Initial studies on quantitative urine cultures obtained from large numbers of patients have established so-called significant (true) bacteriuria at a threshold of ≥10 colony-forming units per milliliter [1]. Because asymptomatic bacteriuria (ABU) has been found with particular frequency in populations more likely to develop pyelonephritis (ie, individuals with diabetes mellitus, pregnancy, obstructive uropathy, past history of instrumentation of the urinary tract), a strong relationship between bacteriuria and pyelonephritis was assumed. This was consolidated by the observation that in pregnancy elimination of ABU decreases the risk for a symptomatic infection [2]. Although bacteriuria is present in a relatively asymptomatic population, it is virtually always necessary for the development of symptomatic disease. Therefore, it was assumed that the presence of bacteriuria defines a population at risk and the elimination of bacteriuria minimizes the risk for a clinically symptomatic disease [2]. The discrepancy between the frequency of pyelonephritis found in autopsies and that diagnosed during life in only about one-fifth of the cases was explained by a high incidence of clinically atypical or inapparent infections [3]. At that time bacteriuriawas considered dangerous in any case, because bacteriuria detected at a significant quantity, even if asymptomatic, was associated with a substantially increased risk of pyelonephritis and premature delivery. Subsequently well-performed, randomized clinical studies in adult women, schoolgirls, long-term care facility residents, spinal cord–injured patients, and diabetic women, however, have consistently documented that the treatment of bacteriuria in asymptomatic patients does not provide any benefit for the patient [4, 5]. Therefore, the term “asymptomatic urinary tract infection” (UTI) was abandoned and redefined as ABU. The diagnosis of ABU is made independent of the presence of pyuria commonly found in patients with ABU [4]. Nowadays ABU is considered a stable bacterial colonization of the urinary tract, similar to commensalism at other mucosal sites [6]. Apart from clinical trials, ABU has been investigated through molecular methods [6]. ABU Escherichia coli isolates from outpatients or hospitalized patients after catheterization or other urological invasive procedures were compared with commensal E. coli isolates from the intestinal flora of healthy individuals [6]. The ABU isolates had a similar overall virulence gene repertoire, which sets them apart from many commensals. Typical uropathogenic E. coli (UPEC) virulence genes, however, were less frequently observed in hospital ABU strains than in outpatient ABU strains or commensals [6]. The diminished virulence from outpatient ABU isolates compared with that of ABU strains from hospitalized patients shows that loss of expression or decay of virulence genes facilitate longterm carriage and adaptation to host environments [6]. A prototype ABU strain, E. coli 83972, isolated from a schoolgirl with long-lasting ABU with this strain, has been completely sequenced in the meantime [7]. Comparing this ABU strain with UPEC strains, the ABU strain has a smaller genome than the UPEC strains with deletions or point mutations in several virulence genes, suggesting that ABU strains undergo a programmed reductive evolution within human hosts [6, 8]. In asymptomatic patients colonized in the lower urinary tract with this ABU strain, superinfection with other strains seems to be prevented even if left untreated [8–11]. This phenomenon, the socalled bacterial interference, is due to the fact that within our body’s bacterial habitats microbial interaction exists, in competing for nutrients and producing toxic molecules. Thus, a microbial balance is established on colonized surfaces, such as the skin and mucosal orifices. This socalled human microbiome is considered a potent defense mechanism against superinfecting pathogenic bacteria [8]. The idea of bacterial interference was further developed. The ABU E. coli Received 29 May 2012; accepted 31 May 2012; electronically published 7 June 2012. Correspondence: Kurt Naber, Karl-Bickleder-Str. 44c, D-94315 Straubing, Germany (kurt@nabers.de). Clinical Infectious Diseases 2012;55(6):778–80 © The Author 2012. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. permissions@oup.com. DOI: 10.1093/cid/cis541
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Sep 9, 2024
Ciara Kenneally + 3
Open Access
