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