Primary Care
1st Edition

Chapter 69
Sexually Transmitted Infections
Carol Buck-Rolland MS, PNP, OGNP
Deborah Wachtel MPH OGNP
This chapter begins with a discussion of sexually transmitted infections (STIs) in general, followed by sections covering chlamydia, gonorrhea, syphilis, herpes simplex virus, human papillomavirus, bacterial vaginosis, trichomoniasis, and moniliasis. The anatomy and physiology of the male reproductive system are described in Chapters 68 and 70. Female reproductive anatomy is described in Chapter 71. The pathology of each of the STIs is discussed in this chapter. Patient history is not specifically discussed; the provider should ask questions using the standard sexual history and symptom format when screening for STIs. For more specific information on history taking, refer to Chapters 66, 67, and 70. Comprehensive epidemiologic statistics are not provided for trichomoniasis, moniliasis, or bacterial vaginosis because these are not reportable infections; interested readers are referred to current gynecologic texts. Teaching and self-care is covered in the section on STIs in general.
STIs, also known as sexually transmitted diseases (STDs), present a major public health problem in the United States. STIs comprise more than 25 infectious organisms that are transmitted through sexual activity (vaginal, oral, and anal intercourse), along with the dozens of clinical syndromes they cause. Studies show that STIs enhance the risk of sexual transmission of HIV infection (Wasserheit, 1992; Laga et al, 1993, Kreiss, 1994; U.S. Department of Health and Human Services [USDHHS], 1993, 1997). The spectrum of health consequences of STIs ranges from mild acute illness to serious long-term complications (Eng & Butler, 1997).
In young female adolescents, the ectocervix has not yet changed from columnar cells to the more protective-type epithelial cells, biologically increasing their vulnerability to the invasion of sexually transmitted infections. Adolescents who initiate intercourse at a young age are more likely to be exposed to multiple partners and risk factors. Any or all of these factors increase the risk of infections over time. Men who are uncircumcised may be at a greater risk (as are their partners) of acquiring certain STIs, such as HIV and chancroid (see Chap. 70). Women who douche are at a higher risk for bacterial vaginosis as well as for later complications of STIs, such as pelvic inflammatory disease (PID). A correlation exists between PID and the frequency of douching (Eng & Butler, 1997) Douching alters the pH of the vaginal mucosa, resulting in an increased susceptibility to transmission of STIs.
STIs are transmitted among all sexually active people, including heterosexuals, bisexuals, and homosexuals. Men who have sex with men are at a greater risk for many life-threatening STIs, including AIDS and hepatitis B and C (American Medical Association, 1995). Women who have sex only with women seem to be at less of a risk for some bacterial STIs. Bacterial vaginosis and genital human papillomavirus infections, however, are not uncommon (Berger et al, 1995).
Certain sexual practices are more likely to facilitate the transmission of STIs. Unprotected receptive rectal intercourse is likely to result in tissue trauma and bleeding, which can facilitate invasion by pathogens. Unprotected vaginal intercourse may also result in tissue trauma, although generally to a lesser degree. Tissue damage facilitates the transmission of both bloodborne pathogens and other viral STIs. Vaginal intercourse during menstruation may facilitate STI transmission. Oral sex is less likely to promote the transmission of STIs.
Currently, AIDS, syphilis, and gonorrhea are reportable diseases in all 50 states. Primary care providers need to be knowledgeable about the reporting requirements in the areas where they practice. Health departments in many states provide anonymous tracking and notification of partners of patients found to be infected with an STI that falls into the category of a reportable disease. Partner notification can help prevent the spread of reportable infections. According to recent data from the Centers for Disease Control and Prevention (CDC; USDHHS, 1996):
  • More than 12 million Americans, including 3 million teenagers, are infected with STIs each year.
  • Two thirds of persons who acquire STIs are under age 25.
  • 87% of all STI cases reported were among the top 10 most frequently reported diseases in the United States in 1995.
  • Since 1980, eight new sexually transmitted pathogens have been recognized in the United States.
  • Every year, about $10 billion is spent on major STIs (other than AIDS) and their preventable complications.
  • Women and adolescents are disproportionately affected by STIs and their consequences of transmission (Eng & Butler, 1997; USDHHS, 1996).
Risk Factors
Behaviors that place patients at risk for STIs include:
  • Initiation of sexual intercourse at an early age
  • Greater number of partners
  • High-risk partners
  • Increased frequency of intercourse
  • P.747

  • Certain sexual practices
  • Lack of circumcision of male partner
  • Vaginal douching
  • Lack of barrier contraceptive use (USDHHS, 1996).
Because of the prevalence and consequences of STIs, all primary care providers need to participate actively in prevention efforts. These efforts should focus on preadolescents, before sexual activity begins, and should be driven by current research and surveillance data and re-evaluated frequently. Prevention efforts need to target high-risk populations and provide appropriate messages. These messages must be repeated often and in a variety of ways, altering the strategies depending on the target audience. Clinical services for prevention education as well as for diagnosis and treatment must be available and effective. Local primary care providers can provide such access. STI education should be included in all routine patient encounters. All sexually active patients need to be informed of how sexually transmitted infections are acquired. Primary care providers can work with local health departments and local schools to provide comprehensive STI services. Primary care providers should implement the recommendations of the U.S. Preventive Services Task Force (1996) and the CDC (1993, 1997) for prevention, screening, and management of STIs. The CDC publishes an annual STD surveillance report. Their guidelines for treating STDs are updated every 3 years.
Infections caused by Chlamydia trachomatis are among the most common STIs. Complications in women caused by chlamydia include PID, tubal factor infertility, and ectopic pregnancy. If not adequately treated, 20% to 40% of women infected with chlamydia will develop PID. Pregnant women can transmit the infection to their babies during delivery, potentially causing conjunctivitis or pneumonia. Adolescents and young adults are at a substantial risk of becoming infected with this infection. Unrecognized infection is believed to be highly prevalent in this group (USDHHS, 1993).
Anatomy, Physiology, and Pathology
Infection by chlamydia is insidious. Approximately 70% of chlamydial infections are asymptomatic. The rectum is a common site of initial chlamydial infection for men who engage in receptive anal intercourse. Exposure to chlamydia in females is a result of sexual intercourse. The site of the initial infection is typically the cervix. The urethra and the rectum may also be infected. The infection travels up through the cervix to the vagina, endometrium, and fallopian tubes. This upward migration may induce lower abdominal pain and minor irregular bleeding, such as postcoital bleeding. The proportion of women with chlamydial infection who develop upper reproductive tract infection (endometritis, salpingitis, and pelvic peritonitis) is uncertain. Chlamydia, alone or with other microorganisms, has been isolated from 5% to 50% of women seeking care for symptoms of PID. In 1991, more than 275,000 women were hospitalized and more than 100,000 surgical procedures were performed as a result of PID (USDHHS, 1993). Approximately 17% of women treated for PID will be infertile; an equal proportion will have chronic pain as a result of infection; and 10% of those who do conceive will have an ectopic pregnancy.
Chlamydial salpingitis may progress to perihepatitis. Chlamydia may be a cause of cystitis in women who have leukouria but negative urine cultures. Pregnant women with chlamydia are at risk for postpartum PID and endometritis (USDHHS, 1993).
By 1995, 48 states had implemented legislation mandating reporting of chlamydia. The CDC has tracked chlamydial infections since 1984. The sharp increases in the prevalence of infection since 1984 primarily reflect increased screening, recognition of asymptomatic infection (mainly in women), and improved reporting capacity. In 1995, 477,638 chlamydial infections were reported to the CDC. For a second consecutive year, reported cases of chlamydia exceeded the 392,848 reported cases of gonorrhea in 1995. Reported cases of chlamydia for women (290.3 per 100,000 population) exceed those for men (52.1 per 100,000 population) (USDHHS, 1996).
Diagnostic Criteria
Symptoms rarely occur in either gender. When they do occur in females, symptoms include vaginal discharge and dysuria. Most men infected with chlamydia are asymptomatic. Chlamydial infections among heterosexual men may typically induce urethral symptoms of dysuria and discharge. Rectal infections in either gender are generally asymptomatic but may cause symptoms of proctitis (rectal discharge, pain during defecation) or proctocolitis (USDHHS, 1993).
History and Physical Exam
Female partners of males with chlamydial infection should be offered a pelvic exam, chlamydia testing, and treatment. The testing and exam of female partners is recommended because:
  • A positive test result may mean that additional partners may be infected.
  • Asymptomatic women may have signs of PID on examination, requiring more intensive therapy.
  • Women may be asymptomatically infected with other STIs.
Male partners of females with chlamydial infection should be evaluated for symptoms of chlamydia and other STIs and for allergy to the treatment medication. A physical exam of

male sex partners should be encouraged, but the exam is less important than treatment. The exam is recommended because:
  • A positive test may lead to the treatment of additional partners who may be infected.
  • Men may be asymptomatically infected with other STIs.
  • Male partners may be allergic to the treatment medication.
If it is not possible for a male partner to be examined, the provider must determine that the man does not have symptoms suggestive of another STI and is not allergic to the treatment medication.
Diagnostic Studies
A number of nonculture tests are marketed for the detection of chlamydia. Nonculture tests are easier to perform and are less expensive than cultures. Tests available include:
  • Enzyme immunoassays to detect chlamydia antigens
  • Fluorescein-conjugated monoclonal antibodies for the direct visualization of chlamydia elementary bodies on smears
  • Nucleic acid hybridization tests
  • Rapid tests.
Endocervical specimens should be obtained after obtaining Pap smears or cervical cultures. Urethral specimens should be delayed until 2 hours after the patient has voided. Specific instructions for the various tests must be followed.
The disadvantages of cell cultures include:
  • Delayed results (3 to 7 days)
  • Only viable organisms are detected, necessitating a special transport medium with control of temperature, and additional cost.
Both enzyme immunoassay and direct fluorescent antibody assay of a first morning urine sample can identify as many infected symptomatic men as does a culture of urethral swabs. Few if any false-positive results are associated with these tests. However, they fail to identify more than 40% of cases in women (Lee et al, 1995).
Urine collection for chlamydia assay uses the nucleic acid amplification method to detect the presence of chlamydia DNA in the specimen. Two methods are the polymerase chain reaction and the ligase chain reaction. Urine collection for detection is less invasive, and early studies have shown a high rate of infection detection, almost 30% greater than that of endocervical swab culture (Chernesky et al, 1994; Epidemiology Newsletter, 1996; Lee et al, 1995).
The leukocyte estrase test is a dipstick that is applied to urine specimens to screen for urinary tract infection. Data are being collected to determine the role of this tool in the diagnosis of chlamydia.
Culture is the preferred method for detecting chlamydia in rectal specimens. The performance of nonculture tests with conjunctival specimens has been at least as effective as with genital specimens. Chlamydial serology has little value in the routine clinical care of genital tract infections. Chlamydial infections elicit long-lasting antibodies that cannot be easily distinguished from the antibodies produced in a current infection.
Everyone with whom the patient has had ongoing sexual exposure within 60 days of the positive test result should be treated. The primary care provider should inform infected patients to have their partners examined and treated. Public health department providers can anonymously contact exposed partners if the patient chooses not to inform them.
Treatment Options, Expected Outcomes, and Comprehensive Management
The recommended antimicrobial agent for uncomplicated urethral, endocervical, or rectal chlamydia in adults is doxycycline or azithromycin. Table 69-1 gives treatment guidelines for both chlamydia and the complication of PID.
TABLE 69-1 Sexually Transmitted Infections Treatment Guidelines
TABLE 69-1 Sexually Transmitted Infections Treatment Guidelines
Chlamydial infection is especially prevalent among adolescents. Prevention strategies must be targeted toward young people and their sexual partners. Community-based prevention programs should target all sexually active adolescents and young adults. These can include school-based programs, adolescent recreation programs, television programs and ads, and newspaper ads. Posters and patient education materials can be placed in settings where there is a high traffic flow of adolescents and young adults. These measures can help promote increased awareness and vigilant screening and treatment. The principal goal is to prevent both overt and silent chlamydial salpingitis and PID sequelae. Prevention of perinatal and postpartal infection is also critical.
Strategies should target infection prevention. Specific strategies include:
  • Recommending behavioral changes that reduce the risk of acquiring or transmitting chlamydia
  • Advising teens to delay having intercourse, to decrease the number of sexual partners, and to use barrier contraception
  • Identifying and treating patients with genital chlamydial infection before they infect their sexual partners, and infected pregnant women before they infect their infants.


Efforts aimed at preventing complications among patients found to be infected with chlamydia include careful screening to identify and treat asymptomatic infection, and treatment of the female partners of men infected with chlamydia.
Because of the high incidence of chlamydial infection among sexually active females, the CDC’s screening recommendations include (USDHHS, 1993):
  • Women younger than 20 should be tested when undergoing a pelvic exam, unless sexual activity since the last test for chlamydia has been limited to a single, mutually monogamous partner.
  • All other women who meet the suggested screening criteria:
    • Mucopurulent cervical discharge Sexually active and younger than 20
    • Age 20 to 24 who meet either of the following criteria, or older than 24 who meet both criteria:
      • Inconsistent use of barrier contraception New or more than one sex partner during the last 3 months.
Anatomy, Physiology, and Pathology
Gonorrhea is transmitted almost exclusively sexually, because the gonococcus cannot survive outside the body. Sexual transmission occurs more easily from man to man or man to woman rather than the reverse. Men may have symptoms after a short incubation period of 3 to 7 days. Typically, men note urethritis and a purulent penile discharge. If left untreated, the infection may spread to the urethra, prostate, seminal vesicles, and epididymis. This may result in urethral stricture and obstructive uropathy. Proctitis may result after anal intercourse, although anal transmission is most often asymptomatic. Anoscopy may reveal punctate ulcerations and intraluminal pus. Pharyngitis may occur after oral–genital sex, although these patients are typically asymptomatic.
Conjunctivitis may occur as a result of inoculation into the conjunctiva. Lack of treatment may progress to corneal ulceration. Newborns may acquire gonococcal ophthalmia from contact with infected vaginal discharge during vaginal birth.
In females, the infection ascends to the uterus and fallopian tubes if untreated. This may lead to salpingitis and PID.
Gonococci may disseminate; this occurs more often in women than in men. Gonococcemia manifests as bacteremia, fever, chills, and characteristic hemorrhagic, painful, vesicopustular skin lesions. Frequently seen is tenosynovitis, particularly of the small joints of the hands and feet. Less common manifestations include endocarditis and perihepatic involvement (Fitz-Hugh-Curtis syndrome).
Antimicrobial resistance remains an important consideration in the treatment of gonorrhea. The resistance, caused mainly by the production of a beta-lactamase (penicillinase), affects 5% to 20% of patients in the United States. In 1995, 31.6% of isolates collected by the Gonococcal Isolate Surveillance Project were resistant to penicillin, tetracycline, or both (USDHHS, 1996). Resistance to ciprofloxacin was first identified in 1991 but remains rare (USDHHS, 1996).
Infections caused by Neisseria gonorrhoeae are a major cause of PID, tubal infertility, ectopic pregnancy, and chronic pelvic pain in the United States. Epidemiologic studies provide strong evidence that gonococcal infections facilitate HIV transmission (Eng & Butler, 1997). An estimated 1 million new infections with gonorrhea occur in the United States each year. The rate

of gonorrhea has continued to decline since 1975. From 1994 to 1995, the rate decreased from 165.1 per 100,000 population to 149.5. Teens age 15 to 19 had higher rates than the general population; young adults age 20 to 24 from minority populations had the highest rates.
History and Physical Exam
The exam of the external female genitalia may demonstrate swelling and discharge from Bartholin’s glands. In men, the exam includes assessing for discharge and regional lymphadenopathy. The prostate should be palpated for signs of acute prostatitis (see Chaps. 68 and 70).
Diagnostic Studies
Cell cultures may be obtained from the sites of exposure (ie, urethra, endocervix, throat, rectum). Microscopic examination of gram-stained specimen discharge may be diagnostic in clinical settings where this is possible, although this method is less sensitive than cell culture. Nonculture tests such as enzyme immunoassays and DNA probes are available and reliable but do not provide information on antibiotic sensitivity (U.S. Preventive Task Force, 1996). Urine tests to detect gonorrhea using the DNA amplification method have a high rate of accurate detection. The directions for specimen collection must be followed carefully.
Treatment Options, Expected Outcomes, and Comprehensive Management
Refer to the general guidelines presented at the beginning of this chapter for the prevention and control of STIs. The CDC recommends screening all pregnant women and all women presenting to STD clinics for gonorrhea (USDHHS, 1993). The U.S. Preventive Task Force (1996) recommends screening all people who are at high risk, including women who have multiple sex partners, a partner with multiple partners, a partner with gonorrhea, or a history of repeated infections. Gonorrhea screening programs have attempted to establish screening criteria that would apply across a variety of provider sites. Frequently used criteria include age (less than 25), marital status, number of recent sexual partners, and repeat clinic visits (Mertz et al, 1997).
When selecting a treatment regimen for gonorrhea infection, the provider must consider the anatomic site of infection, the resistance of gonorrhea strains to the antimicrobials, the possibility of concurrent infection with chlamydia, and side effects and costs. Table 69-1 gives specific treatment guidelines for gonorrhea.
A test of cure is unnecessary for any of the antimicrobial treatments. Patients with persistent symptoms should be evaluated by culture.
Anatomy, Physiology and Pathology
Syphilis is a systemic disease caused by Treponema pallidum. It progresses through three stages.
Primary syphilis is characterized by a chancre or painless lesion that occurs about 3 weeks after exposure. The chancre is usually a solitary erythematous macule that ulcerates, with a well-defined indurated border. The lesion initially has a clear red base that becomes encrusted. Chancres most frequently occur in the genital area but may occur elsewhere on the body, often near the lips or in the mouth. Systemic symptoms rarely occur during this stage. The chancre often goes unnoticed and resolves without treatment within 3 to 6 weeks.
Secondary syphilis occurs within 6 weeks of the chancre and is characterized by adenopathy and a generalized rash that extends to the palmar and plantar surfaces. The lesions may be macular, maculopapular, or papular and are generally not itchy. The lesions may be accompanied by fever, headache, malaise, fatigue, muscle or joint pain, or lymphadenopathy. The mucous membranes are involved in 20% to 70% of patients with secondary syphilis. Diagnosis at this stage may be difficult because the symptoms frequently mimic those of other conditions, such as psoriasis, tinea corporis, or genital warts. Condylomata lata are secondary syphilis lesions found mainly in the genital and perianal regions; they may be mistaken for genital warts, or condylomata. Pharyngeal erythema without a sore throat occurs in about 25% of patients (Clayton & Krowchuk, 1997).
Tertiary syphilis marks the end of latency and is characterized by neurologic and cardiovascular disease, gumma, auditory or ophthalmic involvement, or cutaneous lesions. Thirty percent to 40% of untreated patients progress to tertiary syphilis in 2 to 30 years after initial infection (Clayton & Krowchuk, 1997).

The rate of primary and secondary syphilis peaked in 1945, then declined until the 1960s because of penicillin treatment. An increase in incidence occurred in the 1960s because of the “sexual revolution” and dramatic cuts in funding of programs to reduce transmission of STIs. Another upsurge was noted in large cities in 1985 and 1986, among disadvantaged minority populations. Prostitution and drug use appeared to play a role in outbreaks. The most recent increase was in 1990, in women and also in congenital syphilis. Since 1990, a decline in incidence has been observed (Eng & Butler, 1997).
History and Physical Exam
The exam is as described in previous sections. The provider should pay special attention to signs of ulcerative lesions, as well as any generalized rashes that have spread to the palmar and plantar surfaces.
Dark-field examination and direct fluorescent antibody tests of lesion exudate are the definitive methods for diagnosing early syphilis. Serologic tests provide presumptive diagnosis and should be performed sequentially by the same laboratory. Serologic tests are of two types:
  • Nontreponemal (VDRL and RPR): may be negative in 40% of recent infections
  • Treponemal (FTA-ABS) antibody tests: positive 5 to 7 days after chancre appears.
No single test can be used to diagnosis neurosyphilis. This diagnosis is made using a combination of serologic tests and tests on cerebrospinal fluid.
Treatment Options, Expected Outcomes, and Comprehensive Management
Screening must continue in high-risk populations, including prostitutes and drug users and their partners. Syphilis should be in the differential diagnosis whenever a patient presents with ulcerative lesions or a generalized rash that spreads to the palmar and plantar surfaces. Prevention strategies include discussing with the patient the value of delaying the onset of sexual activity, reducing the number of sexual partners, and using effective barrier methods.
Parenteral penicillin G is the preferred pharmacologic treatment for syphilis. The preparation used, the dosage, and the duration of treatment depend on the stage and clinical manifestations. Table 69-1 presents specific treatment guidelines. Parenteral penicillin G is the only therapy with documented efficacy for neurosyphilis and in pregnant women.
Sexual contacts of patients being treated for syphilis should be evaluated and treated presumptively if their exposure to the patient was less than 90 days ago. If the exposure was more than 90 days ago, serologic tests may be done to determine infection.
No definitive criteria for cure or failure exist. Serologic studies should be done 3 and 6 months after treatment. Patients with persistent symptoms or whose titers sustain a fourfold increase over baseline can be considered to have failed treatment or to have become reinfected. Such patients should be retreated. They should also be evaluated for HIV infection. When patients are retreated, the recommended regimen is benzathine penicillin G 2.4 million units given intramuscularly once a week for 3 weeks, for a total of three doses.
Anatomy, Physiology, and Pathology
Genital herpes is acquired through direct contact with virus and can penetrate intact mucous membranes. Viral particles are transported along peripheral sensory nerves to the dorsal root ganglion, where latent infection is established (Clark et al, 1995). The incubation time for herpes simplex virus (HSV) is 3 to 14 days after primary infection. There may be a significant delay in or total absence of symptoms if pre-existing immunity is present. Primary outbreaks are generally more severe than secondary outbreaks and last 2 to 3 weeks.

There are two forms of genital herpes: HSV1 and HSV2. HSV2 causes approximately 80% of infections, manifesting primarily as genital lesions. HSV1 is responsible for the remaining 20%, usually seen as oral lesions. There is significant crossover between the two strains and their locations. Oral herpes is one of the causative organisms in the condition commonly referred to as cold sores; these are intraepidermal vesicles on the lips and buccal mucosa that ulcerate easily and produce tender lesions that crust over before healing without a scar. HSV2 has a much greater propensity toward symptomatic recurrence and asymptomatic shedding then HSV1 (Pereria, 1996). The majority of genital herpes infections are asymptomatic.
In many countries, successful control of bacterial STIs has coexisted with an increase in the prevalence of viral STIs (Kinghorn, 1996). The continued increase in the incidence of clinical and subclinical genital HSV infections is of particular concern due to the association of increased HIV transmission in the presence of concurrent ulcerative, herpetic lesions. In addition, there is concern that HSV may increase the likelihood of the sexual transmission of hepatitis C (Scott, 1995).
HSV is the most common cause of genital ulcerative disease in industrialized countries (Clayton & Krowchuk, 1997), affecting more than 30 million people in the United States (Eng & Butler, 1997). More than 500,000 new cases of HSV occur in the United States each year (Conant et al, 1996). Genital herpes is generally thought of as an STD, but it should probably be considered an infection transmitted by physical contact (Scott, 1995). Undiagnosed HSV and asymptomatic viral shedding may play a large role in the growing number of new infections. Controlled studies have documented viral shedding between HSV recurrences, asymptomatic shedding in the genitourinary tract, and shedding during the prodromal period that precedes an active outbreak of lesions (Conant et al, 1996). The success of HSV as a pathogen—indeed, its key to survival—is its ability to establish latent infection in the sensory ganglia for the lifetime of the host (Pereria, 1996).
Diagnostic Criteria
Criteria include the presence of fluid-filled lesions on an erythematous base. The selective use of viral culture is an important criterion for diagnosis (Clark et al, 1995).
History and Physical Exam
Clinical diagnosis of genital herpes requires obtaining a standard history for HSV signs and symptoms. Question the patient about past or current presence of the characteristic lesions of HSV. Inquire whether these lesions were accompanied by any of a variety of symptoms, such as superficial to deep pain, burning sensations, and swollen, tender lymph nodes in the area of infection. Note any history of sexual contacts who were possible sources for HSV. Identify whether the patient has a history of HSV1.
Patients with primary infection may experience prodromal flulike symptoms of fever and malaise, headaches, and myalgias and frequently remember pain and pruritus in the area where the lesions emerge. The vesicles rupture within 1 to 2 days of forming, leaving painful superficial ulcers that become crusted until they heal. For men, symptoms tend to be less severe and are often atypical.
The physical exam involves assessing for the presence of fluid-filled vesicles, which appear singly or in groups on an erythematous base. Genital HSV infection can manifest atypically as edema, fissures, erythematous patches, or fleeting irritations. Lesions on the buttocks are frequently misdiagnosed as insect bites or rashes of undetermined significance. Vulvar lesions are often preceded by increased vaginal discharge and irritation, often mistaken for a monilial infection. Other companion symptoms can be lower back pain, pain or aching radiating down one leg, burning with urination, and urinary retention.
Because HSV remains dormant in nerve ganglia, recurrences range from frequent to rare, depending on factors such as endogenous or exogenous stressors and immune system status. Recurrences tend to decrease in frequency over time and may disappear altogether after the primary episode. At the onset of a secondary episode, prodromal symptoms such as aching, burning, and increased vaginal discharge will alert the patient that the eruption of vesicles will follow.
Diagnostic Studies
There are several laboratory methods available to assist with the diagnosis of HSV. Viral culture is the easiest way to separate HSV1 from HSV2. Lesions must be at an early stage; 20% to 30% of culture results are falsely negative (Clark et al, 1995). Results may take 1 to 2 days. If lesions are atypical, equivocal, or old, biopsy or polymerase chain reaction should be considered. Direct immunofluorescence of early vesicular or crusted lesions is as accurate as viral culture and is quicker; results can be available in a few hours (Pereria, 1996)
Treatment Options, Expected Outcomes, and Comprehensive Management
Antiviral medication is started as soon as the diagnosis is established in initial infections, and specific treatment guidelines are given in Table 69-1 during the prodromal period to prevent or shorten recurrent episodes. In recurrent genital herpes, the ulceration is somewhat milder and the associated symptoms are slight or absent, even without pharmacotherapy.
There are three forms of pharmacologic therapies for the treatment of HSV: initial, episodic, and suppressive. Refer to Table 69-1 for specific treatment guidelines.
The treatment of herpes infections includes diet, lifestyle, pharmaceuticals, and attention to psychosocial needs. Genital herpes can have considerable psychological and psychosexual consequences. These may manifest as depression, anger, and lowered self-esteem. The psychological morbidity in patients with a first episode of genital herpes is statistically significantly greater than that occurring in nonherpes patients attending STI clinics (Mindel, 1996). Some patients may express profound regret for poor judgment. They may view this infection as punishment for sexual practices they characterize as promiscuous or unsavory (Conant et al, 1996).

Patients experiencing recurrent episodes have a broad spectrum of concerns. There are questions regarding long-term health issues and future pregnancies. Some patients focus on concerns about disclosure of infection to future partners and family members. People with recurrent genital herpes may experience shame and guilt, withdrawing from intimate relationships for fear of rejection and disapproval. This can lead to self-imposed social isolation (Conant et al, 1996). Treatment must include addressing the issue of self respect. Ideally, this will lead to better management and healing strategies as well as strengthened communication between provider and patient.
Human papillomaviruses (HPVs) are small DNA viruses capable of inducing the proliferation of epithelial cells in the natural hosts (Zheng & Vaheri, 1995). Of the 60 types of HPV that have been identified, 20 are known to cause genital warts. HPV types 6 and 11 are the most prevalent types associated with condylomata acuminata and are not considered to have malignant potential. Types 16, 18, 30, 31, 33, 35, 39, and several more in the 40, 50, and 60 ranges are most frequently associated with genital neoplasia. Genotypes 30 and 40 are associated with laryngeal cancers.
As of 1994, the estimated annual incidence of HPV was 500,000 to 1 million (Carson, 1997; Eng & Butler, 1997). It is believed that approximately 40 million Americans are infected with HPV. HPV causes condylomata acuminata (genital warts), considered the leading cause of cervical neoplasia. HPV infection is often subclinical, exhibiting no visible evidence of disease (Eng & Butler, 1997).
Factors that may influence a patient’s susceptibility to HPV and the immune system’s response to the infection are sexual practices, parity, diet, smoking, other STIs, and immunogenic characteristics. These factors may play a contributory role in the subsequent development of cervical carcinoma (Birley et al, 1995). HPV is transmitted via contact with the virus to sensitive areas of the body. Genital HPV genotypes infect particular membranes such as labial, vaginal, cervical, rectal, oral, and penile tissue. Viral shedding without apparent lesions may occur, but condylomata are highly infectious sources of contact. The role of hand–genital transmission in the etiology of genital warts is unclear. Incubation periods range from 3 to 9 months.
History and Physical Exam
The clinical presentation of genital warts is a diagnostic indicator of HPV. They appear most frequently in the urogenital and rectal areas. Lesions are typically pedunculated or broad-based and mostly papillary, with a lobulated or irregular surface. They may occur as individual lesions, ranging from 0.2 to 1 cm. When in clusters, they may become confluent and involve large areas of the genitalia. In men who are uncircumcised, lesions are most prevalent on the inner aspect of the prepuce and at the frenulum and coronal sulcus. Conversely, men who have been circumcised often present with involvement of the penile shaft. Lesions may also occur within the urethral meatus (Palefsky & Barrasso, 1996).
During a routine exam in a woman, the provider must perform a careful inspection within the folds of the labia and beneath the clitoral hood; these are classic hiding places for condylomata. Women may be asymptomatic, or they may complain of itching and friability of the lesion. Lesions on the cervix may be flat and endophytic during a routine exam (Palefsky & Barrasso, 1996).
Of all urologic tumors, penile carcinoma is the closest male analogy to cervical cancer. McCance (1994) found HPV in 27 of 53 (51%) penile cancers, and Villa (1997) reported HPV in 8 of 18 cases.
Diagnostic Studies
Laboratory detection of HPV includes cytology, colposcopy, histology, HPV antigen detection, and HPV DNA detection. A Pap smear of the cervix must be performed whenever warts are suspected on the external exam. The Pap smear will detect any evidence of viral damage to the cervical tissue. On microscopic examination, condylomata appear as papillated epidermal hyperplastic lesions showing parakeratosis, koilocytosis, occasional atypia of the nucleus, and hyperemia.
Treatment Options, Expected Outcomes, and Comprehensive Management
There are a variety of reasons for treating HPV infection, including reduction of viral transmission, prevention of cervical or penile neoplasia, and symptomatic improvement. The management of HPV-induced disease remains rooted to the strategy of repeated local destruction. It is unclear whether treatment affects either the transmission or natural course of the infection. With time, host immunity generally will attain dominance (Reid, 1996). If left untreated, warts resolve spontaneously, proliferate, or remain unchanged.
The usual treatment for warts is cytotoxic or ablative therapy. The CDC’s STD treatment guidelines (USDHHS, 1993, 1997) remain current. This document advises cryotherapy with

liquid nitrogen or cryoprobe as first-line management for anogenital warts. This is inexpensive and will not result in scarring if properly applied. The topical chemodestructive agents recommended by the CDC are podophyllin, podofilox, and trichloroacetic acid (TCA). Podophyllin acts by poisoning the mytotic spindle.
Laser therapy has the advantage of precise control and hemostasis and is used primarily for proliferative disease. Electrocautery for small lesions and surgical extirpation for large lesions are also available options. 5-fluorouracil is a pyrimidine antimetabolite that is used as a 5% cream and washed off a few hours after application. A high level of irritation may accompany its use, so this treatment should be used with caution. Interferons may be given intramuscularly, subcutaneously, or intralesionally. Side effects are common but self-limited and for the most part well tolerated.
The only safe recommended treatment during pregnancy includes TCA, cryotherapy, and CO2 laser.
Teaching and Self-Care
Refer to the section on HSV.
Anatomy, Physiology, and Pathology
Bacterial vaginosis is thought to occur as a result of an increase in the normal vaginal pH, mediated by the metabolic activity of anaerobic bacteria (Neri et al, 1994). The exact microbes responsible for BV are unknown. The high concentrations of anaerobic gram-negative rods, peptostreptococci, and other opportunistic pathogens in the lower genital tract place women with BV at increased risk for genital infections and adverse pregnancy outcomes (Hill, 1993). Hormonal factors probably play a role, because BV is a condition that typically affects women of reproductive age. BV is a polymicrobial condition distinguished by symptomatic abnormalities of the vaginal secretions. Until recently, BV has not been characterized as an inflammatory process. This has resulted in what may be an underestimation of the long-term consequences to fertility and morbidity. Hillier et al (1996) examined 178 women with PID, looking for the role of BV-associated microorganisms in endometritis; a positive association was found. This suggests an alteration to the historical notion that BV is not an infection but a vaginal inflammation.
Bacterial vaginosis (BV) is found in up to 25% of women seen in gynecologic and obstetric offices and up to 64% of women seen in STI clinics. Fifty percent of women with BV are asymptomatic (American College of Obstetrics and Gynecology [ACOG], 1996).
Diagnostic Criteria
There are four criteria for the diagnosis of BV:
  • pH greater than 4.5
  • Clue cells (vaginal epithelial cells studded with a large number of bacteria that obscure the cell border). At least 20% of the epithelial cells must be clue cells for this to be a significant finding.
  • Positive whiff test. To perform this test, mix one or two drops of 10% KOH with the vaginal discharge. The test is positive when an amine or fishy odor is produced.
  • Homogenous discharge.
The diagnosis of BV is made by finding at least three of these four signs on the vaginal and microscopic exam. Using these criteria will produce a diagnostic accuracy of 90% and will reduce the false-positive rate to less than 10% (ACOG, 1996).
History and Physical Exam
When confined to the vaginal canal, an overgrowth of normal bacteria typically creates a change in vaginal odor, an increase in discharge, and occasionally labial and urethral irritation. The odor is a result of metabolic byproducts, produced primarily by anaerobic bacteria. It is described as fishy and is exacerbated by contact with semen (ACOG, 1996). The discharge has been described as homogenous, white or gray, soupy, frothy, or milky, adherent to the vaginal walls, and pooling at the introitus.
Treatment Options, Expected Outcomes, and Comprehensive Management
All symptomatic infections should be treated. These include grossly apparent cervicitis and PID.

Refer to Table 69-1 for specific criteria for managing BV.
Teaching and Self-Care
In general, BV is a result of vaginal imbalance. Women should strive toward healthy lifestyle practices to encourage normal vaginal flora. A diet low in sugar, adequate rest and exercise, and adequate hydration can all help. Other factors may be exposure-based, such as preventing contact with alkaline semen by using condoms. Some women may find that latex or spermicide sensitivity causes BV. They can avoid these substances by using nonlatex condoms without spermicide. Other strategies for self-care in BV are discussed in the subsection on monilial infections.
Anatomy, Physiology, and Pathology
Trichomoniasis is caused by a parasitic protozoan flagellate and is usually sexually transmitted. The infection is typically found in the vagina and urethra in women and the urethra in men.
History and Physical Exam
The physical exam reveals perineal excoriation, erythema, and possible ulcerations. The vaginal exam typically reveals a strawberry-like appearance of the cervix, red papules on the vaginal walls, and a greenish or gray, frothy or bubbly, malodorous discharge. The pH of the discharge is usually more than 5 (5 to 7). Microscopic evaluation reveals motile cells, slightly larger than leukocytes and smaller than epithelial cells. Typically, the white cell count exceeds 10 per high-power field. The whiff test may or may not be fishy.
Treatment and Comprehensive Management
Refer to the treatment guidelines found in Table 69-1.
It is important that the provider also treat the patient’s sexual partners to prevent reinfection in the patient.
Anatomy, Physiology, and Pathology
Moniliasis is a common STI, usually caused by Candida albicans. It may also be caused by Candida tropicalis, Torulopis glabrata, or other candidal species. These fungi are normal inhabitants of the mouth, gastrointestinal tract, and vagina. Overgrowth occurs as a result of a change in vaginal pH or other changes in the vaginal flora. Systemic antibiotics frequently cause a disruption in the normal balance of the vaginal flora, resulting in a monilial infection. Persistent elevation of the blood glucose level above normal also can cause a monilial infection.
History and Physical Exam
The physical exam in the female typically reveals vulvar and vaginal erythema and irritation. Vaginal discharge is typically thick, odorless, and curdlike, with a pH in the normal range (3.8 to 4.2).
Diagnostic Criteria
Microscopic evaluation reveals hyphae, pseudohyphae, spores, or buds. In male patients, erythema is evident, with satellite lesions.
Treatment Options, Expected Outcomes, and Comprehensive Management
See the treatment guidelines presented in Table 69-1. Many antifungal creams are available over the counter. The patient who self-treats and does not respond to the treatment should be examined to rule out other conditions.
Teaching and Self-Care
Symptom resolution is better ensured if the patient refrains from sexual intercourse during treatment. Women should avoid the use of tampons during this period. Encourage the patient to allow ventilation to the affected area and to avoid tight clothing. Underwear should not be worn when sleeping.
Preventive strategies include wearing cotton rather than nylon underpants. Women should wear cotton underwear underneath their pantyhose. They should reconsider douching and using “feminine hygiene” products; avoiding these products helps maintain healthy vaginal flora.
Community-based resources for education and patient support are widely available in all 50 states. Local or regional public health departments offer current information on STI management standards. Public health departments are an excellent resource for patient education posters and brochures as well. They can also provide information about support groups.
  • National STD Hotline, 800-227-8922
  • American Medical Women’s Association, 801 N. Fairfax St., Suite 400, Alexandria, VA 22314, 703-838-0500
  • American Social Health Association, P.O. Box 13827, Research Triangle Park, NC 27709
  • National Herpes Hotline, 919-361-8488
  • P.757

  • The CDC’s Morbidity and Mortality Weekly Report,
  • CDC National Center for HIV, STD, & TB Prevention, Division of STD Prevention,
  • Sexually transmitted diseases,
  • Virtual Hospital: What you need to know about sexually transmitted diseases, HIV disease, and AIDS,
  • STD Homepage,
  • JAMA Women’s Health, Sexually Transmitted Disease Information Center,
  • Association of Reproductive Health Professionals,
  • National Women’s Health Resource Center,
American College of Obstetrics and Gynecology. (1996). Vaginitis. ACOG Technical Bulletin, 226.
American Medical Association, Council on Scientific Affairs. (1996). Health care needs of gay men and lesbians in the U.S. JAMA, 275, 1354–1359.
Berger, B., Kolton, S., Zenilman, J., Cummings, M., Feldman, J., & McCormack, S. (1995). Bacterial vaginosis in lesbians: A sexually transmitted disease. Clinical Infectious Disease, (21), 1402–1405.
Birley, H., Hart, C., & Stacey, S. (1995). Human papillomaviruses and the genital tract: Old viruses, new developments [Editorial]. Journal of Medical Microbiology, 43(2), 81–84.
Carson, S. (1997). Human papillomatous virus infection update: Impact on women’s health. Nurse Practitioner, 22, 24–37.
Chernesky, M., Jang, D., Lee, H., et al. (1994). Diagnosis of Chlamydia trachomatis infection in men and women by testing first-void urine by ligase chain reaction. Journal of Clinical Microbiology, 32(11), 2682–2685.
Clark, J., Tatum, N., & Noble, S. (1995). Management of genital herpes. American Family Physician, 51(1), 175–188.
Clayton, B., & Krowchuk (1997). Skin findings and STDs. Contemporary Pediatrics, 119–137.
Conant, M., Berger, T., Coates, T., Longo, D., Robinson, J., & Drake, L. (1996). Genital herpes: An integrated approach to management. Journal of the American Academy of Dermatology, 35(4), 601–605.
Eng, T., & Butler, W. (Eds.). (1997) The hidden epidemic: Confronting sexually transmitted diseases. Washington, D.C.: Institute of Medicine, National Academy Press.
Epidemiology Newsletter. (1996). Chlamydia: New detection methods. Utah Department of Health, Bureau of Epidemiology.
Hill, G. (1993). The microbiology of bacterial vaginosis [Review]. American Journal of Obstetrics and Gynecology, 169 (2 Pt. 2), 450–454.
Hillier, S., Kiviat, N., Hawes, S., et al. (1996). Role of bacterial vaginosis-associated microorganisms in endometritis. American Journal of Obstetrics and Gynecology, 175(2), 435–441.
Kinghorn, G. (1996). Limiting the spread of genital herpes. Scandinavian Journal of Infectious Diseases, 100, 20–25.
Laga M, Manoka, A. Kivuvu, M. et al. (1993). Nonulcerative sexually transmitted diseases as risk factors for HIV-1 transmission in women: Results from a cohort study. AIDS, 7:95–102.
Lee, H., Chernesky, M., Schachter, J., et al. (1995). Diagnosis of Chlamydia trachomatis genitourinary infection in women by ligase chain reaction assay of urine. Lancet, 345, 213–216.
McCance, D. (1994). Human papillomaviruses [Review]. Infectious Disease Clinics of North America, 8(4), 751–767.
Mertz, K., Levine, W., Mosure, D., Breman, S., Dorian, K., & Hadgu, A. (1997). Screening women for gonorrhea: Demographic screening criteria for general clinical use. American Journal of Public Health, 87(9), 1535–1538.
Mindel, A. (1996). Psychological and psychosexual implications of herpes virus infection [Review]. Scandinavian Journal of Infectious Diseases, 100, 27–32.
Neri A., Rabinerson, D., & Kaplan, B. (1994). Bacterial vaginosis: Drugs versus alternative treatment [Review]. Obstetrical & Gynecological Survey, 49(12), 809–813.
Palefsky, J., & Barrasso, R. (1996). HPV infection and disease in men [Review]. Obstetrics and Gynecology Clinics of North America, 23(4), 895–916.
Pereria, F. (1996). Herpes simplex: Evolving concepts. Journal of the American Academy of Dermatology, 35(4), 503–516.
Reid, R. (1996). The management of genital condylomas, intraepithelial neoplasia, and vulvodynia [Review]. Obstetrics & Gynecology Clinics of North America, 23 (4), 917–991.
Scott, L. (1995). Perinatal herpes: Current status and obstetric management strategies. Pediatric Infectious Disease Journal, 14(10), 827–830.
U.S. Department of Health and Human Services. (1993). Recommendations and management of Chlamydia trachomatis infections. Atlanta, GA: Centers for Disease Control and Prevention.
U.S. Department of Health and Human Services. (1993, 1997). Sexually transmitted diseases treatment guidelines. Washington, D.C.: U.S. Government Printing Office.
U.S. Department of Health and Human Services. (1996). Sexually transmitted disease surveillance 1995. Atlanta, GA: Centers for Disease Control and Prevention, National Centers for HIV, STD, and TB Prevention.
U.S. Preventive Task Force. (1996). Guide to clinical preventive services. Baltimore: Williams & Wilkins.
Villa, L. (1997). Human papillomaviruses and cervical cancer. Advances in Cancer Research, 71, 321–341.
Wasserheit, J. (1992). Epidemiologic synergy. Interrelationships between human immunodeficiency virus infection and other sexually transmitted diseases. Sexually Transmitted Diseases 9, 61–77.
Wiener, J., & Walther, P. (1995). Human papillomaviruses, biology and role in cervical and penile malignancy. Infections in Medicine, 635–641.
Zheng, J., & Vaheri, A. (1995). Human epithelial cells immortalized by human papilloma viruses [Critical Review]. Oncogenesis, 6(3–6), 235–250.