Chapter 42
Sexually Transmitted Diseases in Pregnancy
Patrick J. Sweeney
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Patrick J. Sweeney, MD, PhD
Associate Professor of Obstetrics and Gynecology, Brown University Program in Medicine; Director of Medical Education, Women and Infants Hospital of Rhode Island, Providence, Rhode Island (Vol 2, Chap 42)



The sexually transmitted diseases (STDs) quite possibly represent medicine's most interesting and most frustrating challenge. The range of their clinical manifestations extends from being totally asymptomatic to being fatal. Between these two extremes, the STDs can be responsible for minor discomforts as well as considerable physical and emotional pain. Some can affect primarily every organ system, producing irreversible damage. For some there is no cure; for most there is a lack of adequate epidemiologic control.

As their name indicates, all of the STDs can be transmitted through sexual contact. However, the significance of the role of direct sexual contact and the long-term medical and psychological consequences vary considerably among the diseases. Based on incidence and relative importance during pregnancy, four STDs are discussed in this chapter: syphilis, gonorrhea, herpes, and chlamydia.

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Although the incidence of syphilis decreased markedly with the discovery of antibiotics, it nevertheless remains a formidable foe. On the one hand, there are several reasons why one would expect the incidence to continue to decrease: (1) the clinical manifestations of primary and secondary syphilis have remained unchanged since their original description, (2) a better-informed, health-conscious public is more likely to seek early treatment for suspicious lesions, (3) the stigma of syphilis is considerably less in today's society, and (4) mandatory premarital and prenatal screening programs can identify patients at earlier, treatable stages of disease. On the other hand, the disease persists, which some claim is due to changing sexual attitudes and the increased use of antibiotics, corticosteroids, and immunosuppressants, resulting in atypical presentations of the disease.1

Syphilis remains one of medicine's mysteries. The causative agent, the spirochete Treponema pallidum, has failed to develop any significant resistance to penicillin. Under such circumstances one would expect the incidence of the disease to fall to progressively lower levels until reaching an irreducible minimum or being eradicated. Such has not been the case.

In fact, from 1986 to 1987 the Centers for Disease Control reported a 25% increase in the incidence of syphilis in the United States, the largest single-year increase since 1960. The 1987 incidence of 14.6 cases per 100,000 persons matched the 1982 rate, which had been the highest rate since 1950. The increase in incidence was highest for blacks and Hispanics, with the highest rates being concentrated in the urban areas. In all racial and ethnic groups, the increases were greater for females than for males, with obvious implications for the incidence of congenital syphilis.2

Clinical Manifestations

Primary syphilis is characterized by the classic hunterian chancre, a painless ulcer that generally develops within 6 weeks of exposure. Treponema pallidum has a propensity for moist areas and so is likely to be found wherever mucous membranes are a frequent site of sexual contact, principally the genital canal, the anorectal area, and the oropharynx. If untreated, the chancre will usually heal in 3 to 6 weeks and occasionally will leave a scar.

Secondary syphilis appears 3 weeks to 6 months after the primary lesion. The systemic nature of the disease is much more obvious in the secondary stage. In addition to constitutional symptoms, such as malaise and low-grade fever, patients may demonstrate one of several varieties of nonpruritic rashes, lymphadenitis, mucous patches, condylomata lata, neurologic involvement, alopecia, or (less frequently) involvement of bone, liver, spleen, or kidneys.

Tertiary (late-acquired) syphilis appears 3 to 10 years following the primary lesion in 25% to 40% of patients who are not diagnosed and treated.3 With the widespread use of antibiotics, this late stage of syphilis has become very uncommon and is not discussed in this chapter.

Implications for Pregnancy

The clinical manifestations of primary and secondary syphilis are the same in the pregnant patient as in the nonpregnant. The principles of management have to do with early diagnosis and treatment in an effort to prevent fetal infection. Until recently it was believed that the spirochetal organism could not cross the placenta prior to 16 week's gestation. Harter and Benirschke reviewed the studies on which this theory was based, posed some possible explanations for the inability of earlier investigators to detect the spirochete in early abortuses, and reported finding T. pallidum in abortion specimens as early as 9 and 10 weeks' gestation.4 Spence states that T. pallidum can cross the placenta as early as 6 weeks.5

The fetus may escape infection. This is more likely to happen if the mother has been infected for a long time or if she contracts the disease very late in pregnancy. This information is of academic interest only, because once the diagnosis of syphilis in pregnancy is confirmed, the patient should be treated regardless of the time since infection.

Congenital syphilis¾a potentially eradicable disease¾persists due to treatment failures, lack of prenatal care, and inadequate prenatal screening. A recent report by McKown and Kapernick6 demonstrates the need for repeat screening in late pregnancy. They found that 37% of 73 women with syphilis in pregnancy failed to receive antepartum treatment, because they developed the disease following an initial negative prenatal screening test.

The clinical manifestations of congenital syphilis depend on the severity of the infection and the gestational age at the time of exposure. Although the organism has been shown to cross the placenta in the first trimester, it remains controversial as to whether or not syphilis is causally related to first-trimester losses, particularly early first-trimester losses. However, late pregnancy complications are well recognized, and intrauterine infection can result in premature labor, growth retardation, still-birth, or neonatal death.

Signs and symptoms of early congenital syphilis will appear within the first 2 years of life. Although most affected children will develop syphilitic rhinitis (“snuffles”) and perhaps a rash, numerous other organ systems may be involved, not unlike the adult secondary stage of the disease. By definition, late congenital syphilis appears in children after the age of 2 years. The clinical presentation can vary from patients who are totally asymptomatic to those who exhibit any combination of the following: Hutchinson's triad (interstitial keratitis, eighth nerve deafness, Hutchinson's teeth), saddle nose, prominent frontal bones, rhagades, gumma formation, and other complications of the skeletal and central nervous systems.


All pregnant patients should be screened for syphilis when they initiate prenatal care. Patients at high risk for developing syphilis should be rescreened in the third trimester, including such patients as those with multiple partners (if known), those with suspicious lesions, victims of sexual assault, and patients who have had sexual contact with persons known to have the disease. It is also recommended that the infant's cord blood be tested for syphilis whenever the mother's serologic status is unknown.

Aside from clinically suspicious signs and symptoms, three laboratory tests are commonly used to assist in the diagnosis and treatment of syphilis.

Darkfield microscopy permits direct visualization of the living spirochete and can accurately diagnose syphilis when interpreted by a qualified person; other treponemes, particularly those found in the oral cavity, can strongly resemble T. pallidum. The obvious limitation of the darkfield examination is that its usefulness is restricted to those stages of the disease during which an active, accessible lesion is present.

Nontreponemal serum tests (e.g., VDRL and rapid plasma reagin, or RPR) are relatively inexpensive, fairly sensitive tests that are widely used to screen general populations. These tests detect reagin, and biologic false-positive reactions can be associated with numerous acute and chronic infections, autoimmune diseases, debilitated states, and pregnancy. These tests generally will not become positive until at least 1 to 2 weeks after the appearance of the primary chancre (i.e., several weeks after infection) and thus may be negative in the primary stage of disease.

Interpretation of serologic tests for syphilis in the neonate requires a basic understanding of the antigen-antibody response. For example, a negative serology in a newborn does not necessarily indicate that the child has escaped infection; the fetus may have been infected too late in the prenatal period to induce an antibody response prior to the date of birth. Therefore, if maternal history or clinical findings place the infant at risk for developing congenital syphilis and the initial screening test is negative, the serologic test should be repeated monthly for 6 months.

Conversely, a positive neonatal serology does not mean that the infant has congenital syphilis. The antibody may have been passively transferred from the mother; if this is the case, the neonatal titer should not be greater than the maternal titer, and it should be completely cleared from the infant's circulation in a few weeks. Newborn infection should be seriously considered if the infant's titer is greater than the mother's, if the infant's titer continues to rise, or if the infant has IgM antibodies.

Treponemal antibody tests--fluorescent treponemal antibody absorption (FTA-ABS), Treponema pallidum immobilization (TPI), treponemal hemagglutination (TPHA), and enzyme-linked immunoabsorbent assay (ELISA)--while not specific for T. pallidum, can distinguish between treponemal disease and the biologic false-positives mentioned earlier. Thus, patients with a positive nontreponemal screening test should be further evaluated with one of these more specific tests to help confirm the diagnosis. The FTA-ABS is the most commonly used of these tests and is the first of all the serologic tests to turn positive. Once positive, however, the specific treponemal antibody tests remain positive indefinitely, regardless of treatment, and are therefore not good parameters on which to base a therapeutic response.


Once the diagnosis of syphilis in pregnancy is confirmed (or if the diagnosis cannot be excluded), the patient should be treated according to the stage of the disease. The treatment guidelines currently recommended by the Centers for Disease Control (CDC) are as follows:7

Primary, secondary, or latent syphilis of less than I year's duration should receive a single intramuscular injection of 2.4 million units of benzathine penicillin G. If allergic to penicillin, patients should receive erythromycin (base or stearate), 500 mg orally four times a day for 15 days.

Syphilis of more than 1 year's duration (except neurosyphilis) should be treated with 2.4 million units of benzathine penicillin G intramuscularly once a week for three successive weeks (7.2 million units total).

Patients who are allergic to penicillin should receive erythromycin, 500 mg orally four times a day for 30 days.

Erythromycin is not as effective as penicillin, it is less well tolerated, it may not produce adequate drug levels in the cerebrospinal fluid, and it may not cross the placenta in sufficient concentrations. Consequently, patients receiving this regimen must be followed with serologic titers and their infants should be given penicillin. Alternatively, recent studies have reported the successful desensitization of penicillin-allergic pregnant women by administering increasing doses of penicillin orally--an alternative which deserves serious consideration, particularly when erythromycin therapy appears to have failed or is unacceptable.8

The CDC guidelines should be followed for treatment of neurosyphilis and congenital syphilis, including recommendations for spinal fluid examinations.

Patients who can provide documentation of adequate prior treatment do not need to be retreated unless clinically or serologically they appear to have been reinfected.

All patients who have been treated for syphilis should have a VDRL test repeated at 3, 6, and 12 months following therapy and should demonstrate at least a fourfold decrease in titer during the first year. If adequately treated, most patients will eventually become serologically negative or will maintain a very low titer.

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Although gonorrhea remains the most common of the reported STD, its incidence has been decreasing since it peaked in the mid seventies; 780,000 cases were reported in 1987, the lowest number since 1972.9

In actuality, herpes and chlamydial infections may be equally as common as gonorrhea; that they are reported less frequently may simply reflect the fact that due to technology and expense widespread screening programs for these two STDs are not yet practical.

With respect to the female genital tract, gonorrhea is perhaps the most destructive of the venereal diseases. It may be totally asymptomatic, allowing its victim to unknowingly infect others; it may also produce severe, debilitating pelvic inflammatory disease, tubo-ovarian abscesses, and tubal occlusion, resulting in sterility. Thus, untreated disease can cause significant long-term psychological sequelae, as well as considerable physical discomfort.

Contrary to T. pallidum, which has remained susceptible to penicillin, Neisseria gonorrhoeae has developed partially resistant strains requiring higher doses of penicillin. Of greater concern is the fact that in the mid-1970s a strain of gonococcus was isolated that was totally resistant to penicillin. This penicillinase-producing N. gonorrhoeae (PPNG) seems to have originated in Southeast Asia and the South Pacific but has become an increasingly significant public health problem in the United States.

While the overall incidence of gonorrhea has declined, the percent of cases due to resistant strains has increased markedly. The first case of PPNG in the United States was reported in 1976 and by 1980 the annual incidence had risen to approximately 1000. In 1987 over 25,000 cases of resistant strains were reported, representing 3.2% of the total cases. In addition to PPNG, other resistant strains have been identified¾chromosomally mediated resistant strains (CMRNG) were first identified in 1983, followed by tetracycline resistant forms in 1985.10

Clinical Manifestations

As mentioned earlier, the disease may be completely asymptomatic or minimally symptomatic by producing dysuria or a vaginal discharge. The clinical picture depends on the site and severity of the infection. The causative organism, N. gonorrhoeae, primarily infects columnar and pseudostratified epithelium. Because its mode of transmission is by sexual contact, it is therefore not surprising that the major sites of infection are the urogenital, anorectal, and oropharyngeal areas.

Rectal infections may be asymptomatic or may produce symptoms of proctitis with a mucopurulent discharge. Although transmitted through sexual activity, patients do not have to participate in actual anal intercourse to develop anorectal infection. It can be transmitted by penile contact in the perineal region, by hand, or by toilet paper. Rectal infections are usually associated with genital infections.

Gonococcal pharyngitis is usually asymptomatic but may present as mild sore throat. In some cases the pharynx may be the only site of infection, depending on the person's sexual practice.

The genitourinary tract is the site of most infections. In the nonpregnant female, the organism can produce inflammation of the lower genital tract glands (Bartholin's, Skene's) or ascend by way of the cervix to produce salpingitis, peritonitis, and adnexal abscesses. Pregnant patients rarely have symptomatic intraperitoneal disease; manifestations of acute gonococcal infection in pregnancy usually are limited to the vulvovaginal area.

Cases that are inadequately treated can progress to gonococcal septicemia characterized by low-grade fever, migratory polyarthritis, and dermatitis. The skin lesions can appear anywhere on the body, although the face seems to be spared. They are frequently found on the extremities, sometimes near joints, and progress from a maculopapular rash through a pustular stage to finally become a hemorrhagic-necrotic lesion that eventually disappears altogether. If untreated, the affected joints can proceed to radiologically evident articular destruction. Other less common consequences of gonococcal septicemia include endocarditis, myocarditis, pericarditis, and meningitis.

Implications for Pregnancy

All prenatal patients should be cultured for gonorrhea during their initial visit; in addition, it is highly desirable to reculture prenatal patients in the third trimester, particularly those who are at high risk for STDs. Solola and colleagues studied patients who had been attending their prenatal clinic by reculturing them at the time of admission for delivery.11 They found that 9.4% of these patients had gonorrhea; one third of these patients had negative antenatal cultures, while two thirds had positive cultures that were treated. Any patient with a positive culture should be treated appropriately and recultured following therapy to verify cure.

The two major concerns during pregnancy are maternal septicemia and neonatal infection. For whatever reasons, patients in the second and third trimesters of pregnancy seem to be particularly susceptible to developing disseminated gonococcal infection. Therefore, pregnant patients with positive cervical cultures, highly suspicious skin lesions, or acute arthritic complaints should be evaluated closely to rule out disseminated disease.

Ophthalmia neonatorum is the most common manifestation of neonatal infection. This is a purulent conjunctivitis that can result in blindness if left untreated. The usual method of infection is by direct contact with the bacteria during a vaginal delivery through an infected cervix. The conjunctival infection can be prevented by applying one of several prophylactic agents to the newborn's eyes (e.g., silver nitrate, tetracycline, or neomycin); such a procedure should be routine in any hospital that provides maternity care.

Infants can also be infected in utero. If a patient should be unfortunate enough to have premature rupture of the membranes while harboring an active cervical infection, she could develop gonococcal amnionitis and her infant could suffer significant morbidity from widespread disease. This combination of events has been termed the amniotic infection syndrome.


Although researchers continue to seek new diagnostic tools, to date none of the new methods has been simple enough, accurate enough, and cheap enough to replace the time-honored Gram stain and culture.


Due to its low cost, technical simplicity, and instantaneous results, the Gram stain remains a valuable aid in the diagnosis of gonorrhea; it is particularly useful for situations in which patient follow-up is likely to be suboptimal (e.g., emergency rooms). Its limitations include the fact that its lack of specificity for the gonococcus and possible errors in staining technique can yield false-positive or false-negative results. For these reasons a culture should also be done, whenever possible, even though the need for immediate treatment may be determined by the Gram stain. Lossick and associates reported that the Gram stain detected 70% of their 1675 cases of gonorrhea, permitting institution of therapy at the initial clinic visit.12 Of the 124 patients who were not treated at the initial visit, 9 developed pelvic inflammatory disease during the interval between their first visit and their return to the clinic for treatment. To make the presumptive diagnosis of gonorrhea on the basis of a Gram's stain, one should be able to identify gram-negative, intracellular diplococci. It should be emphasized that the gram stain is not reliable for smears taken from the pharynx, because the oral cavity normally can harbor meningococci and saprophytic Neisseria.


Culturing the organism is the only method of definitive diagnosis. Depending on the person's sexual history, cultures should be taker of any possible site of infection, including the cervix, urethra, rectum, and pharynx. Several commercially prepared culture kits are available many with their own means of creating a carbon dioxide atmosphere. Culture media may be nonselective or selective. The former contains the basic substances to permit growth of the gonococcus as well as other organisms; the latter also contains antibiotics to inhibit the growth of contaminant such as Proteus, other bacteria, and fungi. Most laboratories will have one or more additional test: available to confirm the diagnosis should any doubt exist with the interpretation of the culture results. Antibiotic sensitivity tests should also be. performed on patients at risk for harboring one of the PPNG strains or on patients for whom initial therapy appears to have been unsuccessful.


Because administration of tetracycline is contraindicated, pregnant patients with uncomplicated gonorrhea should be treated with one of the following regimens:10

  1. Amoxicillin, a single dose of 3.0 g orally, with 1.0 g probenecid
  2. Ampicillin, a single dose of 3.5 g orally, with 1.0 g probenecid
  3. Aqueous procaine penicillin G, 4.8 million units intramuscularly with 1.0 g probenecid by mouth. This injectable regimen offers no significant advantage over the previously mentioned oral therapies and carries with it the possibility of anaphylactic reactions.
  4. Ceftriaxone, 250 mg intramuscularly.

Regardless of which of the above treatments is prescribed, the patient should also receive erythromycin (base or stearate), 500 mg by mouth four times daily for seven days.

Patients who are allergic to penicillin or who have documented infections with a PPNG should be treated with the ceftriaxone-erythromycin combination. Physicians who practice in areas in which PPNG is endemic (1%-3% of all gonorrheal: strains) or hyperendemic (>3%) should consider using the ceftriaxone-erythromycin regimen for all cases of uncomplicated gonorrhea.

Suggested treatment schedules for other complications of gonococcal infections, including septicemia, can be found in the CDC treatment guidelines.

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Although not as common as gonorrhea or chlamydia, genital herpes is probably the most feared and potentially the most devastating of the STDs discussed in this chapter. It is the only one for which there is no cure. Once infected, a person is subjected to periodic recurrences, which can result in considerable emotional distress or sexual dysfunction. In addition, herpes is known to be the cause of life-threatening neonatal infections and is strongly associated with the development of cervical cancer in later years.

Because herpes is not a reportable disease, accurate incidence statistics are not available for the general population. Although genital herpes accounted for more than 450,000 physician-patient consultations in 1984, many cases escape detection.13 There are several reasons for this marked underreporting: (1) the lesions may spontaneously heal before the patient seeks medical attention, (2) the patient may diagnose herself and decide to forego the expenses of an office visit, particularly if she is aware that there is no cure, (3) the patient may be asymptomatic, (4) the cultures may be falsely negative.

Herpes simplex virus (HSV) infections in man can be caused by either the type I (HSV-1) or the type II (HSV-2) virus. Most infections of the head and upper torso are due to HSV-1; most genital infections are caused by HSV-2. There is considerable overlap, however, and the virus can be transmitted by masturbation, orogenital contact, or poor hygiene.

Clinical Manifestations

Primary infections are generally more severe than recurrent episodes and are frequently associated with signs and symptoms of viremia, such as fever and malaise. Patients may experience paresthesias or other unusual sensations of the infected area just prior to the appearance of vesicles. The vesicular stage is often pruritic, becoming quite painful when the vesicles rupture. Unless the vesicles become secondarily infected, they will eventually spontaneously heal without a scar.

Recurrent episodes can be highly variable in frequency and severity, but generally are less symptomatic than the primary infection. The virus remains dormant in the nerve ganglia until reactivated by another systemic illness, emotional stress, a debilitating disease, or an immunosuppressed condition.

Implications for Pregnancy

The importance of genital herpes in pregnancy cannot be overemphasized. There is some evidence to suggest that pregnancy is associated with an increased incidence of disseminated herpes infections, usually seen only in the otherwise medically compromised adult.14,15 Although rare, such cases of disseminated infection have maternal mortality rates as high as 50%.16 Fortunately, in most cases the course of maternal herpes will not differ from that in the nonpregnant patient.

The principal concern caused by herpes in pregnancy is the potential devastation that could be caused if the infant becomes infected. Although the incidence of neonatal herpes infection is low--ranging from 1/3000 to 1/20,000 live births--infected newborns have a 60% mortality rate, with more than half of the survivors being neurologically damaged.17

The infants usually contract the virus during a vaginal delivery through an infected birth canal. If the membranes have ruptured, the possibility of an ascending, transcervical infection also exists. However, intact membranes do not guarantee the absence of infection. Transplacental infections can occur. In fact, in a nationwide surveillance, 12% of all infants diagnosed as having HSV infections had been delivered by cesarean section prior to rupture of the membranes.17

Primary infections in pregnancy are much more likely to result in significant infant morbidity than recurrent episodes. 18,19 Although controversial it is quite possible that the infants of mothers with recurrent infections may benefit from passive immunity secondary to maternal antibody production.20 HSV titers are reported to be lower and the virus is less likely to involve the cervix with recurrent infections. Following a primary first episode of HSV-2, 10.6% of weekly cultures detected asymptomatic cervical shedding, compared with only 0.5% of visits following a nonprimary first episode.18

While researchers continue to seek a cure, clinicians must concentrate on prevention by detecting maternal infections during the prenatal period and by managing infected patients according to a protocol based on sound judgment and established results. Obviously, the most effective way to detect HSV infection in pregnancy is to routinely culture all prenatal patients; this would be particularly ideal as 33% to 50% of infected pregnant women are asymptomatic and have no visible external lesions.21,22 Such massive screening, however, is not practical in view of the fact that prenatal screening studies indicate a very low incidence of positive cultures--in the range of 0.65–1%.17

Admittedly, certain groups of patients are at greater risk for having herpes in pregnancy, including patients with suspicious lesions, patients with a history of herpes, and patients whose sexual partners have a history of past or present infection. However, recent evidence that antepartum maternal cultures fail to predict the infant's exposure to HSV at delivery has significantly altered the management of these patients.23 Until recently a variety of protocols suggested that pregnant patients at risk for genital herpes be cultured at their initial prenatal visit and several times (even weekly) after 32 weeks' gestation. The objective of this intense surveillance was to minimize the infant's potential exposure to active virus by recommending a cesarean section if the most recent culture was positive or active lesions were present at the time of delivery. There were several problems with this approach: (1) asymptomatic virus shedding can be very brief and thus missed even though weekly cultures are performed; (2) cultures may not become positive for 6–7 days, limiting the value of any cultures done within one week of delivery; and (3) over 60% of infected infants are born to asymptomatic mothers, most of whom have no prior history of herpetic infection and would not, therefore, be included in the high-risk group to be cultured antenatally.17,24

Current recommendations for the management of patients at risk for genital herpes infection during pregnancy are:25

  1. For women with a history of genital herpes, but without lesions, there is no need to do weekly prenatal cultures and a vaginal delivery should be anticipated. Cultures should be obtained at the time of delivery to identify potentially exposed infants.
  2. For women with lesions
    1. If lesions are present when labor begins or membrane rupture occurs, a cesarean delivery can reduce the risk of neonatal infection and should be performed as soon as possible.
    2. If lesions are present near term, but prior to labor or membrane rupture, cultures should be obtained at three- to five-day intervals to document the absence of virus at the time of delivery.

Infants of mothers with positive herpes during late pregnancy should be followed closely during the first month of life, because the average age at onset of illness is 11 to 16 days.

Postpartum care should be dictated by the degree of risk of infection. Aside from emphasizing good puerperal hygiene, the infected mother can be treated as a routine postpartum patient, although her contact with others should be restricted. Breast-feeding is permissible as long as the infant does not come in direct contact with any lesions, and rooming-in is probably beneficial. Infants at high risk of infection should have viral cultures, liver function tests, and spinal fluid examinations; circumcision should be delayed. Such infants should be closely observed--hospitalized, if necessary--for 2 weeks.


The physical findings are frequently so characteristic that the diagnosis can often be made clinically. However, due to the serious social and medical implications mentioned earlier, laboratory confirmation is desirable whenever possible.

Cell culture is the most accurate method of diagnosis, but has many disadvantages. Because the amount of live virus recoverable from any given lesion decreases following rupture of the vesicle, older lesions may yield falsely negative cultures. Strict attention must be paid to culture technique and the type of transport media used. Many laboratories are reluctant to report a culture as negative unless it has been incubated for at least 6 to 7 days. Lastly, herpes cultures are generally quite expensive, although newer techniques have resulted in recent cost reductions.

Cytologic examination of smears taken from suspicious lesions may demonstrate characteristic cellular changes. Routine Pap smears, however, have been reported to be positive in only three-fourths of cases with culture-proven herpes.26 Improvements in cytologic diagnosis based on enzyme-linked (ELISA) or fluorescein-tagged herpes antibodies have made cytologic evaluation considerably more accurate. Some even prefer these antibody-dependent reactions to cell culture, as the former can be positive in the presence of dead virus.

Diagnostic methods of the future include nucleic acid hybridization techniques that include both DNA and RNA probes and rapid viral diagnosis (also known as accelerated culture technique).

Serum antibody titers are not very useful. Many adults are already seropositive due to childhood or asymptomatic adult infections. Thus, they may be of value only if one can document either seroconversion (from negative to positive) or a significant rise in titer, both of which occur following a primary infection. The antigenic stimulus in recurrent infections is generally not strong enough to elicit a significant rise in the patient's basic titer.


Because there is no cure for herpes, therapy should be directed toward relief of discomfort and appropriate treatment of complications (e.g., secondary bacterial infection or urinary retention). Painful perineal lesions can be treated with sitz baths, good hygiene, and topical anesthetics.

Acyclovir is an antiviral drug that has been shown to decrease the severity and duration of primary genital herpes infections. Although initially not thought to be effective for the treatment of recurrent infections, oral acyclovir can reduce the duration of the acute phase of recurrent disease by approximately two days.27 Long-term suppressive therapy significantly reduces the frequency of recurrent episodes; however, the drug can only be taken for a maximum of six months, and once treatment is discontinued clinical episodes recur at the same frequency. The safety of systemic acyclovir during pregnancy has not been established. Consequently, except for life-threatening clinical situations, pregnant women should not be treated with acyclovir and women who are receiving suppressive therapy should be counselled to avoid pregnancy during treatment.

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Chlamydial infection is the most prevalent STD in the United States today. Because it is not a reportable disease, accurate nationwide statistics are not available. However, several studies from family planning and venereal disease clinics, using both symptomatic and asymptomatic patients, have reported the incidence of chlamydial infection to be significantly higher than either herpes or gonorrhea.28 Current estimates indicate that the incidence of Chlamydial infections exceeds 3 million cases annually in the U.S.29 Although Chlamydia has long been known to cause ophthalmologic infections and lymphogranuloma venereum, more recent interest has focused on its association with pelvic and perinatal infections similar to those caused by gonorrhea: urethritis, cervicitis, salpingitis, conjunctivitis. Much of this interest was stimulated by the discovery that Chlamydia was a major cause of nongonococcal urethritis (NGU) in males. As more accurate, less expensive methods of diagnosis have been developed, Chlamydia has been confirmed as a significant human genital tract pathogen. So far, 15 immunotypes of Chlamydia trachomatis have been identified, eight of which are responsible for the above-mentioned STD (three others cause lymphogranuloma venereum, the remaining four produce trachoma).

The chlamydial organism has been particularly interesting to microbiologists because it shares certain characteristics with both viruses and bacteria and is considered a parasitic bacterium owing to its obligatory intracellular existence.

Clinical Manifestations

In the female, C. trachomatis has been directly or indirectly associated with the following:

  Pelvic inflammatory disease
  Fitz-Hugh-Curtis syndrome

As is the case with most STDs, patients with chlamydial infection may be completely asymptomatic. Also, certain groups of women are at greater risk for developing the infection. About 5% of the general population has genital Chlamydia; this percentage increases fivefold for patients attending venereal disease clinics and can be as high as 70% for female patients whose partners have NGU or culture-proven Chlamydia.

Twenty-five to 50% of infants exposed to the chlamydia organism at birth will develop acute conjunctivitis of the newborn. Although the disease should be treated if diagnosed, most cases will resolve spontaneously without significant sequelae. Ten to 20% of exposed infants will develop pneumonia in the first few months of life and chlamydial organisms are very likely responsible for many cases of undiagnosed upper respiratory trace infections during this same period. Although otitis media is not as common, it is associated with the pneumonia in about 50% of cases. Chlamydial pneumonia usually does not produce a febrile response, yet may cause apneic episodes and airway obstruction; for these reasons it has been suggested that Chlamydia may play a role in the sudden infant death syndrome, and the possibility of such a relationship deserves further study.

Implications for Pregnancy

There are conflicting reports regarding the importance of chlamydial infection during pregnancy. Chlamydia trachomatis has been named as a possible cause of spontaneous abortions, preterm labor, premature rupture of the membranes, low-birth-weight infants, fetal deaths, and postpartum endometritis. Studies continue to report conflicting results, however, and these claims remain to be substantiated.29,30,31 One variable that may help to explain some of the apparently contradictory reports is the severity of infection. Several authors have reported that although chlamydial infection alone did not increase the risk of an adverse pregnancy outcome, a subset of chlamydia-positive patients who also had IgM antibody against Chlamydia trachomatis did demonstrate increased incidences of premature rupture of the membranes, preterm delivery, low-birth-weight infants, and postpartum endometritis.29,32 Further clarification of this controversy will be necessary to implement appropriate interventions--that is, should all pregnant patients with chlamydia be treated or should therapy be reserved for those in the third trimester, the primary intent of which would be to prevent neonatal infection.

Universal screening of all pregnant patients is not warranted and studies have indicated that it is not cost-effective in low-risk groups--for example, patients undergoing chorionic villus sampling.33 Patients at risk for the infection may benefit from testing at the time of their first prenatal visit and again in the third trimester.34 Risk factors for chlamydial infection include single marital status, age less than 20, low socioeconomic status, presence of other STDs, or a partner with NGU. In areas with high prevalence rates, routine prenatal screening for C. trachomatis has been reported to be cost effective.35


Cytology is not a good method of diagnosing chlamydial infections of the female genital tract, owing to its poor sensitivity. However, just as is the case with gonorrhea, cytologic examination still has usefulness in the diagnosis of these infections when other methods are not available. Serologic tests are equally unrewarding, particularly since many adults already have antichlamydial antibodies. Although there appears to be a direct correlation between antibody titer and severity of disease, the significance of this information is of limited clinical value.

Two nonculture-dependent methods for the detection of Chlamydia trachomatis have achieved considerable recognition. One utilizes direct fluorescent antibody staining, while the other is an enzyme immunoassay technique. Both methods are less expensive, faster, and less susceptible to errors in technique than routine culture. Recent studies report that these nonculture-dependent methods are equally sensitive and perhaps more sensitive than routine cell culture in the detection of C. trachomatis during pregnancy.36,37

Culture remains the most consistently accurate method of diagnosis. The disadvantages of cell culture include cost, technical difficulty, problems with specimen handling and transport, possibility of contamination, and time required for incubation and preparation. Regardless of which diagnostic method is utilized, the clinician should not assume that a negative test excludes the possibility of infection and should retest suspicious cases when appropriate.


During pregnancy treatment should be administered to all women who have a proven infection with C. trachomatis; if diagnostic tests are not performed, treatment should be given to women with mucopurulent cervicitis and to women whose partners have NGU or nongonococcal epididymitis.7 The drug of choice for C. trachomatis is tetracycline. However, because tetracyclines are contraindicated in pregnancy, one of the following drug regimens should be prescribed:

  1. Erythromycin, 500 mg orally four times a day for at least 7 days
  2. Erythromycin, 250 mg orally four times a day for at least 14 days

All male partners should simultaneously be treated with either tetracycline or doxycycline for seven days. Currently, there are no acceptable alternatives to erythromycin in pregnancy. Treatment failures or reinfection should be retreated with erythromycin.

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1. Charles D: Syphilis. Clin Obstet Gynecol 26: 125, 1983

2. Centers for Disease Control: Syphilis and Congenital Syphilis, United States, 1985-1988. MMWR 37:486, 1988

3. Willcox RR, Willcox JR: Diseases caused by spirochaetal organisms. In Venereological Medicine, p 190. London, Grant McIntyre, 1982

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7. Centers for Disease Control: 1985 STD Treatment Guidelines. MMWR 34(4S):21, 1985

8. Wendel GD, Stark B J, Jamison RB et al: Penicillin allergy and desensitization in serious infections during pregnancy. N Engl J Med 312: 1229, 1985

9. Centers for Disease Control: Summary of notifiable diseases. United States, 1987. MMWR 36(54):54, 1988

10. Centers for Disease Control: Antibiotic-resistant strains of Neisseria gonorrhoeae. MMWR 36(5S):1, 1987

11. Solola AS, Ryan GM, Ling FW: Gonorrhea during the intrapartum period. Am J Obstet Gynecol 144: 351, 1982

12. Lossick JG, Smeltzer MP, Curran JW: The value of the cervical gram stain in the diagnosis and treatment of gonorrhea in women in a venereal disease clinic. Sex Transm Dis 9: 124, 1982

13. Becker TM, Stone KM, Cares W: Epidemiology of genital herpes infections in the United States: The current situation. J Reprod Med 31: 359, 1986

14. Kobbermann T, Clark L, Griffin WT: Maternal death secondary to disseminated herpesvirus hominis. Am J Obstet Gynecol 137: 742, 1980

15. Baker DA, Phillips CA, Roessner K et al: Suppression by progesterone of nonspecific in vitro lymphocyte stimulation in mice as a mechanism for the enhancement of herpes simplex virus type II vaginal infection. Am J Obstet Gynecol 136: 440, 1980

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18. Brown ZA, Vontver LA, Benedetti J et al: Effects on infants of a first episode of genital herpes during pregnancy. N Engl J Med 317: 1246, 1987

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20. Prober CG, Sullender WM, Yasukawa LL et al: Low risk of herpes simplex virus infections in neonates exposed to the virus at the time of vaginal delivery to mothers with recurrent genital herpes simplex virus infections. N Engl J Med 316: 240, 1987

21. American College of Obstetricians and Gynecologists: Sexually transmitted Diseases (ACOG Technical Bulletin 51). Chicago, ACOG, 1978

22. Grossman JH, Wallen WC, Sever JL: Management of genital herpes simplex virus infection during pregnancy. Obstet Gynecol 58: 1, 1981

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25. Gibbs RS, Amstey MS, Sweet RL et al: Editorial: Management of genital herpes infection in pregnancy. Obstet Gynecol 71: 779, 1988

26. American Academy of Pediatrics: Perinatal herpes simplex virus infections. Pediatrics 66:147, 1980

27. Baker DA, Milch PO: Acyclovir for genital herpes simplex virus infections--A review. J Reprod Med 31: 433, 1986

28. Sweet RL, Schacter J, Landers DV: Chlamydial infections in obstetrics and gynecology. Clin Obstet Gynecol 26: 146, 1983

29. Sweet RL, Landers DV, Walker C et al: Chlamydia trachomatis infection and pregnancy outcome. Am J Obstet Gynecol 156: 824, 1987

30. Rees E: Infections of the female genital tract--A report from the Fifth International Symposium on Human Chlamydial Infection. Sex Transm Dis 9: 218, 1982

31. Rettig PJ: Perinatal infections with Chlamydia trachomatis. Clin Perinatol 15: 321, 1988

32. Harrison HR, Alexander ER, Weinstein L et al;Cervical Chlamydia trachomatis and mycoplasmal infections in pregnancy: Epidemiology and outcomes. JAMA 250: 1721, 1983

33. Moncada JV, Schachter J, Golbus MS: Chlamydia trachomatis infection among patients undergoing chorionic villus sampling. Am J Obstet Gynecol 156: 915, 1987

34. Frigoletto FD, Little GA (eds): Guidelines for Perinatal Care, 2nd ed. Elk Grove Village, American Academy of Pediatrics, 1988

35. Schachter J, Sweet RL, Grossman M et al: Experience with the routine use of erythromycin for chlamydial infections in pregnancy. N Engl J Med 314: 276, 1986

36. Smith JW, Rogers RE, Katz BP et al: Diagnosis of chlamydial infection in women attending antenatal and gynecologic clinics. J Clin Microbiol 25: 868, 1987

37. Baselski VS, McNeeley SG, Ryan G et al: A comparison of nonculture-dependent methods for detection of Chlamydia trachomatis infections in pregnant women. Obstet Gynecol 70: 47, 1987

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