Urinary tract infection: providing the best care

Urinary Tract Infection: Providing the Best Care
Introduction
Urinary tract infections (UTIs) account for more than 8 million office visits per year and as many as 100,000 hospitalizations. Although UTIs are typically thought to be easy to detect and cure, a number of factors must be taken into account to provide the most appropriate and effective care. Recommendations on the diagnosis and treatment of this common infection vary according to patient's age and sex as well as comorbidity, level of risk of infection with resistant pathogens, previous response to therapy, the use of a urinary catheter, and pregnancy.[1] The choice of antimicrobials has increased, as has the prevalence of resistant pathogens. Those involved in the care of patients who have a UTI are faced with a number of questions: What causes this common clinical condition? How can it be prevented? What is the optimal clinical evaluation? Which antimicrobials should be used empirically, and which should be avoided? Do the antimicrobials long used in the treatment of UTI, such as nitrofurantoin and trimethoprim-sulfamethoxazole (TMP-SMX), still have a role to play in the age of resistant organisms? And when should newer agents such as the fluoroquinolones be used? Recognizing the Clinical Presentation
The urinary tract, adjacent to the bacteria-rich lower gastrointestinal tract, produces
and stores urine. The periurethral area is typically colonized with gut and other flora, some capable of causing UTI.[2] While the process of urination flushes bacteria from the urethral orifice, periurethral pathogens on occasion enter the urethra and ascend, reaching the bladder and resulting in UTI; this is the most common route for UTI acquisition. On rare occasion, hematogenous UTI can occur when a pathogen is delivered to the urinary tract via the bloodstream from a distant source of infection, such as the lungs in a patient with pneumonia.[3] Urinary tract infections can involve mucosal tissue (cystitis) or soft tissue
(pyelonephritis, prostatitis). Anatomically, the infection can be limited to the lower
urinary tract (cystitis involving the bladder and urethra) or the upper tract (pyelonephritis). Complicated UTI can occur in either the upper or lower urinary tract but is accompanied by an underlying condition that increases the risk for failing therapy, such as obstruction, urologic dysfunction, or resistant pathogens. Most UTIs occur via an ascending route.[4] UTI is typically diagnosed by clinical presentation and a limited number of physical exam findings. In the otherwise healthy woman, history of the present illness usually reveals a complaint of dysuria, often reported as an internal discomfort, with urinary frequency and urgency but without fever or constitutional symptoms. Although suprapubic tenderness and pain are often considered part of the clinical presentation, they are only found in about 20% of women with an uncomplicated UTI. Back pain, fever, nausea, and vomiting are more often associated with pyelonephritis, and rarely with cystitis; many with pyelonephritis will also report lower UTI symptoms. While vaginal infection and irritation can cause dysuria, most women who have
dysuria without vaginal discharge have a UTI, not vaginitis.[5]
In urethritis, the inflammation and infection is limited to the urethra only, or
urethra and vagina in women; its etiology is usually a sexually transmitted pathogen such as Chlamydia trachomatis, Ureaplasma urealyticum, Neisseria gonorrhoeae, or Trichomonas vaginalis.[6] Found in men and women, complaints include discomfort during voiding, but there are usually no symptoms of postvoid suprapubic pain or urinary frequency.
Hemorrhagic cystitis is characterized by large quantities of visible blood in the
urine. Its etiology can be bacterial or adenovirus types 1-47 infection or as a result of radiation, cancer chemotherapy, or select immunosuppressive medication. Clinical presentation usually depends on its origin; with all causes, irritative voiding symptoms are typically reported. When infectious in origin, signs and symptoms of infection may also be encountered. Adenovirus is a common cause and is self-limiting in nature. Hemorrhagic cystitis is often confused with glomerulonephritis, but hypertension and abnormal renal function are absent in the former. When radiation-induced, symptoms may develop months after cessation of treatment.[7,8] Acute pyelonephritis is an infection of the renal parenchyma and renal pelvis,
caused by an ascending cystitis; most episodes are uncomplicated and not
accompanied by risk of treatment failure such as obstruction, urologic dysfunction, or
a multidrug-resistant uropathogen.[4] Irritative voiding symptoms similar to cystitis are usually reported, along with fever and flank pain, often with vomiting. Clinical findings usually include an acutely ill appearance, costovertebral tenderness, and pyuria. Table 1 outlines the clinical findings in women with dysuria and pyuria. Table 1. Clinical Findings in Women With Dysuria and Pyuria[3,9] Clinical Findings in Addition to
Possible
Dysuria and Pyuria
Etiology
saprophyticus). Pathogenic organisms revealed by urine Irritative voiding symptoms, purulent or mucopurulent vaginal or cervical discharge, report of postcoital bleeding, edema and/or endocervical swabbing, numerous white blood cells found on microscopic wet mount examination cervix or cervical os, brisk bleeding Pelvic induced by endocervical swabbing, inflammatory influenzae, enteric cervical motion tenderness, possible disease
Selecting Laboratory Tests
Laboratory testing has traditionally been used to support the diagnosis of UTI. Urine
sampling for diagnostic testing is obtained through midstream voiding. A midstream urine sample can be used for dipstick, microscopic urinalysis, and urine culture. Urine dipstick testing is commonly done in the office setting when UTI is suspected because it is simple and convenient and yields immediate results. Leukocyte esterase, nitrates, protein, and blood are the important features in evaluating for UTI. The presence of leukocyte esterase on a urine dipstick is equivalent to >/= 4 white blood cells per high-power field (WBC/hpf). Nearly all (>/= 96%) patients with UTI have pyuria equivalent to > 10 WBC/hpf.[5] Some uropathogens are capable of reducing dietary nitrates in the urine to nitrite; this is an indirect test for bacteriuria. When coupled with a leukocyte esterase response, the likely offending organism is a Gram-negative pathogen (Escherichia coli, Proteus spp., Klebsiella pneumoniae). The nitrite test may be falsely negative in UTI with a low colony count, or in recently voided or dilute urine. In addition, this test does not detect organisms unable to reduce nitrate to nitrite, such as enterococci, staphylococci, or adenovirus.[10] Small amounts of protein and red blood cells may also be positive on dipstick in cases of UTI. Table 2 highlights common urinalysis dipstick findings in UTI. However, in one study of healthy young adult women with dysuria for less than 1 week without vaginal discharge, signs of pyelonephritis, or predisposing conditions, empiric therapy guided by clinical presentation alone was the most cost-effective strategy; culture and treat-later strategies were significantly more expensive, and use of the dipstick alone was the most expensive approach.[11] Further prospective clinical trials will be helpful in establishing the most cost-effective and clinically effective strategy, including patient-directed therapy. Table 2. Common Urinalysis Dipstick Findings in Urinary Tract Infection[12,13] Significance
Comment
Change in urine color is not
presence of neutrophils > 4 WBCs/hpf, an indicator of UTI, Test for enzyme present 90%. Results not valid in in white blood cell (WBC) neutropenic patient. Decreased sensitivity with increased urinary glucose concentration, high urinary SG, and presence of antimicrobial in urine. Surrogate marker for bacteriuria. Presence Escherichia coli, Proteus conversion to take place; dietary spp. Normally absent in sterile False negative possible with low urine and infection represents presence of protein-containing substance such as 30 mg/dL (1+), seldom >/= 100 mg/dL. If alkaline urine is found in presence of UTI symptoms and into CO2 and ammonia, causing a rise in the urine's normally Microscopic urinalysis can be used to confirm UTI but requires additional equipment and considerable technical skill if done in the office, or delay in time if performed in a laboratory. When coupled with classic symptoms, a finding of 2-5 WBCs or >/= 15 bacteria per hpf in a centrifuged urine sediment is consistent with UTI.[10] The presence of many epithelial cells usually indicates a contaminated specimen. Urine culture is important when diagnosis is not clear or UTI is recurrent. The presence of more than one organism may indicate a contaminated urine specimen and collection and testing should be repeated. The presence of >/= 105 CFU/mL of bacteria is the traditional diagnostic indicator for UTI. However, in the presence of dysuria and other symptoms for UTI, 102 CFU/mL confirms the diagnosis. Approximately 10% to 20% of women with acute uncomplicated pyelonephritis will have blood cultures positive for the offending pathogen. However, this is not predictive of a poorer outcome or need for protracted length of treatment in the otherwise healthy woman. While typically obtained when a patient pyelonephritis needs to be hospitalized, obtaining blood cultures will likely be of benefit only when there is evidence of complicated infection, multidrug-resistant pathogen or treatment failure.[4] What Factors Determine the Risk of UTI?
Certain factors protect against or increase the risk for UTI. Male sex is recognized as
a potent protective factor, in part due to the longer urethral length compared with
women. In addition, certain women with a closer proximity of the urethral orifice to the anus appear to be at increased UTI risk.[14] In addition, the scrotum provides a physical barrier between the glans and the perianal region, a potential source of uropathogens. Unlike the periurethral area in women, the male periurethral area does not support bacterial growth. Zinc-rich prostatic secretions are antibacterial, further discouraging pathogen growth.[15] In women, the intestinal tract or periurethral area becomes colonized with uropathogens. Once colonization occurs, the organisms may remain in place, whether or not these cause a urinary tract infection. In either sex, efficient bladder emptying helps prevent urine stagnation and minimizes UTI risk. Factors that can alter efficient bladder emptying, such as cystocele, rectocele, and benign prostatic hyperplasia (BPH) increase UTI risk. In addition, robust fucosyltransferase activity discourages bacterial adherence; the presence of relatively few bacterial adhesion receptor sites in the bladder and urethra acts similarly. Women with these receptors who do not have mucosal secretion of the fucosyltransferase enzyme to help block bacterial adherence are more likely to have colonization of E coli and other coliforms from the rectum and less likely to have lactobacilli in the periurethral area, resulting in frequent episodes of cystitis. The uroepithelial receptors can also be found in the upper urinary tract, increasing the risk of pyelonephritis.[6] Women who are nonsecretors of ABH blood group antigens show enhanced adherence of uropathogenic E coli to uroepithelial cells compared with women who are secretors; this becomes a major UTI risk factor when coupled with spermicide use or frequent vaginal sexual intercourse.[16] The woman who is exposed to the spermicide nonoxynol-9, either through vaginal use or with a male partner who uses condoms with this spermicide, is at increased risk of UTI. The proposed mechanism of this risk is due to the spermicide's antibacterial effect, reducing lactobacilli, a normal component of the periurethral flora. Lactobacilli produce hydrogen peroxide and lactic acid, providing the periurethral area and vagina with a pH that inhibits bacterial growth and blocks potential sites of attachment, as well as being toxic to uropathogens.[17] Recent studies also propose that spermicides containing the antibacterial detergent benzethonium chloride, often used as a preservative, may contribute to this problem. Although often recommended, voiding at regular intervals, wiping patterns, and postcoital voiding have not been proven to provide uncomplicated UTI protection[14,18]; hot tubs, pantyhose, douching, and obesity have not been demonstrated to increase UTI risk.[14] In postmenopausal women, estrogen deficiency leads to a marked reduction in lactobacilli colonization in the vaginal-perineal areas; topical estrogen use results in reestablishment of the normal protective flora and a reduction of UTI risk.[17] Recent antimicrobial use potentially increases UTI risk by the same mechanism.[14] The replenishment of urogenital microflora with probiotics or exogenous application of protective, "friendly" bacteria, via vaginal douche or capsule or taken orally in capsules, drinks, or yogurt, is gaining popularity for genitourinary tract infections.[19] In children and elders, constipation has been noted to contribute to bladder instability and may encourage UTI.[20] Elders often have a number of risk factors for UTI, including alterations in urinary tract structure such as uterine prolapse, cystocele, rectocele, and BPH, and limited functional status impairing mobility, hygiene, and toileting.[20] UTI in Special Populations
Most uncomplicated UTIs occur in women of reproductive age who otherwise do not have chronic health problems or voiding disorders; assessment is often straightforward and treatment is effective. However, certain populations, including elders, pregnant women, and people with clinical conditions such as asymptomatic bacteriuria, bear special mention.
Asymptomatic Bacteriuria
Asymptomatic bacteriuria, in which urine culture reveals a significant growth of a
pathogen (> 105 bacteria/mL)[20] but the patient has no symptoms of UTI, can be
found at equal rates in pregnant and nonpregnant women during the reproductive years. Incidence increases with age. Asymptomatic bacteriuria is noted in approximately 20% to 25% of community-dwelling women age 65 and older and in around 10% of community-dwelling men age 65 and older. In the nonpregnant woman of reproductive age or the well elder, asymptomatic bacteriuria poises no health threat and should only be treated if bladder instrumentation or surgery is planned. In fact, treatment may result in the development of resistant organisms. A course of an appropriate antimicrobial is indicated if bladder instrumentation is planned.[10,21] The incidence of asymptomatic bacteriuria among elders residing in long-term-care facilities increases to 20% to 50% for those without an indwelling urinary catheter, but virtually all with an indwelling catheter have bacteriuria. Risk factors for bacteriuria in the elderly include altered elimination (fecal impaction and the use of medications that encourage constipation and urinary retention such as anticholinergic drugs), anatomic variations in the urinary tract (cystocele, BPH), hygienic issues (fecal soiling, poor perineal hygiene), neurologic impairment affecting mobility and bladder emptying, and postmenopausal hormonal changes. In the person with an indwelling urinary catheter and evidence of sepsis, bacteriuria should be treated.[18] Cunha proposes the following formulas to assist with the differentiation between UTI and bacteriuria: pyuria alone = inflammation; bacteriuria without pyuria = colonization; pyuria + bacteriuria + nitrites = infection.[22]

Symptomatic UTI in the Elderly
The healthy elder with an uncomplicated lower UTI, regardless of gender, is likely to
have a classic presentation including urinary frequency, urgency, and suprapubic discomfort; new-onset urinary incontinence may also be reported. The frail elder with multiple health problems and complicated UTI may have an atypical or subtle presentation of infection, including change in appetite, delirium, and agitation. An elder with urinary incontinence and UTI may experience an increase in the number of
episodes of urine loss.[20,22]

UTI and Asymptomatic Bacteriuria During Pregnancy
Pregnancy-related anatomic changes in the urinary tract, such as pressure on the
bladder from enlarging uterus and increase in the size of the ureters, contribute to urinary reflux. UTI in the pregnant woman is a significant risk factor for low- birthweight infants and prematurity. Asymptomatic bacteriuria occurs in 5% to 9% of both nonpregnant and pregnant women. If left untreated in pregnancy, progression to symptomatic UTI including acute cystitis and pyelonephritis occurs in 15% to 45%, or 4-fold higher than in nonpregnant women. This is due largely to the lower interleukin-6 levels and serum antibody responses to E coli antigens that occur during pregnancy, resulting in less robust immune response. Since asymptomatic bacteriuria, usually caused by aerobic Gram-negative bacilli or Staphylococcus haemolyticus, can lead to UTI, a urine culture should be obtained from all women early in pregnancy, even in the absence of UTI symptoms.[10] Approximately 20% to 40% of women with bacteriuria will develop UTI during the course of the pregnancy; only 1% to 2% of those with a negative urine culture develop UTI. Bacteriuria should be treated with a 3- to 7-day course of antimicrobials, which reduces the risk of symptomatic UTI by 80% to 90%.[10,21] Therapeutic options for the treatment of asymptomatic bacteriuria and symptomatic UTI during pregnancy are guided by pathogen susceptibility, and preferred antimicrobials include those with US Food and Drug Administration (FDA) pregnancy risk category B. Table 3 identifies FDA pregnancy risk and Hale's lactation risk categories for commonly prescribed antimicrobials in UTI. Antimicrobials in pregnancy risk category B include the beta-lactams (amoxicillin, cephalexin, cefpodoxime, cefixime, and amoxicillin/clavulanate) and nitrofurantoin. Nitrofurantoin has the advantage of sparing disruption of normal vaginal flora and consistent efficacy against E coli and Staphylococcus saprophyticus. Nitrofurantoin should be avoided after the 36th week of gestation due to the potential (though unlikely) risk for hemolysis if the fetus is G6PD-deficient and in infections caused by Proteus mirabilis. Beta-lactam use usually fails to eradicate the offending pathogen from the periurethral and perivaginal area, increasing the risk of reinfection. Table 3. FDA Pregnancy Risk and Hale's Lactation Risk Categories for Commonly Prescribed Antimicrobials in Urinary Tract Infection Cat B, L1, L2
Nitrofurantoin Amoxicillin with clavulanate Lactation Risk Category[23]
L1 -- Safest, controlled study = Fails to demonstrate risk
L2 -- Safer, limited number of woman studied without risk
L3 -- Moderately safe, no controlled study or controlled study
shows minimal, nonlife-threatening risk
L4 -- Hazardous, positive evidence of risk, may be used if
maternal life-threatening situation
L5 -- Contraindicated, significant, and documented risk
FDA Pregnancy Risk Categories[23]
Category
Category Category
Category B
Category X
fetal risk but controlled evidence of demonstrate The fluoroquinolones and TMP-SMX are FDA pregnancy risk category C; TMP-SMX is also associated with a higher risk of treatment failure due to resistant pathogens.[6] Women with symptomatic UTI during pregnancy should be treated for 7 days, and asymptomatic bacteruria is usually treated for 3 days. Once UTI is documented, monthly screening urine cultures should be obtained for the duration of the pregnancy. Daily antimicrobial prophylaxis with an appropriate agent should be considered with evidence of 2 days of a symptomatic UTI or persistent, unresolved bacteruria, in spite of effective antimicrobial therapy. Urologic evaluation should also be considered to rule out structural abnormality.[10,21]
UTI in Men
UTI is often thought to be rare in men, but it is the most common cause of male dysuria. It typically occurs during the first 3 months of life or after age 50 years. Potential obstruction to urine flow may be caused by the foreskin in early life and by the prostate in mid and later life.[24] The male presenting with fever, dysuria, and back pain should be evaluated for acute bacterial prostatitis or pyelonephritis; a urology referral should be considered with any male UTI. Table 4 reviews the clinical findings in men with dysuria and pyuria.[25] Asymptomatic bacteriuria in the older man should not be treated unless bladder instrumentation, surgery, or prostatic massage is planned.[21] Table 4. Clinical Findings in Men with Dysuria and Pyuria[25] Clinical Findings
in Addition to
Possible
Dysuria and
Etiology
Pyelonephritis organisms revealed by urine bacilli (Escherichia coli, Proteus, Klebsiella, others) Pyuria rate = approximately 25%. May be caused by uropathogen such as E coli in man with recent urinary tract Uropathogens and Antimicrobial Therapy
The treatment of UTI usually includes an antimicrobial prescription. Selection of an
appropriate agent depends on the anticipated pathogen, which is determined in large part by patient characteristics such as age, sex, pregnancy, the anatomic location of the infection, and comorbid conditions. Antimicrobial characteristics include spectrum of activity, pharmacokinetics (including tissue penetration into the urinary tract), and the adverse effect profile.[3] Table 5 highlights medications for acute uncomplicated cystitis, including dose, and adverse effects. Concern about infection with resistant pathogens can influence the clinician to choose an antimicrobial with broad coverage when one with a narrow spectrum of activity would be more appropriate. The use of any antimicrobial can change the microbiology in the immediate and extended environment.[2,5,25] Table 5. Oral Treatment Regimens for Acute Uncomplicated Cystitis Adverse Effects and Cautions
Dosage
250 mg
trivalent cations Increased incidence of diarrhea for 3 days divalent and trivalent cations day for 3 divalent and trivalent cations day for 3 divalent and trivalent cations Most episodes of community-acquired cystitis in women, the most commonly encountered UTI, are caused by enteric Gram-negative rods from the Enterobacteriaceae group, such as E coli and P mirabilis, as well as the less commonly encountered K pneumoniae. S saprophyticus, a Gram-positive organism, and E coli accounted for more than 90% of the uropathogens in one study of 4324 urine isolates obtained from women with cystitis during a 5-year period; nearly all of these isolates were sensitive to ciprofloxacin and nitrofurantoin, while up to 18% were resistant to TMP-SMX and at least 28% were resistant to beta-lactams Given that E coli is by far the most common uropathogen, recent developments in TMP-SMX-resistant strains bear mention. Factors influencing the development of multidrug-resistant E coli strains include liberal use of TMP-SMX to treat UTI in adults as well as to provide prophylaxis against Pneumocystis carinii pneumonia in patients with HIV. In children, attendance at day care, age younger than 3 years, and repeated TMP-SMX use for respiratory infections are risk factors for infection with a resistant uropathogen; child-to-child and child-to-parent transmission of this organism may then take place.[27,28] TMP-SMX has also been widely used in animal feed, likely contributing to TMP-SMX resistance among E coli strains in animals, although the role of the animal reservoir as a contributor to the origin or spread of uropathogenic E coli has not been demonstrated. Travel to an area with a high prevalence of TMP-SMX resistance may result in what Stamm[28] called "traveler's urinary tract infection" with a multidrug- resistant E coli strain. Multidrug resistance may be transferred on a single plasmid, often yielding resistance to TMP-SMX, ampicillin, cephalothin, and tetracycline; seldom does this multidrug resistance extend to nitrofurantoin. Infectious Disease Society of America (IDSA) Guidelines for Treatment of Uncomplicated UTI advise a 3-day course of TMP-SMX for acute cystitis treatment in regions where E coli TMP-SMX resistance is less than 20%.[27] Alternative therapies in the presence of sulfa allergy or where E coli TMP-SMX resistance rates exceed 20% include a fluoroquinolone or nitrofurantoin. Fluoroquinolones are contraindicated in children aged 18 years and under due to possible disruption of developing cartilage. The Medscape UTI Zone Resource Center[29] provides information on uropathogen susceptibility data for various regions of the United States. Choosing one of these agents will assure infection resolution; nitrofurantoin has a focused spectrum of activity and can spare gut flora exposure to a wider-spectrum antimicrobial and possibly reduce the risk for development of resistant pathogens.[25,28] When prescribing nitrofurantoin for the treatment of cystitis, the IDSA recommends a 7- day course.[27] Although E coli remains the most common uropathogen in the community and long- term-care-dwelling elder, P mirabilis and K pneumoniae account for approximately one third of all infections in this age group. Length of antimicrobial in the elder with uncomplicated UTI should be 7-10 days in women and 10-14 days in men; short-course therapy is not recommended. First-line therapy includes TMP-SMX or fluoroquinolones; nitrofurantoin should not be used in the elderly, as its safe use requires a minimum creatinine clearance of 40 mL/min.[30] In the elder with impaired renal function, TMP-SMX and fluoroquinolone doses need adjustment as well.
Is an Office Visit Needed?
In the adult woman, the clinical presentation of cystitis nearly always includes
dysuria, frequency, and/or urgency; laboratory diagnostics typically add little to the assessment process. As a result, the rationale for insisting on an office visit prior to treatment needs to be questioned. The Institute for Clinical Systems Improvement advises that in the adult woman with dysuria, frequency, and/or urgency without symptoms or risks of genitourinary disease such as sexually transmitted diseases and complicating factors, short-course antimicrobial therapy with patient education may be given without an office or provider visit.[31] Complicating factors include protracted duration of symptoms; signs and symptoms of pyelonephritis; concomitant health problems including diabetes mellitus, renal disease, or recurrent UTI; or the presence of any factor that dictates the need for an office visit and provider assessment. The University of Michigan Health Systems offers similar guidelines,[32] as does a well-designed study presented at the 2001 Interscience Conference on Antimicrobial Agents and Chemotherapy.[33]
Posttreatment Follow-up
Routine posttreatment cultures in uncomplicated cystitis and pyelonephritis are not warranted; follow-up cultures in complicated infection should be obtained as appropriate during the evaluation and treatment of the complicating factors. Urologic imaging (renal ultrasound or computed tomographic scan) should be considered if pyelonephritis symptoms initially resolve but recur within 2 weeks of the end of antimicrobial therapy and urine culture yields the original pathogen with sensitivity profile. Retreatment with a 2-week regimen using another agent should be considered.[4]

Recurrent Infection: Relapse Vs Reinfection
Approximately 20% of patients with UTI will develop a second infection with 6
months. A recurrent infection that occurs within 2 weeks of completing antimicrobial treatment and is caused by the original uropathogen is a relapse of infection. Reinfection occurs after 2 weeks of antimicrobial therapy has been completed and may be caused by the same or a different organism.[10] For women with repeated UTIs, patient-initiated therapy should be considered. In this, the patient has an appropriate antimicrobial available and initiates therapy at first UTI symptom. Recent study on this practice failed to demonstrate an increase in the rate of resistant pathogens.[33] For patient-initiated therapy to be safe and successful, the patient needs to have a clear understanding of length of UTI therapy, signs and symptoms of treatment failure, and when to seek provider assistance.[34] UTI prophylaxis may be indicated for women who experience 2 or more symptomatic UTIs within 6 months or 3 or more UTIs over 12 months, or for those with fewer infections but with severe discomfort. Both continuous prophylaxis, in which an antimicrobial is taken daily for 6 months or more, and postcoital prophylaxis, in which an antimicrobial is taken with each act of coitus, have been demonstrated to be effective in the management of recurrent uncomplicated cystitis. Prior to initiating UTI prophylaxis, resolution of the previous UTI should be confirmed by a negative urine culture 1-2 weeks posttreatment. The method prescribed is dependent upon the frequency and pattern of recurrences and patient preference.[35] Choice of an antimicrobial agent for recurrent UTI should be based on susceptibility patterns of the strains causing the patient's previous UTIs and patient history of drug allergies or intolerance. Long-term TMP-SMX or nitrofurantoin therapy has been used successfully for many years. When compared with TMP-SMX, nitrofurantoin has the advantage of lower rates of resistance of the more common UTI pathogens. The use of a fluoroquinolone for UTI prophylaxis has gained some popularity; concern about emerging resistance is an issue. UTI prophylaxis in the postmenopausal woman should also include the use of a topical estrogen to encourage lactobacilli recolonization.[14] Cranberry juice intake has been touted as a helpful measure to reduce the rate of recurrent infections. Initially believed to cause high levels of benzoic acid that resulted in urinary acidification and bacteriostatic action, further study failed to support this hypothesis. Rather, cranberry-derived substances including glycoproteins, fructose, and condensed tannins (proanthocyanidins) prevent bacterial adherence, especially E coli, to urinary epithelial cells. Infection risk is then minimized as pathogens are flushed from the urinary tract. This property has also been noted with blueberry juice. A minimum of 300-400 mg twice daily in tablet form or 8-16 oz of a >/= 30% cranberry juice blend is needed to yield therapeutic effective. Cranberry juice intake also appears to weaken attachment of E coli to inert surfaces and controls biofilm formation on urinary catheters.[36-38] However, a systematic review of studies indicated a high withdrawal rate and conflicting results. Long-term adherence to cranberry products and expected benefit may be overestimated.[39] Recommendations for Practice
The assessment and treatment of the patient with a UTI is often straightforward, but in certain populations, such as pregnant women and the elderly, diagnosis and therapy can pose complex challenges for the primary care provider. Uncomplicated cystitis needs to be differentiated from pyelonephritis, urethritis, mucopurulent cervicitis, and pelvic inflammatory disease by evaluating clinical findings elicited from the physical examination and appropriate diagnostic tests. While presentation of uncomplicated cystitis in the adult woman does not always require laboratory evaluation for confirmation of diagnosis, the urine dipstick, microscopic urinalysis, and urine culture tests may play a role in other cases. Keeping in mind the most likely uropathogens and patient factors such as age, gender, comorbidity, resistant pathogen risk, previous response to therapy, urinary catheter use, and pregnancy can help guide the clinician to the most cost-effective therapy. References
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