Chapter 74: Pelvic Infections

Infections in the pelvic organs and surrounding structures compose a heterogeneous 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 sexually transmitted infections, major syndromes that will be discussed are genital ulcer disease, vaginitis, cervicitis, pelvic inflammatory disease (PID), urethritis, prostatitis, and epididymitis.

Some of the organisms described in this chapter, such as Treponema pallidum, Neisseria gonorrhoeae, Chlamydia trachomatis, and herpes simplex virus 2, are transmitted from the mother to the fetus. The acronym TORCHES is used to describe certain important fetal or newborn infections acquired from the mother. There are several versions of this acronym. The following is a commonly used one: T = Toxoplasma; O = other (including parvovirus, human immunodeficiency virus, and Zika virus); R = rubella; C = cytomegalovirus; HE = herpes simplex virus 2; and S = syphilis. A more complete list of organisms vertically transmitted from mother to child can be found in Part 12, Table XII–10.

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 of a patient with genital herpes. 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.

Pathogens

Common infectious etiologies of genital ulcer disease include HSV-2 (causing genital herpes) and T. pallidum (causing primary syphilis) primarily, as well as H. ducreyi (causing chancroid). Less common causes of genital ulcers include C. 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. This typically includes the following tests at the initial visit: direct fluorescent antibody (DFA) test for HSV antigens, viral culture for HSV, or nucleic acid amplification methods for HSV DNA using a specimen taken from the base of the ulcer, and syphilis serologic testing (e.g., rapid plasmin reagin, RPR) using a serum sample. 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).

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. There is no vaccine against any of the organisms that cause genital ulcer disease.

Definition

Vaginitis is inflammation of the vagina that can result in discharge, itching, and pain. These symptoms occur primarily in three diseases: candidiasis, trichomoniasis, and bacterial vaginosis (BV). Noninfectious causes include lichen planus and certain medications (e.g., oral contraceptives). Note that a vaginal discharge can occur in both vaginitis and cervicitis. Vaginal symptoms are very common, resulting in millions of visits to health care providers each year.

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 BV is uncertain, but it does not appear to be a sexually transmitted disease. BV can be thought of as a dysbiosis of the vaginal microbiome. Lactobacilli are the predominant organisms in the healthy vagina but other bacteria (see Pathogens section later) predominate in the dysbiotic vagina. 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 BV is thin and grayish and has an unpleasant odor, often described as “fishy.” There is an absence of neutrophils in the discharge. Table 74–2 describes the important clinical features of vaginitis, its diagnostic procedures, and its treatment.

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 BV, but anaerobes such as Mobiluncus and Prevotella and nonanaerobes such as Atopobium vaginae, Mycoplasma hominis, and Ureaplasma 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). If microscopy is negative, Candida culture and Trichomonas nucleic acid amplification test (NAAT) are performed to increase sensitivity.

Trichomonads are shown in Figure 74–5. Figure 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.

Treatment

Metronidazole is the drug of choice for both BV and trichomoniasis. Tinidazole is also used because it has fewer adverse effects than metronidazole. Secnidazole can be used to treat bacterial vaginosis. 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. Following treatment of trichomoniasis, the Centers for Disease Control and Prevention recommends retesting with NAAT to evaluate for reinfection, regardless of whether the partner was treated.

Prevention

There is no vaccine against any of the organisms that cause vaginitis.

Definition

Cervicitis is inflammation of the uterine cervix. Acute cervicitis is usually due to a sexually transmitted infection caused by either C. trachomatis or N. gonorrhoeae or both. Note that a vaginal discharge can occur in both vaginitis and cervicitis.

Clinical Manifestations

A large proportion of persons with cervicitis are asymptomatic but a vaginal discharge and bleeding between menstrual periods may occur. In many cases, cervicitis is detected on speculum examination (Figure 74–8) and/or following routine screening for C. trachomatis and N. gonorrhoeae. Individuals 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.

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, NAAT for C. trachomatis and N. gonorrhoeae is routinely performed. If NAAT testing is not available, then Gram stain and culture for gonococci can be used.

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. There is no vaccine against any of the organisms that cause cervicitis.

Definition

PID is a polymicrobial infection of upper genital tract structures, namely, the uterus, fallopian tubes, and ovaries. Infection of the uterus is called endometritis and infection of the fallopian tubes is called salpingitis.

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. PID is especially common in adolescent and young adult individuals.

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. The abrupt onset of abdominal pain associated with menses is a common finding in PID. On physical exam, tenderness on motion of the cervix and an abnormal vaginal discharge are important diagnostic signs.

Pathogens

PID is primarily caused by N. gonorrhoeae and C. trachomatis, together with Mycoplasma genitalium, 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, such as NAATs for these organisms, can increase the specificity of the diagnosis.

Treatment

If symptoms are mild, persons 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 and clindamycin plus gentamicin are initial options with oral antibiotics only after 24 hours of improvement of the patient.

Prevention

There is no vaccine against any of the organisms that cause PID.

Definition

Urethritis is an inflammation of the urethra. It is usually caused by a sexually transmitted infection, particularly in sexually active persons. Urethritis is often thought of as either gonococcal urethritis or nongonococcal urethritis (NGU). The latter is most often caused by C. trachomatis.

An autoimmune, cause of urethritis is called reactive arthritis (formerly named Reiter’s syndrome), a syndrome that includes urethritis, uveitis, and arthritis. This syndrome is often a sequel to infection by C. trachomatis though other bacteria such as Salmonella, Shigella, Campylobacter, Yersinia, Clostridioides difficile and Chlamydia pneumoniae have been implicated.

Clinical Manifestations

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

Pathogens

N. gonorrhoeae, C. trachomatis, and M. genitalium are the most common organisms implicated. NGU is caused primarily by C. trachomatis followed by M. genitalium but about half of NGU cases have no specific pathogen identified. Other organisms such as T. vaginalis, which are not normally tested, can be involved.

Diagnosis

NAAT for C. trachomatis and N. gonorrhoeae is routinely performed in many centers. Some centers also perform NAAT testing for M. genitalium.

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. There is no vaccine against any of the organisms that cause urethritis.

Definition

Acute epididymitis is characterized by pain and swelling of the epididymis of less than 6 weeks in duration. Sometimes the testes are involved as well (epididymo-orchitis). Chronic epididymitis typically has similar but more muted findings and is longer than 6 weeks in duration.

Pathophysiology

In sexually active persons, the infection begins as a urethritis that ascends into the epididymis. In older, nonsexually active adults, the infection is related to bladder infections, secondary to prostatic hypertrophy. Predisposing factors include prostate biopsy, urinary tract instrumentation, and immunosuppression.

Clinical Manifestations

Acute epididymitis typically presents with unilateral scrotal pain and tenderness and swelling of the epididymis. On physical exam, an enlarged red scrotum is seen. A hydrocele may be present, and a thickened spermatic cord may be palpated. Torsion of the testicle (noted as sudden testicular pain with an asymmetrical and high-riding testis) must be distinguished from acute epididymitis because torsion is a surgical emergency. Torsion of the testicle typically occurs in young adults several hours after physical activity or trauma.

Chronic epididymitis presents with discomfort in the epididymis, scrotum, or testicle lasting 6 weeks or longer.

Pathogens

Acute epididymitis in sexually active adults is typically caused by C. trachomatis or N. gonorrhoeae. Escherichia coli may be the cause in men who have sex with men. E. coli is also a common cause in older adults with a concomitant bladder infection.

Chronic epididymitis can be a granulomatous infection caused by Mycobacterium tuberculosis. However, often no etiology is identified.

Diagnosis

A microbiologic diagnosis of acute epididymitis in sexually active adults can be made by using Gram stain of urethral secretions and/or NAAT for C. trachomatis or N. gonorrhoeae. In nonsexually active adults, urinalysis and urine culture should be done.

Scrotal Doppler ultrasonography is the test of choice used to distinguish torsion from epididymitis. Absence of blood flow on the ultrasound indicates torsion of the testicle.

Treatment

Acute epididymitis in sexually active adults should be treated with ceftriaxone and azithromycin or doxycycline to cover the most common causes. In proven C. trachomatis or N. gonorrhoeae cases, sex partners should also be treated. In nonsexually active patients, oral levofloxacin to cover E. coli is appropriate.

Prevention

There is no vaccine against any of the organisms that cause epididymitis.

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 patients are involved. These organisms include the Enterobacteriaceae (e.g., E. 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.