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Bacteria of preoperative urinary tract infections contaminate the surgical fields and develop surgical site infections in urological operations.

BACKGROUND: The risk factors for surgical site infection (SSI) following urological operations have not been clearly identified, although the presence of a preoperative urinary tract infection (UTI) is thought to be one risk factor. We studied potential risk factors to clarify when and how bacteria contaminate wounds and SSI develop. METHODS: Objects of the present study were patients with SSI after open urological operations that were performed at the Department of Urology, Miyazaki Medical College Hospital, University of Miyazaki, Kiyotake, Miyazaki, Japan, during the period between June 1999 and December 2000. Endourological operations, operations on children and short operations of less than 2 h duration were excluded. Patients were screened for the presence of UTI before the operation and subcutaneous swabs for culture were collected at the end of the operation by brushing with a sterile cotton-swab just before skin closure. RESULTS: Surgical site infections occurred in 20 of 134 patients. Bacteria from the subcutaneous swabs were detected in 15 (75.0%) of the patients with SSI. All patients received antimicrobial prophylaxis (AMP), but bacteria from the subcutaneous swabs of patients with SSI were less susceptible to the agents (20.0%). Preoperative UTI were observed in 11 (55.0%) of the patients with SSI. In these patients, four had the same species of bacteria detected from urine, swab and wound, three had the same species from swab and wound and one had the same species from urine and wound. CONCLUSIONS: Preoperative UTI was the most important risk factor for SSI following urological operations. It is most likely that the bacteria in the urine contaminated the surgical fields and the AMP resistant strains produced SSI.

Adult↗

Clinical significance of the antibody-coated bacteria test in patients with candiduria.

The clinical significance of the antibody-coated bacteria (ACB) test was evaluated with urine from 20 patients with candiduria. The relationship between the in vitro antibody-coating test for Candida albicans, urinary immunoglobulin (Ig) levels and serum antibody titres was evaluated in 40 patients without candiduria, 23 of whom had bacterial urinary tract infection (UTI). Urine specimens from 19 of the 20 patients with candiduria gave a positive result regardless of clinical symptoms; 12/23 specimens of urine from patients with bacterial UTI were positive for antibody-coated C. albicans cells, but there were no positive samples in the patients without UTI. All of the coating-positive patients had serum antibody titres greater than or equal to 1:160, the class of antibody being dependent on the urinary Ig levels. The ACB test for candiduria is of little clinical value in indicating invasive Candida UTI as the Candida cells appear to adhere to antibodies in urine contaminated with circulating fluids.

Aged↗

Bilharzial vesicoureteric reflux and bladder neck stenosis: fact or fiction?

A group of 47 patients with histologically confirmed chronic urinary bilharziasis underwent micturating cystourethrography to look for vesicoureteric reflux (VUR) and bladder neck stenosis (BNS); 13 patients were found to have VUR of varying grades (8 unilateral and 5 bilateral). None had evidence of BNS. Urinary tract infection (UTI), loin pain, hydroureter and renal failure were compared in patients with and without VUR. Of the 13 patients with reflux, 3 had UTI, loin pain was present in 8, 11 had an ipsilateral hydroureter and 2 presented with renal failure. In the 34 patients without reflux, 8 had UTI, loin pain was present in 22, 30 had hydroureter and 3 presented with renal failure. It was concluded that the incidence of UTI, loin pain, hydroureter and renal deterioration associated with bilharzial VUR was not significantly different from that found in bilharzial patients without VUR. Thus the clinical significance and the need for surgical correction of isolated VUR in bilharziasis are questionable.

Acute Kidney Injury↗

Bacterial factors in the formation of renal scars. An experimental study on the role of Escherichia coli P-fimbriation and hydrophobicity.

A model capable of comparing the effects of bacterial virulence factors on renal scarring in vivo has been developed using the female piglet. By creating, at open surgery, unilateral vesicoureteric reflux (VUR) and quantifying scarring both by uptake of an isotope bound to functioning renal parenchyma and by planimetry of the surface area scarred, the effects of 2 organisms, a P-fimbriate Escherichia coli and an E. coli K1 have been compared. The P-fimbriate E. coli was shown to express P-fimbriae in freshly voided urine, was more hydrophobic and produced smaller scars. This indicates that neither the hydrophobicity nor P-fimbriation of the organism causing urinary tract infection (UTI) is of prime importance for the development of renal scars and is evidence against the "big bang" theory for the development of renal scars. Studies on the association of UTI with VUR showed that infection with both E. coli under study led to VUR on the side contralateral to the side undergoing surgery. It seems likely that a non-specific effect of UTI, such as bladder oedema, is responsible for this acquired VUR. An effect of the 2 bacteria under study on the lower urinary tract was observed in that infection with the P-fimbriate E. coli allowed the retention of an intravesical wax plug, whereas infection with E. coli K1 did not. Epidemiological data have shown that the majority of upper urinary tract infections in children are associated with UTI by P-fimbriate organisms. Such an association may be explained in part by an effect of P-fimbriate bacteria on lower urinary tract function rather than an effect on the upper urinary tract.

Animals↗

Split renal function does not change after successful treatment in children with primary vesico-ureteric reflux.

OBJECTIVE: To evaluate the renal growth pattern in patients with primary vesico-ureteric reflux (VUR) using long-term measurements of split renal function with 99mTc-dimercaptosuccinic acid (DMSA) scintigraphy. PATIENTS AND METHODS: In all, 712 children aged < 16 years (466 boys and 246 girls) with primary VUR were referred to our hospital from July 1991 to December 2000. VUR was diagnosed by voiding cysto-urethrography. The patients were treated either surgically (group 1) or conservatively (group 2) and followed with serial 99mTc-DMSA scintigraphy for up to 10 years. There were 942 examinations in 367 of 712 patients who had repeat scintigraphy. Patients with secondary VUR, VUR to a solitary or fused kidney, or upper urinary tract obstruction, were excluded. Five of 298 patients (1.7%) who had ureteric reimplantation had a febrile urinary tract infection (UTI) soon after surgery but none recurred (recurrence is an indication for surgery in children with VUR); there was no febrile UTI in the 69 patients in group 2. Planar scintigraphy with 99mTc-DMSA was used to assess the absolute uptake (AU) of each kidney, measured as a percentage of the injected dose, and the relative uptake (RU = AU of each kidney/AU of both kidneys) calculated. The initial examination was at least 4 weeks after any febrile UTI in most patients. Serial studies were conducted 1 year after surgery and then biannually in group 1. In group 2 the DMSA scan was repeated every 2-3 years. The change in split renal function was compared with the RU of the right kidney. RESULTS: The RU of the right kidney at the initial scan correlated closely with those on repeated scans in both groups. The correlation coefficients were 0.99 in group 1 and 0.94-0.97 in group 2 at every study. The change of RU remained within 0.05 in all patients after treatment. CONCLUSIONS: Under strict control of UTI, split renal function in children with primary VUR does not change. There may be no possibility of accelerated or compensatory growth of the kidney with reflux nephropathy, but no concern about deterioration and atrophy either.

Adolescent↗

Nosocomial urinary-tract infections in a skilled nursing facility.

Fifty-five documented infections reported from an admission unit of a large skilled nursing facility (SNF) during a five-month period were analyzed. Of these, 45 (82 percent) were urinary-tract infections (UTIs), chiefly asymptomatic bacteriuria. Sixty-three percent of the UTIs were acquired in the SNF, and the remainder were acquired during the preceding stay in a general hospital. Statistically, Proteus species infections were more common among the SNF-acquired UTIs, whereas Pseudomonas aeruginosa infections were the most common among the hospital-acquired UTIs. The following recommendations are made: 1) for previously hospitalized elderly patients in whom urinary-tract sepsis develops soon after admission to an SNF, treatment should start with an antibiotic active against Pseudomonas aeruginosa while the results of cultures are pending; 2) symptomatic lower urinary-tract infections caused by SNF-acquired Proteus species should be treated with nalidixic acid or trimethoprimsulfamethoxazole; 3) the term "nosocomial infection" should be broadened to include infections acquired in long-term care institutions; and 4) infection surveillance should be started in selected long-term care institutions for the elderly as part of an expanded National Nosocomial Infections Survey.

Aged↗

Antibiotic resistance patterns of uropathogens in pediatric emergency department patients.

OBJECTIVES: To evaluate the prevalence of resistance of the various urinary tract infection (UTI) pathogens obtained from patients in an urban pediatric emergency department (PED), and to identify risk factors for infection with resistant strains. METHODS: The data were collected retrospectively in an urban, academic PED in northeastern Florida. The microbiology-computerized database was used to identify all positive urine cultures from October 1999 through June 2000. All patients aged 17 years or less, whose urine specimen was collected in the ED and grew cultures with greater than 10,000 colony forming units (CFU) per milliliter of a single organism on Maconkey or blood agar, were included. The medical records of the patients were reviewed and selective demographic and clinical data were collected. Patients were excluded if their charts were unavailable for review or if the pathogen that grew in culture was a suspected contaminant. All patients lacking clinical symptoms of UTI (frequency, dysuria, abdominal pain, fever, or urgency) and whose urine was collected by clean-catch were excluded if their culture grew between 10,000 and 100,000 CFU. Resistance to trimethoprim-sulfamethoxazole (T-S) was estimated for the subset of gram-negative pathogens. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated to compare rates of resistance among patients with and without the following risk factors: age greater than 4 years; current or recent antibiotic use; day care attendance; and previous UTI. RESULTS: A total of 126 urine cultures were identified for inclusion. Of these, 45 patients were excluded, leaving 81 who met the study criteria. The majority of isolated organisms were Escherichia coli, accounting for 89% of the patients (n = 72). Other organisms identified were Klebsiella 3.7%, Proteus 1.2%, Citrobacter 1.2%, Staphylococcus 1.2%, and Enterococcus 3.7% (all in children < 4 years old). The resistance to T-S was 6.5% (95% CI = 0.9% to 12.1%) for gram-negative pathogens. Overall, 48% of gram-negative isolates were resistant to one or more antibiotics, any resistance (95% CI = 36.5% to 59.5%). T-S resistance was nominally higher for older children and for those with a history of antibiotic use, although not to a significant degree. Children less than age 4 were more likely to have any resistance (OR 2.6; 95% CI = 1.0 to 6.7). CONCLUSIONS: The resistance to T-S in this study was 6.7% for gram-negative pathogens. These rates are lower than rates reported in adult populations, international pediatric studies, and the authors' hospital antibiograms, demonstrating the importance of local, population-specific data in selecting antibiotics. This study did not identify any statistically significant risk factors for resistance to T-S, but suggests that those with a recent history of antibiotic use may be at highest risk. While children less than 4 years old with gram-negative pathogens have nominally lower rates of T-S resistance, they are at higher risk for resistance to one or more antibiotics (any resistance) and are at risk for UTI caused by enterococcus (uniformly nonsusceptible to T-S). Prospective studies are needed to validate these results and to identify predisposing factors for urinary pathogens with antibiotic resistance.

Anti-Infective Agents, Urinary↗

The role of cytotoxic necrotizing factor-1 in colonization and tissue injury in a murine model of urinary tract infection.

Cytotoxic necrotizing factor-1 (CNF1) is commonly found in Escherichia coli isolates from patients with urinary tract infection (UTI). To determine whether CNF1 is an important UTI virulence factor we compared the ability of a clinical E. coli UTI isolate and a CNF1-negative mutant of that isolate to colonize and induce histological changes in the urinary tract in a murine model of ascending UTI. We found no evidence that the mutant strain was attenuated.

Animals↗

New aspects of the role of MR/P fimbriae in Proteus mirabilis urinary tract infection.

Proteus mirabilis, a common cause of urinary tract infection (UTI), produces a number of different fimbriae including mannose-resistant Proteus-like fimbriae (MR/P). The precise role of different P. mirabilis fimbriae in ascending UTI has not yet been elucidated. In this study, a clinical isolate of P. mirabilis and an isogenic mutant unable to express MR/P were tested using different experimental approaches. They were tested for their ability to cause infection in an ascending co-infection model of UTI and in a haematogenous model in the mouse. In both models, the mutant was less able than the wild-type strain to colonise the lower and upper urinary tracts although infectivity was not abolished. In vitro adherence to uroepithelial cells was also assessed. Significant differences in adherence between both strains were observed at 1 h but not at 15 min post infection. We have also shown that a wild-type strain carries two copies of the mrpA gene. These data reinforce the importance of MR/P fimbriae in P. mirabilis UTI although other virulence factors may be necessary for efficient colonisation and development of infection.

Animals↗

Influence of P blood group phenotype on susceptibility to urinary tract infection.

Bacterial attachment is an important event in the pathogenesis of urinary tract infection (UTI). Increased receptivity on the host cells has been suggested influence proneness to infection. The dual function of the globoseries of glycolipids both as receptors for attaching E. coli and as P blood group antigens lead us to examine the P blood group phenotype distribution in UTI prone patient populations. A correlation between the P1 blood group phenotype and susceptibility to UTI was found. Patients with recurrent pyelonephritis had 74/79 (94%), P1 compared to 75% in healthy controls. In contrast patients with asymptomatic bacteriuria (ABU) had a reduced frequency of P1, 43/74 (58%). P1 and P2 individuals differ in amount and composition of the globoseries of glycolipids on their erythrocytes. A similar difference in other tissues, e.g. uroepithelial cells might explain the association of P1 with UTI. There was, however, no significant difference in bacterial adherence to uroepithelial cells from P1 and P2 individuals. Other mechanisms explaining the increase in P1 individuals in recurrent pyelonephritis are discussed.

Adult↗

Bacterial adherence as a virulence factor in urinary tract infection.

Escherichia coli (E. coli) causes greater than 90% of urinary tract infections, UTI, in childhood. The capacity to adhere to urinary tract epithelial cells characterizes E. coli strains that cause acute pyelonephritis. Adherence of uropathogenic E. coli is the result of a specific interaction between bacterial adhesins and glycolipid receptors on the host cells, especially the globoseries of glycolipids which share the Galactose alpha 1-greater than 4Galactose beta disaccharide (Gal alpha 1-greater than 4Gal beta). In childhood UTI, Gal alpha 1-greater than 4Gal beta-binding bacteria caused significantly higher body temperature, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and pyuria, and lower renal concentrating capacity, than E. coli lacking this specificity. The Gal alpha 1-greater than 4Gal beta-binding bacteria thus appeared to be more potent inducers of inflammation than other strains. Since inflammation may lead to tissue damage we examined the relationship of infection with Gal alpha 1-greater than 4Gal beta-positive bacteria to renal scarring. The frequency of renal scarring was 5% in boys with Gal alpha 1-greater than 4Gal beta-positive and 40% in boys with Gal alpha 1-greater than 4Gal beta-negative E. coli. Bacterial binding to Gal alpha 1-greater than 4Gal beta can be detected with a commercially available test reagent. This reagent can thus be used as an effective predictor of risk for renal scarring. Interleukin-6 (IL-6) is a pyrogen and inducer of the acute phase reactants. It was shown to be produced locally in the urinary tract, in response to UTI, and to spread systemically. Mucosal challenge with dead bacteria was sufficient to induce the IL-6 response. Circulating IL-6, and/or IL-1 and tumor necrosis factor could explain the fever, as well as increased ESR and CRP found in association with acute symptomatic UTI.

Bacterial Adhesion↗

Effects of sulfamethizole and amdinocillin against Escherichia coli strains (with various susceptibilities) in an ascending urinary tract infection mouse model.

Resistance to antibiotics used for the treatment of urinary tract infections (UTIs) is increasing worldwide. The impact of in vitro resistance on clinical outcome in UTIs requires further study, since most studies of both humans and animals have evaluated only the efficacy of antibiotics toward bacteria susceptible in vitro. We were interested in evaluating the relationship between the in vitro antibacterial effect and the in vivo efficacy after antibiotic treatment. We simulated a natural ascending UTI by use of the ascending UTI mouse model and used Escherichia coli strains with various susceptibilities to amdinocillin (mecillinam) and sulfamethizole. Mice were treated for 3 days with antibiotic doses approximating human urinary tract concentrations after a standard oral dose. For a susceptible strain (MIC, 0.5 micro g/ml) and a resistant strain (MIC, 128 micro g/ml), respectively, there were significant reductions in bacterial counts in the urine, bladder, and kidneys after treatment with amdinocillin, whereas for a strain for which the MIC was 16 micro g/ml, there was a significant reduction in bacterial counts in the kidneys only (P < 0.05). Treatment with sulfamethizole resulted in a significant reduction in bacterial counts in all samples from a susceptible strain (MIC, 128 micro g/ml) and a resistant strain (MIC, 512 micro g/ml). Infection with a sulII gene-positive strain (MIC, >2,048 micro g/ml) could not be treated with sulfamethizole, as no effect could be demonstrated in the urine, bladder, or kidneys. For amdinocillin, there was no clear-cut relationship between the in vitro susceptibility and the in vivo outcome, while for sulfamethizole, we found a relationship between the MIC for the strain and the effect in the urinary tract.

Amdinocillin↗

Iha from an Escherichia coli urinary tract infection outbreak clonal group A strain is expressed in vivo in the mouse urinary tract and functions as a catecholate siderophore receptor.

Virulence factors of pathogenic Escherichia coli belonging to a recently emerged and disseminated clonal group associated with urinary tract infection (UTI), provisionally designated clonal group A (CGA), have not been experimentally investigated. We used a mouse model of ascending UTI with CGA member strain UCB34 in order to identify genes of CGA that contribute to UTI. iha was identified to be expressed by strain UCB34 in the mouse kidney using selective capture of transcribed sequences. iha from strain UCB34 demonstrated a siderophore receptor phenotype when cloned in a catecholate siderophore receptor-negative E. coli K-12 strain, as shown by growth promotion experiments and uptake of (55)Fe complexed to enterobactin or its linear 2, 3-dihydroxybenzoylserine (DHBS) siderophore derivatives. Siderophore-mediated growth promotion by Iha was TonB dependent. Growth and iron uptake were more marked with linear DHBS derivatives than with purified enterobactin. The reported phenotype of adherence to epithelial cells conferred by expressing iha from a multicopy cloning vector in a poorly adherent E. coli K-12 host strain was confirmed to be specific to iha, in comparison with other siderophore receptor genes. iha expression was regulated by the ferric uptake regulator Fur and by iron availability, as shown by real-time reverse transcriptase PCR. In a competitive infection experiment using the mouse UTI model, wild-type strain UCB34 significantly outcompeted an isogenic iha null mutant. Iha thus represents a Fur-regulated catecholate siderophore receptor that, uniquely, exhibits an adherence-enhancing phenotype and is the first described urovirulence factor identified in a CGA strain.

Adult↗

Role of cervicovaginal antibody in the pathogenesis of recurrent urinary tract infection in women.

Introital colonization with Enterobacteriaceae is considered to be one of the principal predisposing factors to recurrent urinary tract infections (UTI) in adult females. One proposed mechanism allowing introital colonization in these patients is the absence of local cervicovaginal antibody. To test this hypothesis, we examined cervicovaginal washings from 22 patients with a history of recurrent UTI and 29 normal controls with no history of UTI for specific local antibody by using indirect immunofluorescence. No significant difference in antibody was found in these populations. Fourteen percent (3/22) of the patients had antibody to their introital Escherichia coli and 34% (10/29) of the controls had antibody to their fecal E. coli. Consequently, a sensitive radioimmunoassay technique was developed to detect cervicovaginal antibody. A solid phase was prepared by coupling to Sepharose 4B a pool of eight serogroups of E. coli which are frequently implicated in UTI. Serial dilutions of cervicovaginal washings were reacted with the solid phase, and the absorbed anti-E. coli antibodies were detected by the uptake of (125)I-labeled anti-human immunoglobulin G (IgG) or anti-human IgA. The antibody levels were quantitated by interpolation on a standard curve prepared by using immunospecifically purified human anti-E. coli antibodies. IgG and IgA levels were measured in washings from 10 colonized patients, 13 non-colonized patients, and 12 controls. There were no significant differences in IgG and IgA levels in cervicovaginal washings among the three groups. In these studies, introital colonization was not related to cervicovaginal antibody.

Antibodies, Bacterial↗

Isolation and comparison of Escherichia coli strains from canine and human patients with urinary tract infections.

We analyzed Escherichia coli strains isolated from dogs with urinary tract infections (UTIs) in an attempt to determine if any of these strains were similar to E. coli isolated from humans with UTIs. Using genotypic and phenotypic traits, we identified four canine and six human E. coli UTI isolates that all appeared to be closely related or identical. All isolates shared similar DNA sequences for pyelonephritis-associated pili (pap), alpha-hemolysin (hly), and insertion sequence 5 (IS5), on the basis of Southern blot analysis. Similar outer membrane protein, pilin, and plasmid profiles were obtained for each of the isolates, although minor heterogeneity was observed. All of these isolates expressed a neuraminidase-sensitive binding phenotype in contrast to the majority of human isolates, which are known to express an adhesin that recognizes terminal digalactoside residues. Taken together, these results suggest that similar E. coli uropathogens may be capable of infecting both dogs and humans. To determine if the intestinal tracts of dogs were a reservoir for uropathogenic E. coli, eight paired rectal and urine pap+ E. coli strains were cultured from dogs with UTIs. By using the same genotypic and phenotypic criteria described above as a basis for strain identity, seven of eight urine-rectal pairs showed intrapair identity. However, each urine-rectal pair displayed a unique overall profile and could be distinguished from the other pairs. We conclude that the uropathogen colonizing the bladders of dog can also be the predominant strain colonizing the intestinal tracts.

Animals↗

Treatment of mice with staphylococcal enterotoxin B enhances resolution of an induced Escherichia coli urinary tract infection and stimulates production of proinflammatory cytokines.

Staphylococcal enterotoxin B (SEB) is a superantigen that causes mass proliferation of murine Vbeta8+ T cells via major histocompatibility complex (MHC) class II molecules and leads to their apoptosis or anergy. SEB also stimulates other MHC class II-bearing cells to proliferate and secrete cytokines, some of which might enhance early host defenses against urinary tract infections (UTIs). We investigated the effect of SEB administration on the course of an induced Escherichia coli UTI in mice. Treatment with SEB 3 or 7 days before the infection had no effect on UTI resolution. However, when SEB was administered at the time of infection, bacterial colonization in the bladders was reduced at time points between 6 h and 3 days. This reduction was not due to a physiological effect, such as increased urinary glycosaminoglycans, or altered pH, nor was SEB bactericidal for the inoculum. Cytokine production in the spleens and bladders of SEB-treated and/or infected mice was evaluated by reverse transcription-PCR. SEB treatment resulted in increased levels of interleukin-2 (IL-2), IL-4, IL-6, and IL-10 mRNAs in the spleen and IL-1alpha, IL-6, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha transcripts in the bladder. Also, liver cells from SEB-treated mice expressed IL-6 mRNA, which induces the production of acute-phase proteins. These data indicate that SEB treatment in vivo leads to enhanced UTI resolution through a mechanism that may include direct stimulation of effector cells in the bladder, the action of cytokines induced in the spleen, or cytokine-mediated induction of acute-phase proteins.

Animals↗

Biofilm formation in a hydrodynamic environment by novel fimh variants and ramifications for virulence.

Type 1 fimbriae are surface-located adhesion organelles of Escherichia coli that are directly associated with virulence of the urinary tract. They mediate D-mannose-sensitive binding to different host surfaces by way of the minor fimbrial component FimH. Naturally occurring variants of FimH that bind strongly to terminally exposed monomannose residues have been associated with a pathogenicity-adaptive phenotype that enhances E. coli colonization of extraintestinal locations such as the urinary tract. The FimH adhesin also promotes biofilm formation in a mannose-inhibitable manner on abiotic surfaces under static growth conditions. In this study, we used random mutagenesis combined with a novel selection-enrichment technique to specifically identify mutations in the FimH adhesin that confer on E. coli the ability to form biofilms under hydrodynamic flow (HDF) conditions. We identified three FimH variants from our mutant library that could mediate an HDF biofilm formation phenotype to various degrees. This phenotype was induced by the cumulative effect of multiple changes throughout the receptor-binding region of the protein. Two of the HDF biofilm-forming FimH variants were insensitive to mannose inhibition and represent novel phenotypes not previously identified in naturally occurring isolates. Characterization of our enriched clones revealed some similarities to amino acid alterations that occur in urinary tract infection (UTI) strains. Subsequent screening of a selection of UTI FimH variants demonstrated that they too could promote biofilm formation on abiotic surfaces under HDF conditions. Interestingly, the same correlation was not observed for commensal FimH variants. FimH is a multifaceted protein prone to rapid microevolution. In addition to its previously documented roles in adherence and invasion, we have now demonstrated its function in biofilm formation on abiotic surfaces subjected to HDF conditions. The study indicates that UTI FimH variants possess adaptations that enhance biofilm formation and suggests a novel role for FimH in UTIs associated with medical implants such as catheters.

Adhesins, Bacterial↗

Effect of trimethoprim-sulfamethoxazole on recurrent bacteriuria and bacterial persistence in mice infected with uropathogenic Escherichia coli.

One of the more perplexing aspects of urinary tract infections (UTIs) is their high propensity to recur. It has been proposed that recurrent infections are a result of the reintroduction of bacteria from the gastrointestinal tract (GIT) to the urinary tract (UT); however, since a significant subset of recurrent UTIs are caused by an identical bacterial strain, it has been challenging to formally prove this hypothesis for same-strain recurrences by using epidemiologic approaches. We present data here obtained by using a mouse model of UTIs in which it was shown that 36% (5 of 14) of mice infected with uropathogenic Escherichia coli (UPEC) will have at least one bacteriuric recurrence, with 21% (3 of 14) having more than one recurrence during a 6-week period after an acute UTI. Intraurethrally infected mice develop UPEC reservoirs in both their feces and their bladders. Ten days of trimethoprim-sulfamethoxazole (SXT) therapy reduces urinary recurrences and eradicates fecal colonization, whereas 3 days of SXT treatment has no effect over a twenty-eight-day observation period despite clearing fecal colonization acutely. Interestingly, SXT is unable to eradicate bacteria from the bladder reservoir even after a 10-day treatment regimen, thus demonstrating that the bladder reservoir can persist even in the face of long-term antibiotic therapy.

Animals↗