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Urinary Tract Infection in Males

  • Author: John L Brusch, MD, FACP; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Oct 22, 2015
 

Practice Essentials

Urinary tract infections (UTIs) are rare in adult males younger than 50 years but increase in incidence thereafter. Causes of adult male UTIs include prostatitis, epididymitis, orchitis, pyelonephritis, cystitis, urethritis, and urinary catheters. Owing to the normal male urinary tract’s many natural defenses to infection, many experts consider UTIs in males, by definition, to be complicated (ie, more likely to be associated with anatomic abnormalities, requiring surgical intervention to prevent sequelae).

Signs and symptoms

Dysuria is the most frequent chief complaint in men with UTI. The combination of dysuria, urinary frequency, and urinary urgency is about 75% predictive for UTI, whereas the acute onset of hesitancy, urinary dribbling, and slow stream is only about 33% predictive for UTI.

Relevant clinical history includes the following:

  • Previous UTI(s)
  • Nocturia, gross hematuria, any changes in the color and/or consistency of the urine
  • Prostatic enlargement
  • Urinary tract abnormalities: Personally and within the family
  • Comorbid conditions (eg, diabetes )
  • Human immunodeficiency virus (HIV) status
  • Immunosuppressive treatments for other conditions (eg, prednisone)
  • Any previous surgeries or instrumentation involving the urinary tract

See Clinical Presentation for more detail.

Diagnosis

Perform a thorough physical examination in males presenting with genitourinary complaints. Focus particularly on the patient’s vital signs, kidneys, bladder, prostate, and external genitalia.

Examination findings may include the following:

  • Fever
  • Tachycardia
  • Flank pain/costovertebral angle tenderness
  • Abdominal tenderness in the suprapubic area
  • Scrotal hematoma, hydrocele, masses, or tenderness
  • Penile meatal discharge
  • Prostatic tenderness
  • Inguinal adenopathy

Laboratory testing

The workup of male UTI is dependent on the suspected diagnosis.

Routine laboratory studies include urine studies, such as urinalysis, Gram staining, and urine culture. The threshold for establishing true UTI includes finding 2-5 or more white blood cells (WBCs) or 15 bacteria per high-power field (HPF) in a centrifuged urine sediment.

Note that a positive nitrite test is poorly sensitive but highly specific for UTI; false-positives are uncommon. Proteinuria is commonly observed in UTIs, but it is usually low grade. More than 2g of protein per 24 hours suggests glomerular disease.

Imaging studies

Consider imaging and urologic intervention in patients with the following:

  • History of kidney stones, especially struvite stones: Potential for urosepsis
  • Diabetes: Susceptibility to emphysematous pyelonephritis and may require immediate nephrectomy; diabetic patients may also develop obstruction from necrotic renal papillae that are sloughed into the collecting system and obstruct the ureter
  • Polycystic kidneys: Prone to abscess formation
  • Tuberculosis: Prone to developing ureteral strictures, fungus balls, and stones

If concomitant obstructive uropathy is suspected, this is an emergent condition that requires prompt intervention, including the following imaging studies of the urinary system:

  • Ultrasonography
  • Contrasted computed tomography (CT) scanning or helical CT scanning (currently preferred by most experts)
  • Intravenous pyelography (IVP) has been replaced by CT scanning techniques and ultrasonography because of its substantial radiation and the necessity of using radiographic dye

See Workup for more detail.

Management

In general, all male UTIs are considered complicated. Consider the potential for renal involvement when planning treatment strategies.

Inpatient management is recommended for patients with the following features:

  • Appear toxic
  • Have obstructive uropathy or stones
  • Unable to tolerate oral hydration
  • Have significant comorbid conditions
  • Unable to care for self at home

Initial inpatient treatment includes the following:

  • Intravenous (IV) antimicrobial therapy with a third-generation cephalosporin (eg, ceftriaxone, ceftazidime), a fluoroquinolone (eg, ciprofloxacin, levofloxacin, ofloxacin, norfloxacin), or an aminoglycoside (eg, gentamicin, tobramycin) (beware ototoxicity)
  • Antipyretics
  • Analgesics
  • IV fluid resuscitation: To restore appropriate circulatory volume and promote adequate urinary flow

Other medications used in the management of male UTIs—or etiologic conditions such as prostatitis; epididymitis; pyelonephritis; or cystitis/urethritis—include the following:

  • Antibiotics such as trimethoprim, trimethoprim-sulfamethoxazole, ampicillin, amoxicillin, ertapenem, erythromycin, vancomycin, doxycycline, aztreonam, nitrofurantoin, rifampin
  • Urinary analgesics such as phenazopyridine

Broaden the antimicrobial coverage and add an antipseudomonal agent in patients with risk factors associated with an unfavorable prognosis (eg, old age, debility, renal calculi, recent hospitalization or instrumentation, diabetes, sickle cell anemia, underlying carcinoma, or intercurrent cancer chemotherapy).

Surgery

Surgical intervention may be required in the patients with the following conditions:

  • Prostatitis involving bladder neck obstruction, prostatic or bladder calculi, or recurrent prostatitis with the same bacteria [1]
  • Emphysematous pyelonephritis (ie, emergent nephrectomy)
  • Epididymitis involving spermatic cord torsion

See Treatment and Medication for more detail.

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Background

The incidence of true urinary tract infection (UTI) in adult males younger than 50 years is low (approximately 5-8 per year per 10,000), with adult women being 30 times more likely than men to develop a UTI. The incidence of UTI in men approaches that of women only in men older than 60 years. (See Epidemiology.)

The causes of male UTI addressed in this article include prostatitis, epididymitis, orchitis, and—as they apply to adult males—pyelonephritis, cystitis, and urethritis. Nosocomial urinary tract infections (UTIs) and their main risk factor, indwelling urethral catheters, are also discussed, with attention directed to unique aspects of the male urinary system. (See Pathophysiology, Etiology, Workup, and Treatment.)

For special hosts (eg, patients with spinal injury, diabetes, or transplants) and special conditions (eg, candiduria, perirenal abscess), see more detailed discussions in Cystitis in Females and Pediatric Urinary Tract Infection.

For issues relating to multidrug-resistant organisms (eg, Acinetobacter) or particular organism infections (eg, gonorrhea, schistosomiasis), consult those specific articles.

Complications

Complications of acute bacterial prostatitis include bacteremia, septic shock, prostatic abscess, epididymitis, seminal vesiculitis, and pyelonephritis. Suspect a prostate abscess if fever does not resolve within 48 hours; if confirmed, add anaerobic coverage and arrange for drainage. (See Prognosis.)

Gonococcal and nongonococcal urethritis may progress to prostatitis, epididymitis, or orchitis, especially in younger patients. Urethral strictures (secondary to inflammation within the urinary tract) may form in up to 5% of patients; this must be kept in mind when evaluating patients with residual obstructive symptoms after treatment.

Other complications from UTI include fistula formation, recurrent infection, bacteremia, hydronephrosis and pyonephrosis, and gram-negative sepsis. Pyonephrosis refers to infected hydronephrosis associated with suppurative destruction of the kidney parenchyma, which results in nearly total loss of renal function.

Complication risk factors appear to be prolonged use of aminoglycosides (>2wk), high serum trough levels (>2), advanced age, baseline renal insufficiency, concomitant conditions (eg, diabetes mellitus), and concomitant nephrotoxic drugs (eg, amphotericin B). (See Presentation and Workup.)

Patient education

For patient education information, see the Cancer Center and the Men's Health Center, as well as Urinary Tract Infections (UTIs), Prostate Infections, Epididymitis, Inflammation of the Testicle (Orchitis), Urethritis in Men, and Bladder Cancer.

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Anatomy

The normal male urinary tract has many natural defenses to infection. Transitional epithelium conducts urine from the kidneys to an elastic bladder, which can store large volumes at low pressures. The male urethra is separated from the rectum by several centimeters of keratinized squamous epithelium; the long urethra provides an additional barrier between the bladder and the perineum.

Because of these many defenses, many experts consider UTIs in males, by definition, to be complicated. Complicated infections are those that are more likely to be associated with anatomic abnormalities, requiring surgical intervention to prevent sequelae. The diagnosis and treatment of UTIs in males should proceed with this concept in mind.

UTIs can be divided anatomically into upper- and lower-tract infections. In the male, lower-tract disease includes prostatitis, epididymitis, cystitis, and urethritis. Upper-tract disease (pyelonephritis) is similar in males and females. The phrase "significant bacteriuria" is sometimes used to emphasize that the number exceeds that which might be caused by contamination during the collection of the specimen. Bacteriuria can be symptomatic or asymptomatic.

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Pathophysiology

As with females, the usual route of inoculation in males is with gram-negative aerobic bacilli from the gut, with Escherichia coli being the most common offending organism. Recent hospitalization, urinary catheter, and fluoroquinolone use in the past 6 months are independent risk factors for fluoroquinolone resistance in community-onset febrile E coli UTI. Fluoroquinolone resistance may be a marker of broader resistance, including extended-spectrum beta-lactamase (ESBL) positivity.[2]

In the normal host, UTI may occur due to infection of other portions of the genitourinary tract, typically the prostate. Older males with prostatic hypertrophy have incomplete bladder emptying, predisposing them to UTI on the basis of urinary stasis. However, in males aged 3 months to 50 years, the incidence of UTI is low; therefore, the possibility of an anatomic abnormality must be entertained in this age group.

Entry of microorganisms into the prostate gland almost always occurs via the urethra; with intraprostatic reflux of urine, bacteria migrate from the urethra or bladder through the prostatic ducts. Other possibilities include entry via the hematogenous route, via the lymphatics from the rectum, and during prostate surgery. However, many patients have no known precipitating event.

Prostatic fluid contains various antibacterial substances, including zinc and antibodies, which are lacking in some patients with chronic bacterial prostatitis. Interestingly, acute prostatitis usually does not result in chronic prostatitis, and chronic bacterial prostatitis is usually not antedated by acute prostatitis. Of men referred for prostatitis, less than 10% have either acute or chronic bacterial prostatitis.

Acute and chronic prostatitis

In the 1800s, prostatitis was thought to be secondary to excessive alcohol consumption or physical or sexual activity. It was often associated with gonorrhea and could be fatal or lead to abscess formation. By the 1920s, most cases were attributed to microorganisms, and antibiotics combined with prostate massage were standard therapy after World War II. Although the role of bacteria was questioned in the 1950s, it was reemphasized in 1968 when Meares and Stamey described their "4-glass test."[3]

Acute prostatitis is caused by an acute infection of the entire prostate gland, resulting in fever and localized pain. Microscopically, neutrophilic infiltrates, diffuse edema, and microabscesses may be seen, which may coalesce into larger collections.

Chronic prostatitis may be caused by inflammatory or noninflammatory diseases. This condition may arise via dysfunctional voiding, intraprostatic reflux, chronic exposure to microorganisms, autoimmune mechanisms, irritative urinary metabolites, and as a variant of neuropathic pain. Chronic bacterial prostatitis often produces few or no symptoms related to the prostate, but it is probably the most common cause of relapsing UTI in men.

Chronic prostatitis has been subdivided by the National Institutes of Health (NIH) into the following categories:

  • Category II: Chronic bacterial prostatitis
  • Category III: Chronic abacterial prostatitis. Category IIIA is chronic, inflammatory abacterial prostatitis, and category IIIB is chronic, noninflammatory abacterial prostatitis, also known as chronic pelvic pain or prostatodynia.
  • Category IV: Asymptomatic, inflammatory prostatitis

Chronic bacterial prostatitis is the most common cause of relapsing UTI in men, with E coli as the main causative organism (80%), but other gram-negative bacteria and enterococci may also be observed. Rare cases may be caused by yeasts (eg, Candida, Blastomyces, Histoplasma, Cryptococcus) and mycobacteria. Whether Staphylococcus epidermidis, S aureus, and diphtheroids are pathogenically significant is doubtful, and the evidence supporting a causative role for Chlamydia and Ureaplasma is not convincing.[4]

Epididymitis

Epididymitis is a clinical syndrome caused by infection or inflammation of the epididymis. This condition is the most common cause of acute scrotum in adult male populations. Long-term complications include abscesses, infarction, recurrence, chronic pain, and infertility

The pathophysiology of epididymitis is divided; Chlamydia trachomatis and Neisseria gonorrhoeae are the most common pathogens in patients younger than 35 years, whereas Enterobacteriaceae and gram-positive cocci are frequent pathogens in older patients. In either case, infection results from retrograde ascent of infected urine from the prostatic urethra into the vas deferens and, finally, into the epididymis.

Orchitis

Because of the widespread use of mumps vaccination, orchitis is no longer a common infection in the United States. Orchitis is one of the few genitourinary infections to result from a viral pathogen.

Mumps orchitis occurs in 18% of postpubertal boys infected with the mumps virus. Other viruses that can cause the disease include coxsackie B, mononucleosis, and varicella. Unlike the majority of genitourinary infections, viral particles are spread to the testicle by the hematogenous route. Granulomatous orchitis is rare and results from hematogenous dissemination of tuberculosis, fungi, and actinomycosis.

Pyelonephritis

Pyelonephritis is an infection of the renal parenchyma. Infection usually occurs in a retrograde, ascending fashion from the bladder, but it may occur hematogenously. The ureteral orifice becomes edematous and loses its one-way valve function during infection. Retrograde flow of bacteria into the upper urinary tracts and into the renal parenchyma results in clinical symptoms.

Bacteremia, particularly with virulent organisms such as S aureus, can result in pyelonephritis with focal renal abscesses. Bacterial adherence allows for mucosal colonization and subsequent infection by an ascending route. Whereas type 1 pili are produced by most uropathogenic strains of E coli, P-pili, which bind to the uroepithelial glycosaminoglycan layer, are found in most strains of E coli that cause pyelonephritis. Genotypic factors may affect uroepithelial susceptibility to these adherence molecules. Endotoxin from gram-negative organisms can retard ureteral peristalsis.

E coli is responsible for approximately 25% of cases in males, with Proteus and Providencia causing many remaining infections; Klebsiella, Pseudomonas, Serratia, and enterococci are less frequent.

Bacterial cystitis

Bacterial cystitis without concomitant infection in other portions of the genitourinary tract is believed to be a rare event in males. The abrupt onset of irritative voiding symptoms (eg, frequency, urgency, nocturia, dysuria) and suprapubic pain are clinically diagnostic.

Most cases of bacterial cystitis occur by an ascending mechanism. Bacterial cystitis in the male is uncommon in the absence of anatomic abnormality, defect in bladder emptying mechanism, or urethral catheterization (eg, poor bladder emptying from prostatic obstruction or dysfunctional voiding). Elevated postvoid residuals allow bacteria to multiply to critical levels. High voiding pressures and poor bladder compliance diminish the natural uroepithelial resistance to infection.

Urethritis

Urethritis has been described for thousands of years. The term gonorrhea (gonus meaning seed, rhoia meaning flow) was coined by Galen. The urethral nonsquamous epithelium can be penetrated by N gonorrhoeae, resulting in periurethral microabscesses. Necrotic debris is sloughed into the urethra lumen, producing a milky penile discharge.

Gonococcal urethritis remains the most commonly reported communicable bacterial disease in the United States.

Urinary catheter–associated UTIs

Up to 25% of hospitalized patients have urinary catheters inserted; of these individuals, 10-27% develop UTIs. In fact, UTI accounts for approximately 40% of all nosocomial infections; 15% of these infections occur in clusters and often involve highly resistant organisms.

The single most important risk factor for nosocomial bacteriuria and UTI is the presence of an indwelling urethral catheter; 80% of nosocomial UTIs are associated with the use of urethral catheters. Once the urethral catheter is in place, the daily incidence of bacteriuria is 3-10%. Because most patients who become bacteriuric do so by 30 days, that is a convenient dividing line between short- and long-term catheterization.

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Etiology

Risk factors for UTI and bacterial causes of prostatitis, epididymitis, orchitis, pyelonephritis, cystitis, and urethritis are discussed in this section.

Risk factors

Obstruction from any cause is a major risk factor for the development of UTI, as are instrumentation of the urinary tract, catheterization, and urologic surgery.

In males older than 50 years, prostatic hypertrophy with partial obstruction is the main contributor to the increase in UTI. Risk factors observed more commonly in elderly or institutionalized males include cognitive impairment, fecal or urinary incontinence, and the use of catheters.

Catheter-associated bacteriuria risk factors include female sex, significant comorbid conditions (especially diabetes mellitus), age older than 50 years, lack of systemic antibiotic(s), and a serum creatinine level greater than 2mg/dL.

Risk factors for bacteremia secondary to catheter-associated UTI (CAUTI) are male sex, UTI caused by Serratia marcescens, older age, underlying urologic disease, and an indwelling catheter.

In young men, risk factors for acute cystitis include homosexual behavior with anal intercourse, intercourse with a female infected or colonized with a uropathogen, lack of circumcision, and human immunodeficiency virus (HIV) infection with CD4 counts of 200/μL or less.

Prostatitis

Gram-negative uropathogens (eg, Enterobacteriaceae, such as E coli, Klebsiella, and Pseudomonas) are acknowledged pathogens of the prostate. Probable pathogens include Enterococcus and S aureus, and possible pathogens include coagulase-negative Staphylococcus, Chlamydia, Ureaplasma, anaerobes, Candida, and Trichomonas. Acknowledged nonpathogens of the prostate include diphtheroids, lactobacilli, and Corynebacterium. Bacterial pathogens cannot be demonstrated in cases of nonbacterial prostatitis.

Viruses and cell wall–deficient bacteria have a controversial association with prostatitis. Rare cases have been reported from Clostridia and Burkholderia (formerly Pseudomonas) pseudomallei (the causative agent of melioidosis).

Unusual pathogens reported in patients with acquired immunodeficiency syndrome (AIDS) include cytomegalovirus (CMV) and some fungi (Aspergillus, Histoplasma, and Cryptococcus). The prostate is a known reservoir for Cryptococcus neoformans.

Epididymitis

Chlamydia trachomatis and N gonorrhoeae are the most common pathogens in patients younger than 35 years with UTI, whereas Enterobacteriaceae and gram-positive cocci are frequent pathogens in older patients.

Orchitis

Orchitis is one of the few genitourinary infections resulting from viral pathogens, such as the mumps, coxsackie B, Epstein-Barr (EBV), and varicella (VZV) viruses. Granulomatous orchitis is rare and results from hematogenous dissemination of tuberculosis, fungi, and actinomycosis. Brucella also been associated with orchitis; clinically, these patients resemble patients with tuberculosis. Colorado tick fever has also been associated with epididymo-orchitis.

Secondary orchitis is a more common condition; it is a late complication of untreated epididymitis.

Pyelonephritis and cystitis

Bacteria responsible for pyelonephritis and cystitis in males include E coli, Klebsiella, Enterobacter, Proteus, Pseudomonas, Serratia, Enterococcus, and Staphylococcus species.

Urethritis

N gonorrhoeae is the most common cause of urethritis in males; nongonococcal causes of urethritis include C trachomatis (in up to 50% of cases), Ureaplasma urealyticum, Trichomonas vaginalis, and herpes simplex virus (HSV). The role of Mycoplasma in urethritis is controversial.

Catheter-associated bacteriuria

Short-term catheters are placed for a mean duration of 2-4 days. The usual indications are for acute illnesses, output measurement, perioperative routine, and acute retention. Approximately 15% of patients develop bacteriuria, usually with a single organism (E coli). Catheter-associated bacteriuria usually resolves after the catheter is removed; however, one third of patients may have symptoms, and bacteremia is the most serious complication. Approximately 10-30% of patients develop a fever, and the risk of postoperative wound infection associated with bacteriuria is increased.

Long-term catheters are placed for chronic medical or neurologic problems, including chronic urinary retention and incontinence. Essentially all patients develop bacteriuria, which is polymicrobial in up to 95% of cases. New pathogens often emerge, whereas many persist because of adherence properties (fimbrial adhesion in Providencia and E coli) or their effect on the local environment (Proteus and Morganella).

Catheter obstruction in long-term catheterization may occur, via an interaction between bacteria, the glycocalyx, protein, and crystals; Proteus mirabilis is a potent producer of urease, which alkalinizes the urine, precipitating struvite and apatite.

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Epidemiology

Although this article exclusively addresses UTI in males, the clinician should appreciate that the incidence of UTI is much higher in females during adolescence and childbearing years (adult women are 30 times more likely than men to develop a UTI). The incidence of UTI in men approaches that of women only in males older than 60 years; in men aged 65 years or older, 10% have been found to have bacteriuria, as compared with 20% of women in this age group.

Internationally, there is a similar incidence in developed countries; however, in developing countries where men have shorter life spans, the incidence of UTI due to prostatic hypertrophy is lower.

Young men rarely develop UTIs, and the prevalence of bacteruria is 0.1% or less. There is an early peak incidence during the first 3 months of life; in neonates, UTIs occur more frequently in boys than in girls (with a male-to-female ratio of 1.5:1), and they are often part of the syndrome of gram-negative sepsis. The cumulative incidence of symptomatic UTI (including pyelonephritis) in boys during the first 10 years of life has been reported at 1.1-1.6%.

The incidence of true UTI in adult males younger than 50 years is low (approximately 5-8 per year per 10,000). In this population, the symptoms of dysuria or urinary frequency are usually due to sexually transmitted disease (STD)–related infections of the urethra (eg, gonococcal and nongonococcal urethritis) and prostate.[5]

In men older than 50 years, the incidence of UTI rises dramatically (range, 20-50% prevalence), because of enlargement of the prostate, prostatism, debilitation, and subsequent instrumentation of the urinary tract. The spectrum of causative agents is also somewhat broader in these older men.

Prostatitis, epididymitis, urethritis, and orchitis

In contrast to UTI, prostatitis affects men of all ages and, from 1990-1994, accounted for almost 2 million office visits per year in the United States. Prostatitis syndromes account for 25% of male office visits for genitourinary complaints, 8% of visits to urologists, and 1% of visits to primary care physicians. Of these men, 5% have bacterial prostatitis, 64% have nonbacterial prostatitis, and 31% have prostatodynia.

Epididymitis has a bimodal distribution, corresponding to different age groups and pathogens. Most cases in men younger than 35 years are due to sexually transmitted pathogens. Older patients are more likely to have obstructive prostatism or a history of instrumentation or catheterization.

Gonococcal urethritis is more common in ethnic minorities, lower socioeconomic groups, and persons living in urban centers. The risk to a male having intercourse with an infected female is 17%. Some of these associations may be limited by confounding. The peak age for urethritis is 20-24 years.

Mumps orchitis occurs in 18% of postpubertal boys infected with the mumps virus.

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Contributor Information and Disclosures
Author

John L Brusch, MD, FACP Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

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, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Bryan P Blair, MD Staff Physician, Department of Urology, Naval Medical Center at Portsmouth

Disclosure: Nothing to disclose.

David S Howes, MD Professor of Medicine and Pediatrics, Section Chief and Emergency Medicine Residency Program Director, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

David S Howes, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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 Thoracic Society, and Society of Critical Care Medicine

Disclosure: Sepracor None None

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.

M Tyson Pillow, MD Assistant Director of Medical Education, Ben Taub General Hospital Emergency Center; Assistant Professor, Baylor College of Medicine

M Tyson Pillow, MD is a member of the following medical societies: Air Medical Physician Association, American College of Emergency Physicians, American Medical Association, American Medical Student Association/Foundation, Emergency Medicine Residents Association, Society for Academic Emergency Medicine, and Student National Medical Association

Disclosure: Nothing to disclose.

Joseph A Salomone III, MD Associate Professor and Attending Staff, Truman Medical Centers, University of Missouri-Kansas City School of Medicine; EMS Medical Director, Kansas City, Missouri

Joseph A Salomone III, MD is a member of the following medical societies: American Academy of Emergency Medicine, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Cindy L Tamminga, MD Consulting Staff, Division of Infectious Diseases, Naval Medical Center at Portsmouth

Disclosure: Nothing to disclose.

References
  1. Doluoglu OG, Gokkaya CS, Aktas BK, et al. Impact of asymptomatic prostatitis on re-operations due to urethral stricture or bladder neck contracture developed after TUR-P. Int Urol Nephrol. 2012 Jan 18. [Medline].

  2. van der Starre WE, van Nieuwkoop C, Paltansing S, et al. Risk factors for fluoroquinolone-resistant Escherichia coli in adults with community-onset febrile urinary tract infection. J Antimicrob Chemother. 2011 Mar. 66(3):650-6. [Medline].

  3. Meares EM, Stamey TA. Bacteriologic localization patterns in bacterial prostatitis and urethritis. Invest Urol. 1968 Mar. 5(5):492-518. [Medline].

  4. Chung SD, Keller JJ, Lin HC. A case-control study of chronic prostatitis/chronic pelvic pain syndrome and colorectal cancer. BJU Int. 2012 Feb 7. [Medline].

  5. Foxman B. Epidemiology of urinary tract infections: incidence, morbidity, and economic costs. Am J Med. 2002 Jul 8. 113 Suppl 1A:5S-13S. [Medline].

  6. Johnson JR. Laboratory diagnosis of urinary tract infections in adult patients. Clin Infect Dis. 2004 Sep 15. 39(6):873; author reply 873-4. [Medline].

  7. Chiang IN, Chang SJ, Pu YS, Huang KH, Yu HJ, Huang CY. Major complications and associated risk factors of transrectal ultrasound guided prostate needle biopsy: a retrospective study of 1875 cases in Taiwan. J Formos Med Assoc. 2007 Nov. 106(11):929-34. [Medline].

  8. Nickel JC. The Pre and Post Massage Test (PPMT): a simple screen for prostatitis. Tech Urol. 1997 Spring. 3(1):38-43. [Medline].

  9. Daunt SW. Accuracy of ultrasonography and plain-film abdominal radiography in the diagnosis of urologic abnormalities in men with urinary tract infection: critically appraised topic. Can Assoc Radiol J. 2004 Feb. 55(1):16-7. [Medline].

  10. Guay DR. Contemporary management of uncomplicated urinary tract infections. Drugs. 2008. 68(9):1169-205. [Medline].

  11. Howes DS, Bogner MP. Urinary tract infections. Tintinalli JE, Kelen GD, Stapczyski JS, eds. Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill; 2008.

  12. Talan DA, Krishnadasan A, Abrahamian FM, Stamm WE, Moran GJ. Prevalence and risk factor analysis of trimethoprim-sulfamethoxazole- and fluoroquinolone-resistant Escherichia coli infection among emergency department patients with pyelonephritis. Clin Infect Dis. 2008 Nov 1. 47(9):1150-8. [Medline].

  13. Cunha BA. Antibiotic Essentials. 7th ed. Royal Oak, Mich: Physicians Press.; 2008.

  14. Killgore KM, March KL, Guglielmo BJ. Risk factors for community-acquired ciprofloxacin-resistant Escherichia coli urinary tract infection. Ann Pharmacother. 2004 Jul-Aug. 38(7-8):1148-52. [Medline].

  15. [Guideline] Workowski KA, Berman SM. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep. 2006 Aug 4. 55:1-94. [Medline]. [Full Text].

  16. Douglas D. Tadalafil confirmed as helpful in LUTS/BPH. Reuters Health Information. August 20, 2013. Available at http://www.medscape.com/viewarticle/809664. Accessed: August 29, 2013.

  17. Wagenlehner FM, Naber KG. Fluoroquinolone Antimicrobial Agents in the Treatment of Prostatitis and Recurrent Urinary Tract Infections in Men. Curr Infect Dis Rep. 2005 Jan. 7(1):9-16. [Medline].

  18. Wagenlehner FM, Naber KG. Current challenges in the treatment of complicated urinary tract infections and prostatitis. Clin Microbiol Infect. 2006 May. 12 Suppl 3:67-80. [Medline].

  19. Luzzi G. Chronic prostatitis. N Engl J Med. 2007 Jan 25. 356(4):423-4; author reply 424. [Medline].

  20. Wagenlehner FM, Weidner W, Naber KG. Therapy for prostatitis, with emphasis on bacterial prostatitis. Expert Opin Pharmacother. 2007 Aug. 8(11):1667-74. [Medline].

  21. Yoon BI, Kim S, Han DS, et al. Acute bacterial prostatitis: how to prevent and manage chronic infection?. J Infect Chemother. 2012 Jan 5. [Medline].

  22. [Guideline] Hooton TM, Bradley SF, Cardenas DD, Colgan R, Geerlings SE, Rice JC, et al. Diagnosis, prevention, and treatment of catheter-associated urinary tract infection in adults: 2009 International Clinical Practice Guidelines from the Infectious Diseases Society of America. Clin Infect Dis. 2010 Mar 1. 50(5):625-63. [Medline]. [Full Text].

  23. [Guideline] Gould CV, Umscheid CA, Agarwal RK, Kuntz G, Pegues DA. Guideline for prevention of catheter-associated urinary tract infections 2009. Infect Control Hosp Epidemiol. 2010 Apr. 31(4):319-26. [Medline]. [Full Text].

  24. Saint S, Elmore JG, Sullivan SD, Emerson SS, Koepsell TD. The efficacy of silver alloy-coated urinary catheters in preventing urinary tract infection: a meta-analysis. Am J Med. 1998 Sep. 105(3):236-41. [Medline].

  25. [Guideline] CDC. Update to CDC's sexually transmitted diseases treatment guidelines, 2006: fluoroquinolones no longer recommended for treatment of gonococcal infections. MMWR Morb Mortal Wkly Rep. 2007 Apr 13. 56(14):332-6. [Medline]. [Full Text].

  26. McNaughton Collins M, Fowler FJ Jr, Elliott DB, Albertsen PC, Barry MJ. Diagnosing and treating chronic prostatitis: do urologists use the four-glass test?. Urology. 2000 Mar. 55(3):403-7. [Medline].

  27. Porst H, Oelke M, Goldfischer ER, Cox D, Watts S, Dey D, et al. Efficacy and Safety of Tadalafil 5 mg Once Daily for Lower Urinary Tract Symptoms Suggestive of Benign Prostatic Hyperplasia: Subgroup Analyses of Pooled Data From 4 Multinational, Randomized, Placebo-controlled Clinical Studies. Urology. 2013 Jul 19. [Medline].

  28. Olson PD, Hruska KA, Hunstad DA. Androgens Enhance Male Urinary Tract Infection Severity in a New Model. J Am Soc Nephrol. 2015 Oct 8. [Medline].

 
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Prostatic calcifications in a male with a urinary tract infection.
Bladder calculi in a male with a urinary tract infection.
 
 
 
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