Although lower urinary tract infections (UTIs) are infrequent in men, in some clinical conditions like prostatitis the demonstration of UTI is paramount in order to correctly classify and threat this disease (1). Urine culture with or without prostate massage is essential to differentiate between bacterial and non-bacterial prostatitis. Urodynamic studies are useful in non-bacterial prostatitis in order to rule out any voiding dysfunction like bladder outlet obstruction or detrusor sphincter dyssynergia that may be present in these diseases. However, infection by Escherichia coli (E. coli) can affect the lower urinary tract function because of the effect of its endotoxin on alpha-adrenergic receptors (2). If this effect can be proved in vivo we cannot rule out that some voiding dysfunctions usually associated to non-bacterial prostatitis may result from bacterial infections. Our hypothesis is that E. coli infection can affect voiding function in male patients. The objective of our study is to compare the urodynamic findings in a sample of men with positive and negative UTI to E. coli bacteria.

Study design 
Cross sectional study

Materials and methods 
We carried out a cross sectional study in men with UTI diagnosed by positive culture urine (>105 colony forming units per millilitre), who underwent a urodynamic study. The sample was divided into two groups: E. coli positive group: formed by 27 men with urinary culture positive for E. coli growth, and E coli negative group formed by 19 men whose urine culture showed the growth of bacteria other than E. Coli. Inclusion criteria were male, 18-year-old or over. Exclusion criteria were neurogenic lower urinary tract dysfunction, antibiotic treatment, anatomical abnormalities of the urinary tract, urolithiasis and genitourinary neoplasms. Patients were asked about the presence of lower urinary tract symptoms (LUTS), and other data like age and presence of indwelling catheters.

Urodynamic studies were performed according ICS specifications and guidelines of Good Urodynamic practices. Urethral resistance was measured by the urethral resistance algorithm (URA) and detrusor contractility by maximum value of Watts Factor (Wmax) and by the difference between the value of Watts Factor at 80% of bladder capacity minus the value of Watts Factor at 20% of bladder capacity (W8020).

Sample size was calculated based on data published by Gobish (2). Assuming that the standard deviation maximum urinary flow rate is 5 ml/s and that the difference between groups is 5 ml/s, with an alpha level of 5%, a statistical power of 80%, the minimum sample size should be 17 patients in each group.

 
For statistical analysis we used the Fisher exact test for qualitative variables and the t-test to compare the means of parametric data, or Mann-Whitney’s U test for nonparametric quantitative data. Quantitative data were tested for normal distribution using the Kolmogorov-Smirnov test. Statistical significance was set at p < 0.05 bilaterally.

The distribution of clinical data for both groups is shown in Table 1. No clinical variable showed significant differences between both groups. The distribution of urodynamic data is shown in table 2. The parameters that showed significant differences were URA (higher in the E. coli negative group), Wmax (higher in the E. coli positive group) and W8020 (higher in the E. coli positive group).

There are several in vitro studies about the effect of E. coli bacteria on lower urinary tract function. However, to our knowledge this is the first urodynamic study that assess this influence on patients. In vitro studies have shown that 
endotoxins liberated from E. coli inhibit alpha-adrenergic receptors in urethral muscle (2). This effect may explain our finding that urethral resistance was lower in patients with E. coli infection that those without it. 

The action of E. coli bacteria in detrusor is more controversial. Some authors state that there is no effect on this muscle (2). While other authors claim that E. coli releases ATP that enhances bladder contractility. This release of ATP has not been shown in other microorganisms like lactobacillus bacteria. Although this mechanism has been proposed to explain the presence of overactive bladder syndrome and detrusor overactivity (DO) in women, so far no clinical study has validated this hypothesis. Our data also did not find any relationship between E. coli infection and the presence of LUTS or DO. However, this mechanism could explain the greater contractility in both contractility parameters (Wmax and W8020) found in our study in patients with E. coli infection.

Providing other non-studied effects are found, the result of E. coli infection in the lower urinary tract is positive because it reduces urethral resistance and improves bladder contractility. Some authors have advocated the deliberate colonization of human urinary tract with avirulent strains of E. in case of recurrent UTI. Although the design of our study does not allow us to stablish a cause-effect relationship, if other studies prove this effect, that procedure would be therapeutically useful.

Male patients with E. coli infection have less urethral resistance and more bladder contractility than male patients infected by other bacteria. The consequences of these findings could be clinically interesting.

Nickel JC. Classification and diagnosis of prostatitis: a gold standard. Andrologia. 2003;35(3):160-7
Nergårdh A, Boréus LO, Holme T. The inhibitory effect of coli-endotoxin on alpha-adrenergic receptor functions in the lower urinary tract. An in vitro study in cats. Scand J Urol Nephrol. 1977;11(3):219-24.
Ghobish A. Voiding dysfunction associated with "chronic bacterial prostatitis".Eur Urol. 2002;42(2):159-62.