eMedicine Specialties > Infectious Diseases > Genitourinary Tract Infections

Urinary Tract Infection, Females: Follow-up

Author: Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Coauthor(s): Jeffrey M Tessier, MD, Assistant Professor, Department of Medicine, Uniformed Services University of the Health Sciences; Mary F Bavaro, MD, Chief, Division of Infectious Disease, Navy Medical Center, San Diego
Contributor Information and Disclosures

Updated: Oct 19, 2009

Follow-up

Deterrence/Prevention

  • Approximately 25% of women with acute cystitis develop recurrent urinary tract infections (UTIs). The number of recurrences experienced varies for each woman (range, 0.3-7.6 episodes per year), and recurrences often cluster in time. Most recurrent infections are from bacteria colonizing the fecal or periurethral reservoirs. The 3 main risk factors are (1) an increased frequency of sexual intercourse, (2) the use of a spermicide and diaphragm, and (3) the loss of estrogen's effect in the vagina and periurethral structures.
    • Women who develop a UTI within 2 weeks of a treated UTI either have a new infection or they have a recurrence of the original uropathogen. The latter is supported by cultures growing the same species, especially if it is biotyped or shares the same antimicrobial sensitivities.
    • Looking for a source of persistent infection, such as a structural abnormality (eg, calculus, abscess, cystic disease) is prudent.
  • Women with recurrent UTIs (less than 2-3 per y) may benefit from behavioral modification and a program of self-initiated antibiotics.
    • Behavioral modifications are generally easy, low-risk, and low-cost maneuvers. Methods include urge-initiated voiding, postcoital voiding, increased fluid intake, and the daily consumption of cranberry juice.
    • Patients using a spermicide should consider alternative methods of contraception.
    • Self-initiated antibiotics may be an acceptable alternative for women with recurrent UTIs. The clinician should educate the patient about the warning signs of a persistent or worsening infection despite therapy. A recent study showed that women with a history of at least 2 UTIs in the past year were capable of self-diagnosing and treating UTIs. Uropathogens were isolated in 84% of 172 UTIs; clinical and microbiologic cures were achieved in about 95% of episodes.
  • Women with recurrent UTIs (more than 3 per y) should be considered for more aggressive prophylactic regimens in addition to the behavioral modifications.
    • Women who associate their recurrent UTIs with sexual intercourse should be offered postcoital prophylaxis. This involves taking a single dose of an effective antimicrobial (eg, nitrofurantoin 50 mg, TMP-SMZ 40/200 mg, or cephalexin 500 mg) after sexual intercourse.
    • Continuous antimicrobial prophylaxis may be required in women who fail a postcoital regimen, do not associate frequent UTIs with a modifiable cause, or who are at risk for recurrent complicated UTIs. Regimens include TMP-SMZ (40/200 mg qhs or 3 times per wk), nitrofurantoin (50-100 mg qhs or 3 times per wk), norfloxacin (200 mg qhs or 3 times per wk), and trimethoprim (100 mg qhs or 3 times per wk).
    • These regimens have been shown to be safe and effective, even after 5 years of use. However, after 6-12 months, a trial without the medication is warranted because as many as 30% of women experience a prolonged UTI-free period. Prophylaxis may be reinstituted if the patient again develops recurrent UTIs.
  • Women who are postmenopausal with recurrent UTIs may benefit from estrogen replacement, either systemically or locally. Estriol in a vaginal cream (0.5 mg every pm for 2 wk, then twice weekly) significantly reduced the incidence of recurrent UTI; the effect probably is related to the restoration of lactobacilli, which replace Enterobacteriaceae and decrease the vaginal pH.
  • For patients with SCI, the efficacy of prophylaxis with TMP-SMZ or nitrofurantoin has been demonstrated. The possibility of developing resistant organisms is a concern, especially in an institutional setting.
    • One option includes the use of methenamine (1 g tid), alternating q2mo with nitrofurantoin (50-100 mg bid). Methenamine is converted into formic acid, which is bacteriocidal. Oral ascorbic acid therapy has not been shown to confer much benefit.
    • Risk can be decreased by the use of intermittent catheterization. Urine cultures should be obtained periodically, and prophylactic or long-term antibiotic therapy may be considered if over 10,000 CFU/mL and pyuria are noted (even in the absence of symptoms).
    • Reflex bladder pressures greater than 50 cm H2O should be avoided through the use of alpha-blockers, anticholinergics, transurethral sphincterotomy, or electrical stimulation.
    • Using a 6% bleach solution to clean reusable leg bags and seat covers decreases the rates of infection and ASB.
  • Neither cefuroxime nor ciprofloxacin was shown to reduce the rate of bacteriuria (about 20%) after lithotripsy.
  • The American Heart Association recommends antimicrobial prophylaxis to prevent bacterial endocarditis in patients with moderate-to-high–risk cardiac conditions. High-risk conditions include prosthetic valves, previous bacterial endocarditis, complex cyanotic congenital heart diseases, and surgically constructed systemic pulmonic shunts. Moderate-risk conditions include most other congenital heart diseases, hypertrophic cardiac myopathy, and mitral prolapse with regurgitation. For patients with moderate- or high-risk cardiac conditions, urologic procedures warranting prophylaxis include cystoscopy and urethral dilatation; prophylaxis is not recommended for inserting a Foley catheter in a patient with uninfected urine. No good evidence supports using such regimens for prophylaxis for patients with prosthetic joints; this is an area that needs further research and study.
    • Regimens for high-risk patients include ampicillin (or vancomycin) plus gentamicin. Ampicillin is administered as 2000 mg IM or IV within 30 minutes of starting the procedure; 6 hours later, 1000 mg of ampicillin (or amoxicillin PO) is administered once. Gentamicin is dosed at 1.5 mg/kg IV or IM (not to exceed 120 mg) and is administered only once with the first dose of ampicillin. For patients allergic to ampicillin, 1000 mg of vancomycin is administered only once, IV over 1-2 hours; it should be completed within 30 minutes of starting the procedure.
    • Regimens for moderate-risk patients include amoxicillin or vancomycin. Amoxicillin is administered only once as 2000 mg PO 1 hour before the procedure. For patients allergic to amoxicillin, 1000 mg of vancomycin is administered only once, IV over 1-2 hours; it should be completed within 30 minutes of starting the procedure.

Complications

  • Bacteremia, sepsis, shock, and death have all been discussed.

Prognosis

  • The prognosis for most women with cystitis and pyelonephritis is good; about 25% of women with cystitis will experience a recurrence.
  • The prognosis for emphysematous pyelonephritis is not as good and is discussed in Special Concerns.
  • Infected cysts in polycystic kidney disease respond to treatment slowly.

Patient Education

Miscellaneous

Medicolegal Pitfalls

  • Many lawsuits arise from the complications of long-term aminoglycosides, especially irreversible cranial nerve (CN) VIII damage (hearing loss and vestibular dysfunction).  
    • Risk factors appear to be prolonged use (>2 wk), high serum troughs (>2.0), advanced age, baseline renal insufficiency, concomitant conditions (such as diabetes mellitus), and concomitant nephrotoxic drugs (such as amphotericin-B). Fortunately, most aminoglycoside use in treating serious urinary tract infections (UTIs) is limited to less than 1 week. Unfortunately, monitoring for CN VIII dysfunction is less than optimal; by the time it is detectable (even subclinically, via weekly audiography and/or electronystagmography [ENG]), the damage has occurred and is irreversible. This is because of differences in half-lives between serum, and the endolymph and perilymph that bathe the inner ear.
    • However, monitoring will allow damage to be minimized; recall that the auditory and vestibular systems function independently, and, therefore, consider monitoring each. Animal models suggest that doses administered at night or to a fasting or dehydrated patient may be more ototoxic. The possibly protective roles of calcium and calcium channel blockers await further study.
  • The differential diagnoses of many complicated UTIs are broad and include some potentially disastrous causes of acute abdomen. Lawsuits may be filed for missing a diagnosis of pyelonephritis, resulting in sepsis or death as an outcome. UTIs in pregnancy have potentially adverse outcomes for both the mother and the fetus. Good communication with patients and their families is essential.

Special Concerns

  • Catheters
    • Nosocomial infections develop in about 5% of patients admitted to hospitals, and UTIs account for 40% of these infections. Two to 4% of these patients become bacteremic, with a mortality rate of 12.5%.
    • Once a catheter is placed, the daily incidence of bacteriuria is 3-10%. Ten to 30% of patients with short-term catheterization (ie, 2-4 d) develop bacteriuria and are asymptomatic. Ninety to 100% of patients with long-term catheterizations develop bacteriuria.
    • Pathogenesis: The presence of potentially pathogenic bacteria and an indwelling catheter predisposes to the development of a nosocomial UTI. The bacteria may gain entry into the bladder during insertion of the catheter, during manipulation of the catheter/drainage system, around the catheter, and after removal. Enteric pathogens are responsible most commonly, but Pseudomonas species, Enterococcus species, S aureus, coagulase-negative staphylococci, Enterobacter species, and yeast also are known to cause infection. Proteus and Pseudomonas species are the organisms most commonly associated with biofilm growth on catheters.
    • Risk factors: The most important risk factor for bacteriuria is the presence of a catheter. Eighty percent of infections are related to a catheter while 5-10% are related to genitourinary manipulation. Catheters inoculate organisms into the bladder and promote colonization by providing a surface for bacterial adhesion and causing mucosal irritation. Risk factors for bacteriuria in patients who are catheterized include longer duration of catheterization, colonization of the drainage bag, diarrhea, diabetes, absence of antibiotics, female gender, renal insufficiency, errors in catheter care, catheterization late in the hospital course, and immunocompromised or debilitated states.
    • Diagnosis: Symptoms generally are nonspecific; most patients present with fever and leukocytosis. Significant pyuria generally is represented by greater than 50 WBC/hpf. Colony counts on a urine culture range from 100-10,000. Infections may be polymicrobial.
    • Prevention
      • At least nine steps can be taken to prevent catheter-associated UTIs. These steps can postpone a UTI for weeks but are not likely to be successful in chronically catheterized patients. Catheterization should be avoided when not required (catheters were found to be unnecessary in 41-58% of patient-days) and should be terminated as soon as possible. Suprapubic catheters are associated with a lower risk of UTI. Patients who require long-term catheterization are more satisfied, but mechanical complications are increased. Contraindications include bleeding disorders, previous lower abdominal surgery or irradiation, and morbid obesity. Intermittent catheterization is an option, but most become bacteriuric within a few weeks as the incidence is 1-3% per insertion.
      • Aseptic indwelling catheter insertion and a properly maintained closed-drainage system are essential. Urinary catheters coated with silver also reduce the risk (silver alloy seems to be more effective than silver oxide). Another approach is the Bard Lubricath, which has a hydrophilic coating that decreases tissue irritation and nosocomial UTIs. It is reasonable to use these more expensive catheters in those who are at highest risk.
      • Receiving systemic antimicrobial drug therapy has been shown repeatedly to lower the risk for developing a UTI in catheterized patients; most benefit was observed in those catheterized for 3-14 days. Most hospitalized patients already are receiving antibiotics for other reasons. Disadvantages include creating resistant organisms. Because many of these infections occur in clusters, good handwashing before and after catheter care is essential.
    • Treatment: Removal of the catheter is adequate in some patients with bacteriuria. If bacteriuria persists 48 hours after removal of the Foley catheter, antibiotics should be started. Antibiotic therapy is directed at the pathogen(s) isolated in the culture. Patients with chronic indwelling catheters who are febrile and not bacteremic should be treated with a 3- to 5-day course of antibiotics. If a patient is bacteremic, then a 10- to 14-day course of antibiotics is recommended.
  • Pregnancy
    • ASB occurs in 5-10% of pregnant women. More than 100,000 CFU/mL of a single uropathogen is the classic definition of ASB, but more recent data support 10,000 CFU/mL from a clean-catch specimen.
    • ASB most commonly appears between the ninth and 17th weeks of pregnancy. ASB predisposes to preterm labor, intrauterine growth retardation, low–birth weight infants, anemia, amnionitis, and hypertensive disorders of pregnancy.
    • Risk factors include sexual activity, increasing age and parity, diabetes, lower socioeconomic class, a history of UTIs, sickle cell disease, and structural/functional abnormalities. Cystitis and pyelonephritis are inevitable complications of ASB.
    • The recommendation is to screen pregnant women at their first prenatal visit and during the third trimester and not again, unless their initial test result is positive or they develop symptoms. Cystitis occurs in 0.3-1.3% of pregnancies but does not appear to be related to ASB. Acute pyelonephritis occurs in 1-2% of pregnancies. Complications of pyelonephritis include pulmonary edema and acute respiratory distress syndrome, transient renal dysfunction, anemia, preterm delivery, and low–birth weight infants.
    • ASB must be treated and not merely observed. Treatment of ASB decreases the risk of persistent bacteriuria from 86-11%, with a significant reduction in the risk of acute pyelonephritis. Sulfonamides, cephalosporins, nitrofurantoin, and broad-spectrum penicillins have been shown to be effective. A 4- to 7-day course of therapy is recommended for treating ASB and cystitis. Sulfonamides just before birth may cause fetal hyperbilirubinemia, while trimethoprim early in pregnancy is teratogenic.
    • Repeat cultures should be obtained during pregnancy given the high risk of relapse. After the second occurrence, nitrofurantoin, amoxicillin, or a cephalosporin is recommended for suppression until after delivery. Hospitalization is indicated for pyelonephritis with nausea/vomiting, evidence of sepsis, or for patients with contractions. Empiric parenteral regimens include a cephalosporin, such as ceftriaxone, or gentamicin plus ampicillin (or a derivative of penicillin). When using an aminoglycoside, the risk of ototoxicity in the fetus must be considered.
    • Antibiotic regimens should be changed based on culture results. Patients may be changed to oral therapy once they are afebrile and able to tolerate an oral regimen. Urolithiasis, a structural abnormality, or an abscess should be considered if a patient fails to respond to appropriate therapy.
  • Urinary tract infections in patients with renal transplants
    • UTIs are the most common type of infection following renal transplantation. UTIs occur in 30-50% of renal transplant patients and frequently are silent.
    • UTIs may, but do not always, predispose the patient to graft loss or rejection. Infection of the allograft may lead to life-threatening bacteremia. Patients are most susceptible the first 2 months following transplantation. Triggering factors include vesicoureteral reflux and immunosuppression.
    • An unusual bacterium, Corynebacterium urealyticum (ie, CDC group D2), has been reported to cause encrusted pyelitis and cystitis in these patients. Treatment of UTIs in renal transplant patients is preferably with either TMP-SMZ or a quinolone.
    • ASB should be treated for 10 days. Parenteral antibiotics should be used for severe infections. The duration of antibiotics for severe infections should be 4-6 weeks.
    • Antibiotic prophylaxis is valuable in patients undergoing renal transplantation. TMP-SMZ (1 PO qd), beginning 2-4 days after surgery and continuing for 4-8 months, reduced the incidence of UTIs from 38-8% (especially after the catheter was removed), cut febrile hospital days and bacterial infections (during and after hospitalization) in half, and reduced graft rejection.
  • Yeast and fungi
    • Removal of a Foley catheter is essential for clearance of funguria. If the catheter is still needed, replace it (preferably a day later).
    • Treatment options vary from topical treatment to systemic therapy.
    • Amphotericin-B bladder washes for 7 days provides a prompt but nonsustained response. It does not treat systemic mycoses and is inconvenient for the nurse to administer. Amphotericin-B, 0.3 mg/kg IV for 1 dose is an option that provides a more sustained and systemic response.
    • Fluconazole, 200 mg PO for 1 d followed by 100 mg PO qd for 4-7 d is a simpler option. This drug is effective against azole-responsive candida. Generally, azole-resistance is observed only in Candida krusei and Candida glabrata. Fluconazole provides a good long-term effect but takes a few days to clear the urine.
  • Diabetes mellitus
    • Complicated UTIs in patients who have diabetes include renal and perirenal abscess, emphysematous pyelonephritis, emphysematous cystitis, fungal infections, xanthogranulomatous pyelonephritis, and papillary necrosis.
    • Emphysematous pyelonephritis is a severe, necrotizing form of multifocal bacterial nephritis with gas formation within the renal parenchyma. Seventy to 90% of cases develop in patients with diabetes. Sixty percent of infections are secondary to E coli. Enterobacter aerogenes and Klebsiella, Proteus, Streptococcus, and Candida species also may play a role.
      • Three factors must be present for the development of renal emphysema—excess tissue glucose, impaired tissue perfusion, and a gas-producing bacterium. The gas may result from fermentation of necrotic tissue or from mixed acid fermentation by Enterobacteriaceae. Predisposing factors include diabetes mellitus, remote or recent kidney infection, and obstruction.
      • Patients may present with fever, chills, and nausea or vomiting. Half of patients have evidence of a flank mass on examination. Rarely, patients have crepitus over the thigh or flank.
      • Lab findings include leukocytosis, hyperglycemia, pyuria, and an elevated BUN and creatinine. A plain film of the abdomen may reveal gas in the kidneys in 85% of infections. Renal ultrasonography may also help establish the diagnosis. If gas is visualized, then a CT scan should be performed to reveal if the gas is in the parenchyma or collecting system.
      • The mortality rate is 60% in cases in which the gas is localized to the renal parenchyma, regardless of treatment. The mortality is 80% if the gas has spread in the perinephric space and the patient is treated with antibiotics alone.
    • Emphysematous pyelitis is defined as the presence of gas localized to the renal collecting system. Emphysematous cystitis is defined as air in the urinary tract.
      • Pathogenesis: More than 50% of these patients have diabetes. Obstruction of the collecting system generally is the rule in emphysematous pyelitis. The left kidney is involved twice as often as the right in emphysematous pyelitis. The most common infectious etiology is E coli, but other gram-negative organisms, S aureus, Clostridium perfringens, and Candida species also may be responsible.
      • Presentation: Patients with emphysematous pyelitis most commonly present with fever, chills, nausea and vomiting, and abdominal pain. Patients with emphysematous cystitis most commonly present with urinary frequency, urgency, and dysuria. Abdominal pain also may be present. Gross hematuria and pneumaturia are occasionally present.
      • Diagnosis: Leukocytosis and pyuria are observed in most patients. In half of the patients, azotemia and hyperglycemia are present. Abdominal films may reveal gas outlining the renal pelvis and in the ureters. Abdominal films may reveal air in the bladder wall or lumen. Renal ultrasonography may reveal diffuse thickening of the bladder wall and echogenicity. CT scans may reveal gas in the bladder wall with extension into the lumen. Cystoscopy may reveal blebs in the bladder mucosa.
      • Therapy: Antibiotics and relief of obstruction usually are sufficient. The mortality rate is 20%.
  • Papillary necrosis
    • Definition: Papillary necrosis is defined as focal or diffuse ischemic necrosis of various segments of the renal medulla.
    • Pathogenesis: This entity is uncommon in people with diabetes, but, when infections occur, more than one half are in people with diabetes. Other causes include sickle cell disease, analgesic abuse, pyelonephritis, renal transplant rejection, cirrhosis, and obstruction. Most infections are complicated by UTI and renal insufficiency.
    • Two types of papillary necrosis have been described. In the medullary form, the fornices remain intact. In the papillary form, the entire papillary surface is destroyed.
    • Presentation: Many patients present with fever, chills, and flank pain. The flank pain is secondary to the passage of sloughed papilla. Some patients may present with symptoms of obstruction or azotemia.
    • Histology and/or radiologic studies may help make the diagnosis. The sloughed papillae may be obtained by straining the urine and sending for histology. The retrograde pyelography is the radiologic procedure of choice, but ultrasonography or CT scan also reveals the diagnosis. Findings of early renal papillary necrosis include a dilated calyceal fornix, retracted or irregular papillary tip, and extension of contrast into the parenchyma. A club-shaped cavity in the medulla or papilla may be formed in later disease. When a separated papilla is surrounded by contrast, a ring may be visualized; this is characteristic of papillary necrosis.
    • Treatment: Antibiotics, drainage, and (occasionally) surgery are the mainstays of therapy. Antibiotics should cover E coli and Enterobacter, Proteus, and Klebsiella species.
    • Treatment for more serious infections also should cover Pseudomonas and Enterococcus species. Initial therapy should not be with an oral regimen. Parenteral agents such as gentamicin, cefotaxime, ceftriaxone, ceftazidime, cefepime, mezlocillin, piperacillin, piperacillin-tazobactam, imipenem-cilastatin, meropenem, or ciprofloxacin should be used empirically pending the result of a urine culture. Parenteral therapy should be continued until the fever and other symptoms resolve. Duration of therapy generally is 14 days.
 


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References
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Further Reading

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Keywords

urinary tract infection, UTI, urinary infection, cystitis, pyelonephritis, bacteriuria, candiduria, urosepsis, sexually transmitted disease, STD, Escherichia coli, E coli, Pseudomonas aeruginosa, P aeruginosa, Klebsiella pneumoniae, K pneumoniae, candidal species, enterococcal species, enterococci, pelvic inflammatory disease, PID, yeast infection, uropathogens, hematuria, indwelling urethral catheter, indwelling urethral catheterization

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Contributor Information and Disclosures

Author

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Jeffrey M Tessier, MD, Assistant Professor, Department of Medicine, Uniformed Services University of the Health Sciences
Jeffrey M Tessier, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine
Disclosure: Nothing to disclose.

Mary F Bavaro, MD, Chief, Division of Infectious Disease, Navy Medical Center, San Diego
Mary F Bavaro, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Medical Editor

Klaus-Dieter Lessnau, MD, FCCP, Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital
Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Artificial Internal Organs, American Thoracic Society, Physicians for Social Responsibility, and Society of Critical Care Medicine
Disclosure: sepracor Ownership interest None

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Mark Jeffrey Noble, MD, Consulting Staff, Urologic Institute, Cleveland Clinic Foundation
Mark Jeffrey Noble, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Urological Association, Kansas Medical Society, Sigma Xi, Society of University Urologists, and Southwest Oncology Group
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center
Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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