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Tufts OpenCourseware
Author: Michael Barza, M.D.
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1. Epidemiology

UTI are far more common in women than in men, probably because of the shorter urethra in the female. Prostatic secretions in the male may have some antibacterial effect.

2. Pathogenesis

Nearly all UTI arise by the "ascending route." Fecal organisms, principally Escherichia coli, colonize the vaginal introitus. Their entry into the bladder is facilitated by sexual intercourse, contraceptive diaphragms, and spermicides. The contraceptive pill has no effect on the incidence of UTI.

Some women are prone to have multiple urinary reinfections. These women may be colonized by strains of E. coli with "stickier" fimbriae (anchoring them to the epithelial cells) or may have "stickier" epithelial cells (a phenomenon related to certain blood groups). In addition, the factors noted earlier may contribute to multiple reinfections. In elderly women, vaginal atrophy leads to a reduction in the counts of lactobacilli in the vagina: thus, the vaginal secretions become less acidic and gram-negative enterics more easily colonize. The most potent risk factors for UTI in women are: sexual intercourse, the use of a diaphragm/spermicide, and a history of UTI. In men, prostatic hypertrophy is the main risk factor. In both sexes, Foley catheters are a major risk factor.

Once bacteria reach the bladder, they may cause cystitis or they may reside there asymptomatically.Symptoms of cystitis are urgency, frequency and dysuria. (The symptom of dysuria can also be caused by certain STDs causing urethritis, and may be confused with the symptoms of vaginitis.)

From the bladder, bacteria may ascend to reach the kidney, producing pyelonephritis, an invasive infection which can cause bacteremia and severe illness.Pyelonephritis is typified by fever, chills, flank pain and tenderness, and an elevated peripheral WBC. Ascent from the bladder to the kidney is facilitated by urinary stasis and obstruction (as occurs in pregnancy and certain neurological conditions). Sticky E. coli have an advantage here, too.

The defenses of the urinary tract against infection are minimal, mainly the flushing effect of urine and the sloughing of colonized epithelial cells.

3. Diagnosis

Laboratory diagnosis of UTI is made problematic by the fact that it is difficult to obtain a truly sterile urine specimen from voided urine: contamination by meatal organisms is frequent. If a urine sample is left at room temperature for hours, these organisms may grow to high numbers. Thus, for patients with asymptomatic bacteriuria (no symptoms), a high threshold is required to document true bacteriuria (vs contamination), i.e. 105 bacteria per ml. By contrast, in patients with typical symptoms, a much lower threshold is accepted, i.e. 102 bacteria per ml. Most patients with true bacteriuria have pus cells in the urine (pyuria), at least 105 per high-power field under the microscope or a positive leukocyte esterase dipstick test. Pyuria is a fairly sensitive indicator for true bacteriuria but it is not very specific as a guide to treatment because many patients with asymptomatic bacteriuria (of whom only selected subgroups should be treated) have pyuria as do some patients with noninfectious inflammatory conditions (e.g. allergic interstitial nephritis).

4. Treatment

The most common causes of UTI are E. coli (85%), Staphylococcus saprophyticus (5-10%), and other enteric gram-negatives (5-10%). These organisms are nearly always susceptible to quinolones. Nowadays, about 20-30% are resistant to TMP-SMX. For reasons not entirely clear, quinolones and trimethoprim-sulfamethoxazole (TMP-SMX) are more effective than beta-lactams for UTI even if the organisms are susceptible to the beta-lactams. For cystitis, a superficial infection, 3 days of treatment usually suffices. For uncomplicated pyelonephritis (no obstruction or other anatomic problem), 2 weeks suffices.

5. Recurrences (relapse vs. reinfection)

While most UTI respond readily to treatment, some are followed by recurrences.These may take two forms:relapse and reinfection.

5.1. Relapses

Relapses signify that the original infection was never eradicated. The organism cultured is identical to that from the previous episode and symptoms usually recur within 2 weeks of the end of treatment for the previous episode. If the previous episode was treated with short course therapy, the first thought should be that there was subclinical pyelonephritis and that a longer course of treatment is needed. If a longer course is followed by another relapse, "imaging" (CT scan or ultrasound) is warranted, to look for an anatomic abnormality.

5.2. Reinfections

Reinfections may be caused by the same or a different organism, and usually occur at intervals > 2 wks after the preceding infection. Multiple reinfections usually point to pathogenetic factors such as those outlined above. They can be addressed by changing the contraceptive to "the pill", applying estriol cream in the postmenopausal woman, and, if necessary, by giving low dose chronic antibiotic prophylaxis.)

6. "Complicated" UTI

This term refers to UTI in the patient with an anatomic or functional abnormality facilitating UTI and making UTI difficult to eradicate. Obstructive lesions are a good example of complicated UTI but the most common association is with the Foley catheter. Patients with complicated UTI undergo many symptomatic episodes and courses of antibiotic treatment, which leads to infection by antibiotic-resistant organisms. The Foley catheter serves as a "highway" for bacteria from the outside world into the bladder: most organisms seem to travel by the extraluminal route. The rate of acquisition of bacteriuria with a Foley catheter is about 5% per day so that, by day 10, more than half of patients have bacteriuria. Irrigation of the urine bag by antibacterials and systemic administration of prophylactic antibiotics are of no benefit in preventing bacteriuria. (There are important technical issues which are of value, e.g. never raising the bag above the level of the patient's bladder.) Despite the frequency of bacteriuria, it is mainly asymptomatic. Nevertheless, long term indwelling urinary catheters should be avoided if possible.

7. Asymptomatic bacteriuria

One of the most important, and common, questions involves patients with asymptomatic bacteriuria. Although it may seem intuitively obvious that bacterial infection should be combated wherever possible, in fact, in most groups of patients, including the elderly and diabetic patients, treatment of asymptomatic bacteriuria has been shown to produce no benefit. It is usually difficult to eradicate, readily recurs, and exposes the patient to the cost and adverse effects of antibiotics - with no clinical benefit. There are three groups of patients in whom there IS a benefit to treating asymptomatic bacteriuria: pregnant women (because, untreated, 30% will go on shortly to develop symptomatic pyelonephritis), newborns (who have a risk of renal scarring from untreated infection), and patients about to undergo a urological procedure (because they have an appreciable risk of pyelonephritis).

8. Ancillary Material

8.1. Readings

8.1.1. Required

Schaechter Textbook, Chapter 60, pages 564-572.

8.1.2. Suggested

  • Stamm WE, Hooton TM: Management of urinary tract infections in adults. New Eng J Med 1993; 329: 1328-34.
  • Hooton TM, Scholes D, Hughes JP et al: A prospective study of risk factors for symptomatic urinary tract infection in young women. New Eng J Med 1996; 335; 468-474.
  • Scholes D, Hooton TM, Roberts PL et al: Risk factors for recurrent urinary tract infection in young women. J Infect Dis 2000; 182: 1177-82.
  • Gupta K, Hooton TM, Stamm WE: Increasing antimicrobial resistance and the management of uncomplicated community-acquired urinary tract infections. Ann Intern Med 2001; 135: 41-50.
  • Harding GKM, Zhanel GG, Nicolle LE et al: Antimicrobial treatment in diabetic women with asymptomatic bacteriuria. New Eng J Med 2002; 347: 1576-83.