Review of Medical Microbiology and Immunology, 13th Edition

74. Pelvic Infections

Contributed by Peter Chin-Hong, MD

CHAPTER CONTENTS

Introduction

Genital Ulcer Disease

Vaginitis

Cervicitis

Pelvic Inflammatory Disease

Urethritis

Prostatitis

INTRODUCTION

Infections in the pelvic organs and surrounding structures comprise a heterogenous group of diseases. They primarily affect sexually active women and men. Many of the pathogens implicated are sexually transmitted, so an important facet of management is partner notification and treatment, as well as patient education regarding safe sexual practices. Among sexual transmitted infections, major syndromes that will be discussed are genital ulcer disease, vaginitis, cervicitis, pelvic inflammatory disease, urethritis, and prostatitis.

GENITAL ULCER DISEASE

Definition

Genital ulcer disease manifests as a breach in the skin or mucosa of the genitalia, usually caused by a sexually transmitted infection. Of these infections, herpes simplex virus type 2 (HSV-2) is the most common etiology in most geographic areas, followed by syphilis and chancroid. The most important noninfectious cause is Behçet’s disease.

Pathophysiology

The mechanisms by which ulcers are produced by pathogens are incompletely understood, and there are different mechanisms of injury depending on the pathogen. In chancroid, a cytotoxin secreted by Haemophilus ducreyi may be important in epithelial cell injury.

Clinical Manifestations

Although the various lesions may have a characteristic appearance, it is important to note that local epidemiology is an important consideration because lesions may appear in an atypical fashion. The appearance of the ulcer, whether it is painful, and the nature of the associated lymphadenopathy may be clues in the etiology of the ulcer. Figure 74–1 shows several vesicles on the shaft of the penis. The vesicular lesions are typically painful. The vesicles can then progress to form shallow ulcers. Figure 74–2 shows the chancre of primary syphilis. It is a painless lesion with a shallow base and a firm, rolled edge. Table 74–1 describes the important clinical features of genital ulcer lesions, their diagnostic procedures, and treatment.

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FIGURE 74–1 Genital herpes caused by herpes simplex virus-2. Note group of vesicles on shaft of penis. (From Wolff K, Johnson R, Saavedra A (eds): Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology, 7th ed. New York: McGraw-Hill, 2013.)

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FIGURE 74–2 Chancre of primary syphilis caused by Treponema pallidum. Note shallow ulcer with clean base and rolled edge. (Used with permission from Goldsmith LA, et al. Fitzpatrick’s Dermatology in General Medicine. 8th ed. New York: McGraw-Hill, 2012. Copyright © 2012 by The McGraw-Hill Companies, Inc.)

Pathogens

Common infectious etiologies of genital ulcer disease include HSV-2 (causing genital herpes), Treponema pallidum (causing primary syphilis), and H. ducreyi (causing chancroid). Less common pathogens include Chlamydia trachomatis serovars L1–3 (causing lymphogranuloma venereum) and Klebsiella granulomatis (causing granuloma inguinale, also known as donovanosis).

Diagnosis

A thorough sexual and medical history, followed by the physical examination, are important for diagnosis. Although clinical characteristics can be very helpful, there is often overlap in presentation, and there may also be multiple syndromes copresenting. Therefore, diagnostic testing is highly recommended. Testing for other sexually transmitted diseases including human immunodeficiency virus (HIV) is also important because there is often cotransmission of multiple pathogens (see Table 74–1).

TABLE 74–1 Genital Ulcers: Clinical Features, Diagnosis, and Treatment

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Treatment

The drug of choice for genital herpes is acyclovir or one of its derivatives, famciclovir or valacyclovir. Primary and secondary syphilis are treated with a long-acting penicillin, benzathine penicillin G. The drug of choice for chancroid is azithromycin, whereas for lymphogranuloma venereum, it is doxycycline (see Table 74–1).

Empiric treatment is often used before diagnostic tests return. As for most sexually transmitted infections, treatment that involves one dose and that is observed is preferred if possible.

Prevention

Consistent use of condoms is an important measure that can prevent genital ulcers. In some cases, primary prevention of HSV infection can be undertaken by treatment of the negative partner in serodiscordant couples with acyclovir or one of its derivatives. Prophylaxis with these drugs can be effective in preventing recurrences of HSV outbreaks in patients who have had frequent occurrences, especially among those who are immunosuppressed. Partner notification and treatment are important prevention strategies as well.

VAGINITIS

Definition

Vaginitis is inflammation of the vagina that can result in discharge, itching, and pain. Common causes of vaginitis are candidiasis, trichomoniasis, and bacterial vaginosis. Noninfectious causes include lichen planus and certain medications (e.g., oral contraceptives).

Pathophysiology

The use of antibiotics that inhibit the normal flora of the vagina, especially lactobacilli, predisposes to Candida vaginitis. Candida is a member of the normal flora of many women. The pathogenesis of bacterial vaginosis is uncertain, but it does not appear to be a sexually transmitted disease. Trichomoniasis, on the other hand, is a sexually transmitted disease.

Clinical Manifestations

Patients are usually prompted to seek medical attention because of an abnormal vaginal discharge. This may be accompanied by pruritus, pain (including dyspareunia), and symptoms of vaginal irritation. Figure 74–3 depicts the white, “cottage cheese” appearance of vaginal candidiasis. Figure 74–4 shows the “strawberry” cervix of trichomoniasis. There are red, punctate lesions on the cervix, and frothy exudate can be seen at the cervical os. The vaginal discharge in bacterial vaginosis is thin and grayish and has an unpleasant odor, often described as “fishy.” Table 74–2 describes the important clinical features of vaginitis, its diagnostic procedures, and its treatment.

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FIGURE 74–3 Vaginal candidiasis caused by Candida albicans. Note areas of whitish, “cottage cheese–like” exudate on cervical mucosa. (Figure courtesy of Centers for Disease Control and Prevention.)

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FIGURE 74–4 Trichomoniasis caused by Trichomonas vaginalis. Note frothy discharge and punctate “strawberry” lesions on cervix. (Courtesy of Richard P. Usatine, MD; used with permission from Usatine RP et al. The Color Atlas of Family Medicine. New York: McGraw-Hill, 2009. Copyright © 2009 by The McGraw-Hill Companies, Inc.)

TABLE 74–2 Vaginitis: Clinical Features, Diagnosis, and Treatment

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Pathogens

Candida albicans is the most common cause of vaginal candidiasis. Trichomonas vaginalis is the cause of trichomoniasis. Overgrowth of bacteria such as Gardnerella vaginalis is implicated in bacterial vaginosis, but anaerobes such as Mobiluncus are also involved.

Diagnosis

A patient’s complaint of vaginal discharge should prompt a careful history, including time of last menstrual period, medications, and sexual activity. The physical examination should include a microscopic examination of the vaginal discharge itself on a glass slide using a drop of 0.9% saline solution (to look for motile trichomonads or clue cells), followed by a drop of 10% potassium hydroxide (to look for Candida). Trichomonads are shown in Figure 74–5Figure 74–6 shows clue cells as large, vaginal epithelial cells dotted with bacteria. A Gram stain of clue cells reveals many gram-variable rods on the surface of the epithelial cells. Figure 74–7 shows the appearance of the yeasts and pseudohyphae of Candida. Cultures for Gardnerella are not done because at least 50% of asymptomatic women carry the organism. See Table 74–2 for additional information.

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FIGURE 74–5 Trichomonas vaginalis in vaginal discharge. Note trichomonads (arrows) mounted in saline and visualized in light microscope. (Courtesy of Richard P. Usatine, MD; used with permission from Usatine RP et al. The Color Atlas of Family Medicine. New York: McGraw-Hill, 2009. Copyright © 2009 by The McGraw-Hill Companies, Inc.)

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FIGURE 74–6 Clue cells in bacterial vaginosis. Note that the lower epithelial cell is a “clue cell” because its surface is covered with bacteria. The upper epithelial cell is not a “clue cell” because its surface has few bacteria. (Used with permission from Usatine, RP et al: The Color Atlas of Family Medicine, New York: McGraw-Hill, 2009. Courtesy of E.J. Mayeaux, Jr., MD.)

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FIGURE 74–7 Candida visualized in KOH preparation. Note yeast cells (red arrow) and pseudohyphae (blue arrow). (Used with permission from Goldsmith LA et al. Fitzpatrick’s Dermatology in General Medicine. 8th ed. New York: McGraw-Hill, 2012. Copyright © 2012 by The McGraw-Hill Companies, Inc.)

Treatment

Metronidazole is the drug of choice for both bacterial vaginosis and trichomoniasis. For candidiasis, either oral fluconazole or vaginally administered miconazole or butoconazole is the drug of choice (see Table 74–2). T. vaginalis is a sexually transmitted infection, so a one-time treatment regimen of patient and partner is preferred.

CERVICITIS

Definition

Cervicitis is inflammation of the uterine cervix. Acute cervicitis is usually due to a sexually transmitted infection caused by either C. trachomatis or Neisseria gonorrhoeae or both.

Clinical Manifestations

A large proportion of women with cervicitis are asymptomatic. In many cases, cervicitis is detected on speculum examination (Figure 74–8) and/or following routine screening for C. trachomatis and N. gonorrhoeae. Women who have concomitant urethral infection may have dysuria. On physical examination, increased friability of the cervical tissue after a swab is inserted may be a clue to the diagnosis.

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FIGURE 74–8 Cervicitis. Note purulent exudate at cervical os. (Used with permission from Knoop KJ, Stack LB, Storrow AB, Thurman RJ: The Atlas of Emergency Medicine, 3rd ed. © 2009 by McGraw-Hill, Inc., New York. Photo contributor: Sue Rist, FNP.)

Pathogens

The usual pathogens are C. trachomatis serovars D–K and/or N. gonorrhoeae. Other less common etiologies include HSV and T. vaginalis.

Diagnosis

A clinical diagnosis may be made based on increased friability of the cervix, with or without mucopurulent discharge. To make a laboratory diagnosis, nucleic acid amplification testing (NAAT) for C. trachomatis and N. gonorrhoeae is routinely performed in many centers. If NAAT testing is not available, then Gram stain and culture may be performed.

Treatment

If there is clinical evidence of cervicitis, empiric treatment for both C. trachomatis and N. gonorrhoeae (ceftriaxone intramuscularly plus azithromycin orally) is recommended, particularly if follow-up of test results by the patient is uncertain. Sex partners of patients with a confirmed diagnosis should also be notified and treated.

Prevention

Consistent use of condoms is an important measure that can prevent sexually transmitted diseases. Partner notification and treatment are important prevention strategies as well.

PELVIC INFLAMMATORY DISEASE

Definition

Pelvic inflammatory disease (PID) is a polymicrobial infection of upper genital tract structures, namely the uterus, fallopian tubes, and ovaries.

Pathophysiology

When the endocervical canal barrier is compromised, vaginal bacteria can ascend into the normally sterile space of the upper genital tract (uterus, fallopian tubes, and ovaries). A sexually transmitted infection affecting the cervix (e.g., N. gonorrhoeae and C. trachomatis) can initiate the process, permitting the anaerobic bacteria of the vagina to ascend.

Having multiple sex partners increases the risk of PID. Multiple episodes of PID lead to scarring of the fallopian tubes and an increased risk of ectopic pregnancy and sterility.

Clinical Manifestations

Patients can present with a range of symptoms, from lower back pain to fever, chills, lower abdominal pain, and cervical and adnexal tenderness. On physical exam, pain and tenderness on motion of the cervix are important diagnostic signs.

Pathogens

PID is primarily associated with N. gonorrhoeae and C. trachomatis, together with enteric gram-negative rods and anaerobes.

Diagnosis

Because it is often difficult to diagnose PID precisely (given the nonspecific findings) and because the consequences of not treating PID can be grave, many opt to treat with minimum diagnostic criteria such as uterine, adnexal, or cervical motion tenderness. Fever, the presence of leukocytes on cervical or vaginal discharge, elevated C-reactive protein, and laboratory evidence of cervical infection with N. gonorrhoeae or C. trachomatis can increase the specificity of the diagnosis.

Treatment

If symptoms are mild, women can be treated as outpatients with cefoxitin or ceftriaxone (one dose) plus doxycycline (14 days). Metronidazole is sometimes added to the regimen. In the inpatient setting, intravenous therapy is preferred. Cefoxitin or cefotetan with doxycycline, or clindamycin plus gentamicin are initial options with oral antibiotics only after 24 hours of improvement of the patient.

URETHRITIS

Definition

Urethritis is inflammation of the urethra. It is usually caused by a sexually transmitted infection, particularly in sexually active men. A noninfectious cause is Reiter’s syndrome, an autoimmune disease that includes urethritis, uveitis, and reactive arthritis.

Clinical Manifestations

Dysuria is a common presenting complaint. Discharge from the urethra (Figure 74–9), pruritus, and burning are also common complaints.

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FIGURE 74–9 Urethral discharge in gonorrhea. Note thick purulent urethral discharge. (Used with permission from Goldsmith LA et al. Fitzpatrick’s Dermatology in General Medicine. 8th ed. New York: McGraw-Hill, 2012. Copyright © 2012 by The McGraw-Hill Companies, Inc.)

Pathogens

N. gonorrhoeae and C. trachomatis are the most common organisms implicated. Other organisms include Mycoplasma genitalium and T. vaginalis.

Diagnosis

Nucleic acid amplification testing (NAAT) for C. trachomatis and N. gonorrhoeae is routinely performed in many centers.

Treatment

If there is clinical evidence of urethritis such as a purulent urethral discharge, empiric treatment for both N. gonorrhoeae and C. trachomatis (ceftriaxone intramuscularly plus azithromycin orally) is recommended.

Prevention

Consistent use of condoms is an important measure that can prevent sexually transmitted diseases. Partner notification and treatment are important prevention strategies as well.

PROSTATITIS

Definition

Acute bacterial prostatitis is characterized by the presence of typical irritative voiding symptoms (urinary frequency, hesitancy, feeling of incomplete voiding, dribbling), fever, pyuria, and positive urine cultures. Chronic bacterial prostatitis is characterized by the same voiding symptoms, but fever and pyuria are typically absent. Prostatitis is also discussed in Chapter 78 on Urinary Tract Infections.

Pathophysiology

Bacteria ascend the urethra, and then reflux into the prostatic ducts where infection occurs.

Clinical Manifestations

Patients appear ill in acute prostatitis with fevers, chills, irritative voiding symptoms, and pelvic or perineal pain. Physical examination may reveal a very tender and enlarged prostate. Symptoms in chronic bacterial prostatitis may be more subtle. Patients may present with recurrent urinary tract infections, but only prolonged treatment of prostatitis will result in a cure.

Pathogens

Generally, gram-negative rods that reflect the range of organisms that cause cystitis in men are involved. These organisms include the Enterobacteriaceae (e.g., Escherichia coli, Klebsiella and Proteus species) as well as Pseudomonas. In sexually active men, N. gonorrhoeae and C. trachomatis can cause prostatitis, especially in association with urethritis and epididymitis.

Diagnosis

A patient with symptoms of prostatitis who has an edematous and tender prostate on examination is considered to have acute bacterial prostatitis. Culture of urine is done to determine the causative organism. Culture of prostatic fluid is not done in acute prostatitis because prostatic massage should not be done during the acute phase. Prostatic massage may be useful in chronic prostatitis.

Treatment

Trimethoprim-sulfamethoxazole or a fluoroquinolone such as ciprofloxacin can be used as empiric therapy until culture results return. These agents exhibit good penetration into the prostate. Therapy is prolonged, usually given for 4 to 6 weeks.