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Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996.

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Medical Microbiology. 4th edition.

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Chapter 97Microbiology of the Genitourinary System

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General Concepts

Clinical Presentations

In women, genital infections may cause a vaginal discharge, mucosal ulceration producing local discomfort and pain on intercourse, or pelvic inflammatory disease. Ongoing infection of the upper genital tract leads to infertility, ectopic pregnancies and chronic pelvic pain. In men, genital infection may cause urethral discharge, pain on voiding, and painful scrotal swellings. Genital ulcers are usually painful. Some diseases cause enlarged inguinal lymph nodes.

Etiology

Primary genitourinary infections are usually sexually transmitted; common pathogens include parasites (Trichomonas vaginalis), bacteria (Treponema pallidum, Neisseria gonorrhoeae, Chlamydia trachomatis, Haemophilus ducreyi), and viruses (herpes simplex virus, human papillomavirus, human immunodeficiency virus). Members of the normal flora, such as the fungus Candida albicans, may cause opportunistic infections.

Pathogenesis

Pathogens may enter the genital tract by local invasion or ascending infection. Treponema pallidum, H ducreyi, herpes simplex virus, etc., locally invade the skin and mucous membranes. T pallidum and Human Immunodeficiency Virus disseminate via the bloodstream to distant sites. Other pathogens such as N gonorrhoeae cause ascending infection through the urethra and cervix. Infants born through a genital tract infected with some of these pathogens may become infected.

Microbiologic Diagnosis

The organisms responsible for genital infections are generally fastidious and often difficult to culture. Specimens must be correctly collected and transported. Dark-field examination and serologic studies are necessary to diagnose syphilis; specialized tissue culture or antigen detection techniques are used for C trachomatis, viral culture for herpes simplex virus, and specialized media for culturing N gonorrhoeae and H ducreyi.

Prevention and Treatment

Education to modify sexual behavior and use of condoms are essential. Screening asymptomatic individuals in some populations and case contact tracing are also effective measures. Effective drug therapies exist for all bacterial genital infections and for herpes simplex.

Urinary Tract Infections

Clinical Manifestations

Urinary tract infections in adults may cause painful, frequent urination with a feeling of incomplete emptying of the bladder, perineal pain, fever, chills, and back pain. Most elderly patients are asymptomatic, and in small children, the symptoms are nonspecific.

Etiology

Most urinary infections are caused by bacteria from the intestinal flora. Eschericia coli causes about 70 percent of all infections. Staphylococcus saprophyticus causes about 10 percent of infections in young women. Pseudomonas aeruginosa, Serratia marcescens, Enterococcus faecalis, and Staphylococcus epidermidis are common hospital-acquired pathogens. Yeasts and, in some parts of the world, protozoa are occasional pathogens.

Pathogenesis

Organisms can ascend through the urethra to infect the bladder and renal pelvis. Occasionally, they may interfere with renal function or produce abscesses within renal tissue. Because of the shorter urethra, intercourse can facilitate urinary tract infections in women. Pyuria is almost always present. Hydrolysis of urea by bacteria (e.g., Proteus mirabilis) can cause the formation of struvite stones.

Microbiologic Diagnosis

Presumptive diagnosis can be made by demonstrating pyuria. Quantitative urine culture is essential for diagnosis. Specimens should be refrigerated until cultured to prevent bacterial replication. Properly submitted urine that contains >105 or 108 organisms/ml indicates significant infection. However, with acute cystitis, bacterial counts may be lower. Blood cultures may be positive in patients with pyelonephritis.

Prevention and Treatment

Antimicrobial agents cure most urinary tract infections. Recurrence is common, and may be prevented by prolonged therapy. Prolonged use of a urinary catheter greatly increases the likelihood of a urinary tract infection.

Introduction

Genitourinary infections fall into two main categories: (1) primary infections due to sexually transmitted pathogenic microorganisms and (2) infections due to members of the resident flora. Genital infections are uncommon in children and increase dramatically in sexually active adults, in whom sexually transmitted diseases are the second most prevalent group of reportable communicable illness in North America. Sexually transmitted pathogens include parasites (Trichomonas vaginalis), bacteria (Treponema pallidum, Neisseria gonorrhoeae, Chlamydia trachomatis, Haemophilus ducreyi), and viruses (Herpes simplex virus, human papillomavirus, human immunodeficiency virus). Genital infections due to the fungus Candida albicans or to members of the endogenous bacterial flora (Bacteroides fragilis and members of the family Enterobacteriaceae) are not known to be sexually transmitted. Bacterial vaginosis occurs when the balance of vaginal flora is upset.

The urinary tract and urine are normally sterile. Numerous mechanical and biologic processes ensure that microorganisms do not enter the urinary tract. Women are more susceptible to urinary infections because the female urethra is short and because the area around the urethral opening is colonized with potential pathogens (e.g. E coli and E faecalis).

Urethritis and Epididymitis

Clinical Manifestations

Urethritis (inflammatory disease of the urethra) is characterized by urethral discharge (Table 97-1). The incubation time varies, averaging 3 days for gonococcal urethritis and 7 days for nongonococcal urethritis. The clinical symptoms range from mild to severe. In both men and women, dysuria is common. Discharge and dysuria are seen in 70 percent of patients with gonococcal urethritis, whereas patients with nongonococcal urethritis are more likely to have one or the other of these symptoms but not both. Other symptoms include itching, frequency, urgency, or a feeling of heaviness in the genitals. Polyarthralgia, involving large joints, characteristic rash, and low-grade fever are typically present in patients with disseminated gonococcal infection.

Table 97-1. Gential Infections in Males.

Table 97-1

Gential Infections in Males.

Orchitis and epididymitis are complications of both N gonorrhoeae and C trachomatis infections that present as a painful, swollen mass in the scrotum. Testicular atrophy follows in some patients with orchitis.

Etiology

Neisseria gonorrhoeae and C trachomatis account for most cases of urethritis in men. Chlamydia trachomatis is responsible for 40 to 60 percent of cases of nongonococcal urethritis (Fig. 97-1). The etiology of chlamydia-negative nongonococcal urethritis is uncertain. Ureaplasma urealyticum can cause nongonococcal urethritis; however, the high incidence of this organism in the normal genital flora makes it difficult to interpret its role in nongonococcal urethritis. Less common agents isolated from nongonococcal urethritis include herpes simplex virus and Trichomonas vaginalis. Although gonococcal urethritis is a more acute disease than nongonococcal urethritis, overlap in the symptoms mandates laboratory confirmation. Patients often have multiple sexually transmitted pathogens. Approximately 1/3 of heterosexual men infected with Neisseria gonorrhoeae are concurrently infected with Chlamydia trachomatis. If only the gonococci are treated, these patients develop a nongonococcal urethritis called postgonococcal urethritis. Therefore, patients with gonorrhea should also be treated with agents that will effectively eradicate C trachomatis.

Figure 97-1. Major causes of urethritis.

Figure 97-1

Major causes of urethritis.

Pathogenesis

Neisseria gonorrhoeae and C trachomatis are transmitted by sexual intercourse (Fig. 97-2). Neisseria gonorrhoeae attaches to mucosal cells via pili and other surface proteins. The organism then is phagocytosed and passes through the mucosal epithelium. Proliferation occurs with subsequent influx of polymorphonuclear neutrophils (PMN), which produce the exudate that is the hallmark of gonorrhea. Neisseria gonorrhoeae spreads to cause disseminated gonococcal infection in approximately 1 to 3 percent of patients with gonorrhea. Disseminated gonococcal infection is more prevalent in women than in men. Up to 80 percent of patients with disseminated gonococcal infection have had an asymptomatic local infection for 7 to 30 days prior to dissemination.

Figure 97-2. Pathogenesis of genital tract infections.

Figure 97-2

Pathogenesis of genital tract infections.

Chlamydia trachomatis is an obligate intracellular parasite with a dimorphic life cycle (Fig. 97-3). Urethral infection is asymptomatic in about 30 percent of men. If left untreated, the infection can progress to cause epididymitis. Proctitis also can occur in homosexual males.

Figure 97-3. Replication cycle of Chlamydia (EB, elementary body; RB, reticulate body).

Figure 97-3

Replication cycle of Chlamydia (EB, elementary body; RB, reticulate body).

Microbiologic Diagnosis

Neisseria gonorrhoeae

Diagnosis of gonorrhea is based on microscopic examination of exudate, culturing of the organism, and rapid methods such as antigen or nucleic acid detection. Urethral exudates should be examined by Gram stain for leukocytes and Gram-negative intracellular diplococci. The Gram stain has good sensitivity (90 percent) and specificity (95 percent) in males. Ideally, urethral exudate should be planted directly onto a split plate containing modified Thayer-Martin and chocolate agar. The Thayer-Martin agar contains vancomycin, colistin, nalidixic acid and trimethoprim. Approximately 5 percent of strains of N gonorrhoeae are susceptible to vancomycin, thus necessitating the use of a non-inhibitory medium such as chocolate agar. The medium is incubated in 5 percent CO2 in a moist environment for 48 hours. Neisseria gonorrhoeae grows as translucent gray colonies that are oxidase-positive. The identity of the cultures is confirmed by carbohydrate utilization: glucose is fermented, but lactose, maltose and sucrose are negative. Fluorescent-antibody analysis using monoclonal antibodies may also be used to confirm the identity of cultures. Culture confirmation can also be performed using DNA probes that detect specific sequences of the rRNA of N gonorrhoeae.

Chlamydia trachomatis

Diagnosis of C trachomatis infection involves growing the organism in tissue culture or using direct bacterial antigen detection techniques. Since the organism is an intracellular parasite, infected urethral cells must be collected on the swab sample. The best transport media are 2-sucrose-phosphate or sucrose-glutamate-phosphate. If swab specimens are not processed immediately, they should be stored at -70°C prior to culturing. The swabs are then used to inoculate cell culture lines that have been treated with cyclohexamide. After 48 to 72 hours, the monolayer is fixed and, after staining, is examined for chlamydial inclusion bodies. Because of the labor intensiveness of tissue culture, direct antigen detection methods have been developed for C trachomatis. These include either direct visualization of the organism using fluorescein-conjugated antibodies or enzyme-like immunosorbent assay (ELISA) methods which detect solubilized chlamydial LPS. Serologic tests based on either complement fixation or microimmunofluorescence are available in specialized laboratories. Nucleic acid detection systems using amplification steps are now commercially available.

Prevention and Treatment

No vaccines exist for N gonorrhoeae or Chlamydia trachomatis. Control requires modification of sexual behavior and cure of the patient and their contacts.

For gonorrhea, ceftriaxone is the drug of choice. Resistance to penicillin due to β-lactamase has been increasing; therefore, all isolates of N gonorrhoeae should be tested for β-lactamase production and susceptibility testing performed if the strain is β-lactamase positive. Gonorrhea is a reportable disease, and contact tracing is one strategy to contain the spread of infection. As mentioned previously, all patients being treated for gonorrhea should be concomittantly treated for the agents of nongonococcal urethritis such as C trachomatis. Thus, ceftriaxone combined with tetracycline is an optimal regime. Recently azithromycin given as a single oral dose has been recommended for treatment of C trachomatis. This approach leads to better compliance.

Vaginitis, Cervicitis, Endometritis, and Pelvic Inflammatory Disease

Clinical Presentation

Endometritis and pelvic inflammatory disease usually result from ascending vaginal or cervical infections (Table 97-2). Vaginal infections seldom have systemic manifestations; they present as an abnormal vaginal discharge that may have an unusual odor. Pruritus may also be present. The consistency of the discharge often reflects the nature of the disease. A thin watery discharge that sticks to the anterior and lateral vaginal walls is seen in bacterial or non-specific vaginosis; the vaginal walls appear normal. In candidiasis the vaginal walls are erythematous, and in trichomoniasis they have a strawberry appearance and the vaginal discharge is green and frothy. A yellow, purulent discharge suggests cervicitis or other forms of vaginitis. In prepubertal girls, gonorrhea causes an inflammatory response in the vagina, whereas following puberty, the infection is primarily a cervicitis. Mucosal ulceration of the vagina results in local discomfort and pain on intercourse. Abdominal discomfort is rare in vaginitis, and is more suggestive of cystitis or pelvic inflammatory disease.

Table 97-2. Genital Infections in Females.

Table 97-2

Genital Infections in Females.

Etiology

About one-half of the cases of vaginitis are due to Candida albicans or Trichomonas vaginalis (Fig. 97-4). The rest are classified as bacterial vaginosis. Bacterial vaginosis involves an upset in the distribution of the normal flora that is associated with an increase in the numbers of Gardnerella vaginalis mobilencus sp. and anaerobes of the Bacteroides group. Since 40 to 50 percent of normal individuals may carry Gardnerella vaginalis, isolation of the organism does not reliably predict bacterial vaginosis. However, the absence of this organism almost rules out bacterial vaginosis.

Figure 97-4. Major causes of vaginitis.

Figure 97-4

Major causes of vaginitis.

Neisseria gonorrhoeae and C trachomatis are responsible for the majority of cervical infections (Fig. 97-5). Sexually transmitted infections with more than one pathogen are common. Due to the overlap in clinical features, accurate diagnosis requires laboratory confirmation. About two-thirds of women infected with N gonorrhoeae or C trachomatis do not exhibit purulent cervical discharge. Therefore, for both gonococcal and chlamydial cervicitis, physical examination is not adequate to exclude these infections. Herpes simplex is an occasional cause of cervicitis in women and can be isolated from approximately 90 percent of women with primary herpes simplex virus infection.

Figure 97-5. Major causes of cervicitis.

Figure 97-5

Major causes of cervicitis.

Pathogenesis

Vaginitis due to T vaginalis and C albicans remains localized, producing vaginal discharge and itching. Yeasts are part of the normal flora in 50 percent of adult women of child-bearing age. Antibiotics such as tetracyclines disturb the balance of the flora and cause overgrowth by C albicans,with resulting vulvovaginal candidiasis.

Trichomonas vaginalis infection is superficial; penetration of the vaginal epithelial cells has not been described. Inflammation of the vaginal walls and exocervix includes erythema, punctate hemorrhages, and small ulcerations. The pH of the vaginal discharge is often greater than 4.5.

Ascending infection may take the form of salpingo-oophoritis or pelvic inflammatory disease. The onset of ascending infection frequently coincides with menses. Ascending genital infection occurs in approximately 10 to 20 percent of women with Neisseria gonorrhoeae with endocervical infection.

Gonococcal ophthalmia neonatorum occurs as a result of the passage of the newborn through the birth canal of infected mothers.

The infective life cycle of C trachomatis is summarized in Figure 97-2. The organism spreads by ascending infection from the vagina and endocervix to the endometrium, fallopian tubes and other contiguous structures. Pelvic inflammatory disease can be an acute or a chronic complication of endocervitis. Infection results in scarring of the fallopian tubes; this accounts for the ten-fold increase in risk of ectopic pregnancies in women with a history of pelvic inflammatory disease. Each episode of pelvic inflammatory disease also increases the incidence of sterility.

Microbiologic Diagnosis

A wet mount is the optimal method for detecting T vaginalis or C albicans in patients with vaginitis. However, the wet mount is negative in 30 percent of symptomatic women with trichomoniasis and therefore does not rule out this infection. Active vaginal candidiasis is characterized by many yeast cells with active budding. Low numbers of Gardnerella vaginalis are often present in women who do not have nonspecific vaginitis. Gram-stained smears that show no lactobacilli but many curved, Gram-negative rods are very suggestive of nonspecific vaginitis. According to current recommendations, a diagnosis of nonspecific vaginitis should be based on a positive Gram-stained smear in conjunction with a vaginal pH greater than 4.5 and a positive “whiff test”.

Microbiologic diagnosis of N gonorrhoeae involves examining Gram-stained cervical exudate, as well as culturing the organism on selected media such as modified Thayer-Martin agar. The sensitivity of the Gram stain is substantially lower for exudates from women than from men: it is positive in only about 80 percent of women with cervical gonorrhea. If pelvic inflammatory disease or pelvic abscesses are suspected, material should, if possible, be aspirated from the infected site, smeared, and cultured.

Microbiologic diagnosis for C trachomatis is performed by either tissue culture or antigen detection techniques. Cervical mucus should be cleared, and then a second sample taken by vigorously rubbing the cervical orifice to ensure that cervical cells are sampled, since C trachomatis is an intracellular parasite. The methods used for culturing and antigen detection are described above.

Prevention and Treatment

There are no vaccines for any of these sexually transmitted diseases. Preventive measures are directed at education with emphasis on safe sexual behavior. Barrier methods such as condoms are essential to decreasing the spread of genital infections. Contact tracing of the reportable infections has also been invaluable. Trichomonas infection is treated with metronidazole either as a single oral dose of 2 g or as 250 mg orally three times a day for 7 days. Treatment of candidal infection requires local application of an antifungal agent. The imadiazoles (e.g. clotrimazole or miconazole) are usually more effective than the polyenes (e.g. nystatin). The usual length of treatment is 3 days. Women who have frequent recurrences may be left on longer courses of systemic or local therapy.

Genital Ulcer Disease

Clinical Manifestations

Genital ulcers are transmitted by sexual intercourse and can be caused by a variety of microorganisms. However, some clinical features are found more commonly with a particular etiologic agent. Up to one-third of the episodes of genital ulceration have a clinical diagnosis that did not agree with the microbiologic diagnosis. This indicates the importance of microbiologic confirmation of diagnosis for genital ulcers. In developed countries, the most common genital ulcer diseases are herpes simplex, followed by syphilis. In developing countries, the most common causes of genital ulceration are chancroid, followed by syphilis, lymphogranuloma venereum and granuloma inguinale. The reason for this difference in prevalence between different geographical locations is not understood. The variable incubation period for genital ulcers and the fact that initial lesions are often overlooked are two factors that lead to the increased dissemination of these diseases. Genital ulcers increase the risk of heterosexual transmission of AIDS.

The incubation period for chancroid ranges from 3 to 10 days. The ulcers begin as small, inflammatory papules that develop into ulcers that have an undermined edge, contain purulent exudate and bleed easily. Chancroid is a sexually transmitted disease that is more prevalent in males than females, with a ratio of approximately 8:1. In men, the ulcer is located primarily on the prepuce and around the coronal sulcus. In women, the forchette, labia and perianal area can be involved. Multiple “kissing” ulcers (ulcers in direct opposition to each other) are common. Approximately one-third of the patients with chancroid also have enlarged inguinal lymph nodes that are extremely tender. These lymph nodes may coalesce and rupture and drain, forming buboes.

Syphilis usually presents as a small papule that develops into a painless, eroded, indurated ulcer. The mean incubation period is 21 days. If untreated, the genital ulcer disappears and, after a variable length of time, the patient may develop secondary syphilis with widespread, protean symptoms usually involving the skin with disseminated diffuse papules. The final stage of the disease, tertiary syphilis, can remain latent or appear as late syphilis consisting of neurosyphilis, cardiovascular syphilis, or gummatous syphilis.

Lymphogranuloma venereum, a disease due to restricted types of C trachomatis, usually begins as a painless papule that frequently goes unnoticed. The second stage of the disease involves enlargement of regional lymph nodes and the third stage manifests as rectal strictures and fibrosis.

Granuloma inguinale also begins as a painless papule that ultimately develops into a painless, raised, beefy-red lesion.

The lesions of herpes simplex initially begin as small papules that develop into extremely painful vesicles or ulcers.

Etiology

Haemophilus ducreyi is the etiologic agent of chancroid (Fig. 97-6). This organism is a fastidious, Gram-negative rod that requires hemin. The incidence of chancroid has been increasing in the United States. Detailed information about herpes simplex virus is available in Chapter 68. Treponema pallidum, a spirochete, is the agent of syphilis.

Figure 97-6. Major causes of genital ulcers.

Figure 97-6

Major causes of genital ulcers.

Chlamydia trachomatis serovars L1, L2, and L3 are the agents of lymphogranuloma venereum. These strains of C trachomatis differ from ocular and nongonococcal urethritis in being more invasive in a mouse model and more resistant to trypsin treatment. Granuloma inguinale is caused by Calmatobacterium granulomatis, which is usually demonstrated as intracellular Donovan bodies visualized by Warthin-Starry silver stain or Giemsa stain of histologic sections. The disease is most prevalent in India, Papua, New Guinea, and the Caribbean.

Pathogenesis

Treponema pallidum invades intact mucosa and, after entering the lymphatics, can disseminate throughout the body to almost any organ. Obliterative endarteritis is the pathologic hallmark of syphilis and is found in all stages of the disease. Treponema pallidum can infect the fetus of a syphilitic mother, producing congenital syphilis.

The pathogenesis of chancroid is poorly understood, but the organism is thought to gain access through minute breaks in the mucosal epithelium. The organism is drained to the regional lymph nodes but does not disseminate further in the body. The organisms remain localized in the superficial layers of the ulcer.

Chlamydia trachomatis serovars L1, L2 and L3 and Calmatobacterium granulomatis both remain localized at the site of ulceration but sometimes may show contiguous spread.

Microbiologic Diagnosis

Because the clinical symptoms of the genital ulcer diseases overlap, and because two or more pathogens may be present simultaneously, culture is critical to confirming the diagnosis. Chancroid is diagnosed by culturing either ulcer or bubo exudate. The organism is fastidious but can be grown in 48 hours by culturing on Mueller-Hinton or GC medium enriched with IsoVitaleX, fetal bovine serum, and vancomycin. The cultures grow best in a water saturated environment at 37°C with 5 percent CO2. Even under optimal culture conditions, the isolation rates are between 50 and 80 percent. The organism is identified by hemin requirement, alkaline phosphatase production, ability to reduce nitrate and a positive oxidase test.

Treponema pallidum cannot be grown in vitro. Diagnosis is made by dark-field examination of ulcer material for spirochetes and by serologic detection of an antibody response. Herpes simplex is diagnosed by submitting appropriate vesicular fluid for a viral culture or antigen detection. Lymphogranuloma venereum is usually diagnosed by culturing C trachomatis and examination for inclusion bodies in the inoculated cell line. Antigen detection methods using fluorescein-conjugated antibody have also proved useful. Calmatobacterium granulomatis is usually detected by staining histologic sections with Warthin-Starry silver stain and observing Donovan bodies within the host cells.

Prevention and Treatment

As with other sexually transmitted diseases, rapid diagnosis, treatment and contact tracing help contain the spread of the disease. Use of condoms and modification of sexual behavior are important preventitive measures. Effective treatment is available for all the genital ulcer diseases. Chancroid is treated with a seven day course of erythromycin. Other useful antibiotics include ceftriaxone, trimethoprim, either with or without sulfonamides, and ciprofloxacin. Syphilis is treated with penicillin. If the patient is allergic to penicillin, tetracycline is an effective alternative. Early treatment of pregnant women with syphilis is crucial to prevent congenital syphilis. The susceptibility profiles of Lymphogranuloma venereum strains are similar to those of other C trachomatis serovars. Tetracyclines, erythromycin and sulfonamides are all effective. Granuloma inguinale has been successfully treated with trimethoprim-sulfamethoxazole, tetracycline and erythromycin. Treatment should be continued for 3 weeks.

Urinary Tract Infections

Cystitis, Pyelonephritis, Asymptomatic Bacteriuria, Renal Abscess

Clinical Manifestations

Acute cystitis is a superficial inflammation of the bladder and urethra which leads to urinary frequency, painful urination, a feeling of fullness following voiding, and suprapubic discomfort. Acute pyelonephritis is due to bacterial invasion of the renal tissue with inflammation and swelling, leading to fever, back pain, and sometimes renal dysfunction. Acute cystitis occurs together with acute pyelonephritis in about one-third of patients. Acute prostatitis occurs when bacteria invade the prostate, causing perineal pain and fever.

Infection can spread within the urinary tract and patients often have recurrences of cystitis, sometimes interspersed with episodes of pyelonephritis. Symptoms that persist and recur are often referred to as chronic cystitis, chronic pyelonephritis or chronic prostatitis. However, these chronic conditions are much more difficult to define. Recurring kidney infection in childhood sometimes leads to renal damage and ultimate kidney failure. Hypertension is also an occasional outcome of chronic renal infection.

Asymptomatic infections of the urinary tract—asymptomatic bacteriuria—are common. In childhood, about 1 percent of girls have asymptomatic bacteriuria. The prevalence increases to 3 to 5 percent among adult women and 10 to 50 percent in elderly men and women. Occasionally, individuals do have symptoms such as incontinence or ongoing malaise that are not recognized as due to bacteriuria until it is diagnosed and treated.

Some patients have what are called “complicated urinary tract infections.” This includes individuals who have congenital or acquired anatomic abnormalities of the urinary tract. Obstruction of the urinary tract as a result of either a stone or a malfunctioning bladder secondary to a neural injury also predisposes to infection and makes infections more difficult to treat. Kidney and bladder stones can be the consequence of infection, and management of the infection is usually only successful if the stone is also removed. Many individuals cared for by urologists have underlying abnormalities of the urinary tract that make infections complicated and difficult to cure without surgical restoration of normal urine flow. Urinary catheters, used to drain the urinary tract in cases of obstruction or incontinence, bypass normal host defenses, and individuals with indwelling catheters are very prone to infections. Nosocomial urinary infections due to catheterization account for almost one-half of all infections acquired in hospital and can lead to invasive, life-threatening sepsis.

Urinary infections are the commonest type of bacterial infection that causes women to seek medical care. In a given year, about 1 in 20 women have acute cystitis. Acute pyelonephritis is one of the most common infections that require hospital admission for intravenous antibacterial therapy.

Urinary infections are recurrent in about 5 percent of women, and the recurring cystitis and pyelonephritis cause substantial morbidity. Recurrent urinary infection in women can be due to a number of underlying causes. Sexual intercourse, the syndrome referred to as “honeymoon cystitis”, is responsible for about one-half of urinary infections in sexually active adult women. These infections are not acquired from the sexual partner but rather are due to the mechanical irritation associated with intercourse. Unfortunately, women who acquire frequent infections that are associated with intercourse often have difficulties developing healthy, normal sexual relations and this may require special attention. The use of a diaphragm for contraception is also a major risk factor, increasing the risk of cystitis threefold.

Etiology

Organisms normally present in the intestinal tract cause most urinary tract infections. The commonest of these by far is Escherichia coli, which is responsible for 80 percent of infections that are acquired outside of hospitals (Fig. 97-7). Other Gram-negative rods such as Klebsiella, Enterobacter, and Proteus spp are relatively common, each accounting for 3 to 5 percent of infections. Within the hospital environment, Pseudomonas aeruginosa, Serratia marscesens, and other, more resistant, hospital-associated pathogens account for many infections.

Figure 97-7. Major causes of urinary tract infections.

Figure 97-7

Major causes of urinary tract infections.

Gram-positive organisms, particularly coagulase-negative staphylococci and enterococci, cause some infections. Staphylococcus saprophyticus causes about 10 percent of urinary tract infections in young women. Candida albicans is also a frequent pathogen in hospitalized patients, particularly if diabetes is present.

Anaerobes and fastidious organisms rarely cause urinary infections. A number of viruses, particularly mumps virus, cytomegalovirus, and coxsackieviruses, can be present in the kidneys and urine, but rarely cause symptoms or any consequences.

A number of sexually transmitted pathogens (e.g., Neisseria gonorrhoeae) may invade the urethra. Chlamydia trachomatis and herpes simplex can present with symptoms that mimic acute cystitis in both men and women.

Pathogenesis

Bacteria invade the urinary tract by ascending or hematogenous routes (Fig. 97-8). The ascending route is the most common, with hematogenous spread causing kidney abscesses.

Figure 97-8. Pathogenesis of urinary tract infections.

Figure 97-8

Pathogenesis of urinary tract infections.

Escherichia coli serogroups 01, 02, 04, 06, 07 and 075 are the most common agents of urinary tract infections. The most important virulence factor for these bacteria is the enhanced ability to adhere to uroepithelial cells. This attachment is mediated by specific pilus adhesins on the surface of E coli. The mucosal epithelial cells of women and children with recurrent urinary tract infections have been shown to have an increased avidity for attachment of E. coli. However, phasic variation (Fig. 97-9) occurs after the organism ascends to the kidney or pelvis, and pili are no longer produced. Motility has been shown to facilitate ascending infection and bacterial endotoxins can decrease urethral peristalsis.

Figure 97-9. Phasic variation of E coli in urinary tract infections.

Figure 97-9

Phasic variation of E coli in urinary tract infections.

Alterations of urine flow by scarring, obstruction due to stones, or catheterization greatly enhances the risk of acquiring a urinary tract infection.

Microbiologic Diagnosis

The diagnosis of a urinary tract infection is confirmed by culturing the organism from urine. Most bacteria that cause urinary infection grow readily, and the clinical diagnosis of urinary tract infection is usually confirmed within 24 hours.

Because urine is an excellent culture media for a variety of microorganisms, considerable effort must be made to ensure that a urine sample is not contaminated during collection and that organisms are not permitted to grow before the urine is cultured. Patients suspected of urinary infection are usually asked to collect a mid-stream sample after cleaning the perineum or glans penis with soap and water. An early-morning collection is best because the concentration of bacteria in the urine is greatest prior to the morning voiding. The urine is then refrigerated or taken to the laboratory for immediate culture. Urine can be stored in a refrigerator for up to 24 hours without any loss of bacterial viability.

In the laboratory, a quantitative loop that samples 0.001 ml is usually used to inoculate both a nonselective medium (blood agar) and a selective medium (MacConkey agar). The cultures are incubated at 37°C. By the following day, the organism can be identified and quantitated. Cultures that represent true infection rather than specimen contamination are identified quantitatively. Approximately 65 percent of patients with acute cystitis have >105 organisms/ml of urine and almost 90 percent of patients with acute pyelonephritis and asymptomatic bacteriuria also have counts in excess of 105 organisms/ml. Unless contaminated or overgrown, most negative urines have <104 organisms/ml. Antibacterial susceptibility profiles of the pathogens are also analyzed. Examination of urine to demonstrate the presence of pus cells is an important part of diagnosing urinary infection. Most infections of the urinary tract are associated with an inflammatory response. Thus, quantitative urine culture and the presence of pyuria are straightforward, reliable means of confirming the clinical diagnosis of urinary tract infection.

Prevention and Treatment

Most antimicrobial agents are excreted in the urine and, therefore many different treatment regimens can be used to cure urinary infections. The most commonly prescribed agents for acute cystitis are oral regimens of nitrofurantoin, a sulfonamide-trimethoprim combination, amoxicillin, cephalexin, and ciprofloxacin or other quinolones. Each of these regimens cure 90 to 95 percent of females with acute cystitis. Amoxacillin which previously was the drug of choice now fails in 10 to 20 percent of patients due to widespread resistance among E coli. Long courses are not necessary, and many studies have shown that single dose therapy or therapy prescribed for 3 days is as effective as longer courses. Intravenous antimicrobials are usually prescribed for patients acutely ill with acute pyelonephritis or acute prostatitis. Aminoglycosides and cephalosporins are frequently chosen. Longer courses of oral antibacterial agents are useful to prevent recurring infections in women who are susceptible to frequent reinfections; women need not live in fear of their next infection. If they wish to not take continuous preventive therapy, the next treatment regimens should be carried for self-initiation with the onset of acute symptoms.

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Copyright © 1996, The University of Texas Medical Branch at Galveston.
Bookshelf ID: NBK8136PMID: 21413302

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