005 guideline from the Infectious Diseases Society of America recommended that ASB should be screened for and treated only in pregnant women or in an individual prior to undergoing invasive urologic procedures. Treatment was not recommended for healthy women; older women or men; or persons with diabetes, indwelling catheters, or spinal cord injury. The guideline did not address children and some adult populations, including patients with neutropenia, solid organ transplants, and nonurologic surgery. In the years since the publication of the guideline, further information relevant to ASB has become available. In addition, antimicrobial treatment of ASB has been recognized as an important contributor to inappropriate antimicrobial use, which promotes emergence of antimicrobial resistance. The current guideline updates the recommendations of the 2005 guideline, includes new recommendations for populations not previously addressed, and, where relevant, addresses the interpretation of nonlocalizing clinical symptoms in populations with a high prevalence of ASB.

Asymptomatic bacteriuria (ASB) is a common finding in many populations, including healthy women and persons with underlying urologic abnormalities. The 2005 guideline from the Infectious Diseases Society of America recommended that ASB should be screened for and treated only in pregnant women or in an individual prior to undergoing invasive urologic procedures. Treatment was not recommended for healthy women; older women or men; or persons with diabetes, indwelling catheters, or spinal cord injury. The guideline did not address children and some adult populations, including patients with neutropenia, solid organ transplants, and nonurologic surgery. In the years since the publication of the guideline, further information relevant to ASB has become available. In addition, antimicrobial treatment of ASB has been recognized as an important contributor to inappropriate antimicrobial use, which promotes emergence of antimicrobial resistance. The current guideline updates the recommendations of the 2005 guideline, includes new recommendations for populations not previously addressed, and, where relevant, addresses the interpretation of nonlocalizing clinical symptoms in populations with a high prevalence of ASB.

No abstract

Mucosal pathogens trigger a local innate host response by activating epithelial cells. Bacterial adherence and Toll-like receptor 4 (TLR4) signaling have been implicated as key events in this process. This study addressed the molecular basis of the epithelial response to gram-negative infection in the human urinary tract. Mucosal biopsies were obtained from kidneys, ureters, and bladders of patients undergoing urinary tract surgery, and epithelial TLR4 and CD14 expression was examined by immunohistochemistry. TLR4 was detected in epithelial cells lining the entire urinary tract and in the renal tubular epithelium. CD14, in contrast, was completely absent from the epithelial tissue. The response of the epithelial cells to infection was studied by in vitro challenge of the biopsies with uropathogenic Escherichia coli bacteria. A rapid cytokine response was observed, with production of interleukin-1␤ (IL-1␤), IL-6, and IL-8 but not of IL-4 or gamma interferon. Adhering, P-or type 1-fimbriated E. coli activated IL-6 and IL-8 production more efficiently than the nonfimbriated control, as shown by cellular staining and analysis of secreted cytokines. The results demonstrate that human uroepithelial cells possess the molecular machinery needed to respond to uropathogenic E. coli. This includes recognition receptors for fimbriae and TLR4 for transmembrane signaling. We speculate that the lack of membrane-bound CD14 allows the epithelium to regulate its sensitivity to lipopolysaccharide and to discriminate between more-virulent and less-virulent strains.Mucosal pathogens use diverse and highly sophisticated mechanisms to gain access to the tissues at their preferred site of infection (6,8,11,35). Adherence is a crucial first step to establish tissue contact and to break the inertia of the mucosal barrier, but in addition, the molecular interactions between bacteria and host alert the host to the danger, and a host response is activated (1,14). In urinary tract cell lines, epithelial cell activation by fimbriated Escherichia coli requires primary recognition receptors for fimbrial adhesins and Toll-like receptor 4 (TLR4) for transmembrane signaling (12). Human urinary tract epithelial cells express both glycosphingolipid and mannosylated surface glycoprotein receptors, which recognize the P fimbrial adhesins (29) and the type1 fimbriae, respectively (30). TLR4 is also expressed in murine urinary tract epithelium, and the tlr4 genotype was found to regulate the in vivo response to experimental urinary tract infection (UTI) caused by P-or type 1-fimbriated E. coli (12,17,36,38).The extent to which TLR4 is expressed by the human urinary tract epithelium remains controversial, however. In addition, there are contradictory reports concerning the lipopolysaccharide (LPS) responsiveness of uroepithelial cells and their expression of CD14. It is well established that cells of myeloid origin express CD14 and MD2 and recruit TLR4 for transmembrane signaling when exposed to LPS (5), but uroepithelial cell lines respond poorly to sol...

Our results indicate that recurrent UTIs have a significant impact on QoL of women in Europe.