SEXUALLY TRANSMITTED DISEASES docx

681 A sexually transmitted disease (STD) is any infection acquired pri- marily through sexual contact. STD is a general term, and the causative organisms, which are harbored in the blood or body se- cretions, include viruses, mycoplasmas, bacteria, fungi, spirochetes, and minute parasites (e.g., crab lice, scabies). Some of the organ- isms involved are found exclusively in the genital (reproductive) tract, but others exist simultaneously in other systems. Additionally, various STDs often coexist, and when one is found, others should be suspected. There is a range of intimate bodily contact that may transmit STDs, including kissing, sexual intercourse, anal inter- course, cunnilingus, anilingus, fellatio, and mouth or genital to breast contact. Physicians are required to report most STDs to lo- cal public health departments. The vast majority of female genital tract infections are acquired sexually. Female genital tract infections are divided into lower geni- tal tract and upper genital tract (or pelvic) infections. The lower gen- ital tract infections (including a number of STDs and their sequelae) are discussed in Chapters 20 and 21, and they include viral infections (herpes simplex, human papillomavirus, and molluscum contagio- sum) and vulvar infestations (pedicularis pubis and scabies). Com- mon types of vulvovaginitis (e.g., Trichomonas, bacterial vaginosis, and Candida) and some of the sequelae of STDs (e.g., infections of Bartholin glands and cervicitis) also are discussed in Chapter 20. This chapter deals with upper genital tract infections, the most serious, most directly sexually transmitted diseases and their sequelae. HUMAN IMMUNODEFICIENCY VIRUS (HIV) INFECTIONS The human immunodeficiency virus (HIV) was first reported to cause disease in 1981. In the United States, AIDS is now the fifth 24 SEXUALLY TRANSMITTED DISEASES CHAPTER Copyright 2001 The McGraw-Hill Companies. Click Here for Terms of Use. BENSON & PERNOLL’S 682 HANDBOOK OF OBSTETRICS AND GYNECOLOGY leading cause of death among women of childbearing age. More- over, it is the leading cause of death in this age group in New York City. This is now a worldwide crisis, with millions affected, especially in developing countries. One of the problems in recog- nition of HIV infection is a long, asymptomatic latency of 2 months to 5 years. The mean age at diagnosis of HIV infection is 35 years. The virus is present in blood and all body fluids and is trans- mitted by sexual contact (.70%), by parenteral exposure to infected blood or body fluids, or by transplacental passage of the virus from mother to fetus. The highest-risk groups for HIV infection are ho- mosexuals, bisexual men, intravenous drug abusers, and hemo- philiacs receiving blood transfusions. Others at high risk are pros- titutes and heterosexual partners of men in the high-risk groups. All blood must be screened for HIV before transfusion to minimize transfusion risk. Women acquire the virus more easily from men rather than the reverse because the concentration of HIV in semen is high and mucosal breaks at the introitus or vagina with inter- course occur more commonly than do breaks in penile skin. Although anti-HIV antibodies develop within 12 weeks of ex- posure, 45%–90% of persons infected with HIV will develop symp- toms of an acute infection similar to mononucleosis within a few months. They experience weight loss, fever, night sweats, pharyn- gitis, lymphadenopathy, and an erythematous maculopapular rash. Most of these symptoms resolve within a few weeks, although the patients remain infectious despite being asymptomatic. Some will progress to develop symptoms of AIDS-related complex (ARC), with early immunosuppression (decreased CD4ϩ lymphocytes). ARC is usually marked by generalized lymphadenopathy, weight loss, diarrhea, malabsorption, and wasting. Some patients experi- ence further immunosuppression and develop AIDS (any of the symptoms of acute sepsis, opportunistic infections, Kaposi’s sar- coma, cognitive difficulties, or depression). Once AIDS has been diagnosed, mortality is Ͼ90%. Immunologic abnormalities associ- ated with AIDS include (but are not limited to) lymphopenia, de- creased T helper cells, decreased T lymphocytes, hypergamma- globulinemia, and an inverted T4/T8 ratio. Because there is no cure for HIV, current therapy only slows the progression of the disease. Hence, there is every reason to stress prevention. Other than abstinence or having a monogamous rela- tionship with a known noninfected partner, using latex condoms lu- bricated with nonoxynol 9 is the most effective method of limiting the risk of infection. If a woman is HIV positive, she should be counseled (1) not to donate blood, plasma, tissue, or organs; (2) to avoid pregnancy; (3) to maintain a monogamous relationship; and (4) to assiduously use condoms lubricated with nonoxynol 9 during any sexual contact. HIV antibody testing begins with the enzyme-linked im- munosorbent assay (ELISA), which has a Ͼ95% sensitivity and a Ͼ99% specificity if repeatedly positive. If the ELISA is positive, a Western blot assay must be performed to confirm the diagnosis. False-negative results are rare unless the patient is too early in the disease to have formed antibodies. HIV screening (after informed consent has been obtained and assurances of confidentiality pro- vided) should be encouraged for women in the following cate- gories: intravenous drug users, prostitutes, sex partner(s) of men who are HIV positive or at risk for HIV, those with other sexually transmitted disease, those who received blood transfusions between 1978 and 1985, those with clinical signs and symptoms of HIV in- fection, inhabitants of a country with high endemic heterosexual HIV infection, prison inmates, and one who considers herself at risk. Pregnancy does not appear to alter the progression of HIV in- fection, but the chance of the fetus acquiring the virus is 20%–50%. The neonate may be infected during labor and delivery by mater- nal blood or body fluids or may be infected during breastfeeding. The mode of delivery does not influence the development of pedi- atric AIDS. The acute illness associated with HIV in pregnancy may be misdiagnosed if HIV serologic testing is not performed. When HIV infection is diagnosed during pregnancy, treatment should be delayed because of the teratogenic potential of the medications used. The pregnant HIV-infected woman should be screened for other STDs, along with evaluation for opportunistic infection. A baseline serologic study for CMV and toxoplasmosis, TB skin test- ing, and chest radiograph are recommended. Recently AZT and other chemotherapeutic agents have been found to decrease maternal–fetal and neonatal transmission of HIV. When caring for HIV positive mothers, health care providers should obtain the very latest infor- mation in this important and rapidly evolving area. Care of the HIV-positive woman and her infant in the peri- partum and postpartum interval includes protection of health care workers by using universal infection control guidelines (e.g., water-repellent gowns, gloves, masks, goggles for potential splash situations, wall or bulb suctioning). Scalp electrodes and fetal scalp blood samples should be avoided (potential entry site for HIV if fetus is not already infected). Circumcision should not be done if the neonate is HIV positive. Because anti-HIV IgG anti- body passes through the placenta, the infant may be seropositive without being infected. Abnormal facial features have been de- scribed in some HIV-positive newborns, but this is not common. CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 683 BENSON & PERNOLL’S 684 HANDBOOK OF OBSTETRICS AND GYNECOLOGY If neonatal/pediatric AIDS develops, the course of the disease is much more rapid than in adults, with death in months rather than years. GONORRHEA Neisseria gonorrhoeae (one of the most common causes of STD) is a gram-negative diplococcus that usually resides in the female in the urethra, cervix, pharynx, or anal canal. The infection primary involves the columnar and transitional epithelium of the genitouri- nary tract. The organism is very fastidious and sensitive to drying, sunlight, heat, and most disinfectants. Special media (e.g., Thayer- Martin) are required to achieve optimal recovery. Culture of the lower genital tract is usually obtained by rotating a cotton swab for 15–20 sec deep in the endocervical canal. If a rectal swab is taken, the incidence of recovery increases from 85% to Ͼ90%. In upper genital tract infections (salpingitis, peritonitis) proven by laparo- scopically obtained culture, only ϳ50% of the lower genital tract cultures will reveal N. gonorrhoeae. After exposure to an infected partner, 60%–90% of women and 20%–50% of men will become infected. Untreated, 10%–17% of women will develop pelvic inflammatory disease (PID). If a woman is positive for N. gonorrhoeae, she has a 20%–40% chance of also having chlamydial infection, syphilis, or hepatitis. Early symptoms typically include vaginal discharge, urinary frequency, and rectal irritation. Some report burning, itching, or in- flammation of the vulva, vagina, cervix, or urethra, although most women are asymptomatic. Bartholin duct(s) and gland(s) may be involved, as evidenced by swelling or abscess formation (Chapter 20). Acute pharyngitis and tonsillitis may occur, but this is uncom- mon. Rarely, the asymptomatic carrier will develop a disseminated infection with polyarthralgia, tenosynovitis, and dermatitis or meningitis or endocarditis. Although ophthalmic infection most commonly occurs in neonates born to an infected mother, adult oph- thalmitis may result from autoinoculation. The diagnosis may be presumed when a stained smear from the involved sites reveals intracellular gram-negative diplococci. How- ever, confirmation after growth on selective medium is essential. The culture for gonorrhea must include penicillin resistance testing because 2%–3% of strains in the United States are penicillin re- sistant. Gonorrhea must be reported to the state public health au- thorities. The patient and all sexual partners must be treated. Other concomitant diseases must be ruled out and treated if present. The preferred adult regimen for uncomplicated disease is ceftriaxone 125 mg IM (single dose), cefixime 400 mg PO (single dose), or spectinomycin 2 g IM (single dose for patients with cephalosporin intolerance). Although spectinomycin is not reliable therapy for pha- ryngeal infection, ceftriaxone and cefixime are effective in all sites. Given the high rate of coinfection, treatment for chlamydial infec- tion (see the following section) is necessary. Because of the emer- gence of resistant organisms, repeat cultures should be performed within 7 d of completion of therapy to ensure cure. Disseminated disease requires hospitalization. Meningitis and endocarditis must be confirmed or ruled out. Recommended therapy is ceftriaxone 1 g IM or IV qd or cefotaxime or ceftrizoxime 1 g IV q8h. Patients with allergy to beta-lactamase drugs may be treated with spectromycin 2 g IM q12h. If sensitivity testing confirms that the organism is penicillin-sensitive, ampicillin 1 g q6h may be given. Whichever regimen is chosen, therapy should be continued for 7 days. The prognosis for properly treated gonorrhea is good, but future fertility may be compromised. CHLAMYDIAL INFECTIONS Chlamydia trachomatis is an obligate intracellular microorganism with a cell wall similar to that of gram-negative bacteria. Although they are classified as bacteria, contain both DNA and RNA, and di- vide by binary fission. Chlamydia grow only intracellularly, as do viruses. Since most of the C. trachomatis serotypes attack only columnar epithelial cells (except the aggressive L serotypes), signs and symptoms tend to be localized to the infected area (e.g., eye or genital tract) without deep tissue invasion. CERVICITIS C. trachomatis cervical and tubal infections occur in women of young age (2–3 times higher in women Ͻ20 years), with numerous sexual partners, of low socioeconomic status, with other STDs, and with oral contraceptive use. Barrier contraception tends to decrease the infection rate. Pregnant women have an incidence of 8%–12%. SIGNS AND SYMPTOMS Typically, a mucopurulent discharge develops with cervical chlamy- dial infection, and the cervix shows hypertrophic inflammation (mu- copurulent cervicitis). The infection may be asymptomatic in 15% of nonpregnant, sexually active women. CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 685 BENSON & PERNOLL’S 686 HANDBOOK OF OBSTETRICS AND GYNECOLOGY LABORATORY FINDINGS The most frequently used method of detection is a direct fluores- cein-conjugated monoclonal antibody test (available in kit form). This is rapid, sensitive (85%–93%), and specific (ϳ99%). Speci- mens are generally obtained as described for gonorrhea (p. 684). Tissue culture is required for culture of C. trachomatis, and because of the high cost, limited availability, and 2–6 day delay, it is used infrequently. Although Giemsa staining of conjunctival specimens in neonates is fairly successful in identifying chlamydial inclusions, this technique is only 40% accurate in genital infections. DIFFERENTIAL DIAGNOSIS N. gonorrhoeae is the only other predominant organism causing a mucopurulent cervicitis. Thus, fluorescent antibody tests or cultures on selective medium are mandatory for differentiation. Both or- ganisms may be present simultaneously. TREATMENT Cure rates of .95% can be achieved with the use of one of several regimens. The preferred regimen is tetracycline 500 mg PO qid for 7 days or doxycycline 100 mg bid for 7 days. If tetracyclines can- not be taken or are contraindicated, erythromycin base 500 mg qid for 7 days or erythromycin ethylsuccinate 800 mg qid for 7 days may be prescribed. COMPLICATIONS The primary complication of C. trachomatis cervical infection is salpingitis. Unfortunately, if the patient is pregnant and untreated, the vaginally delivered neonate will develop chlamydial conjunc- tivitis in 50% of cases and late onset pneumonitis in 10%. Prema- ture delivery and early postpartum endometritis are also associated problems. SALPINGITIS C. trachomatis salpingitis may be as prevalent as that caused by N. gonorrhoeae. However, there are marked differences in the pathophysiology and symptomatology. C. trachomatis salpingitis (which is also an ascending infection) has an insidious onset, it usually causes minimal symptoms, and the organism remains in the tube (primarily in the epithelium) for months. In contrast, N. gonorrhoeae infections have an acute onset, cause more acute symptoms, and remain in the tubes only 24–48 h. Gonorrheal in- fections appear to have a much greater cytotoxic effect on the tubal epithelium. Although C. trachomatis salpingitis usually causes fewer symp- toms, the gross appearance of the tubes suggests even more severe involvement. Salpingitis is a consequence of C. trachomatis cer- vicitis. Treatment of C. trachomatis salpingitis may be accom- plished with tetracyclines or erythromycin. The sequelae of C. tra- chomatis salpingitis include ectopic pregnancy and infertility, although the exact incidence of these complications is unknown. LYMPHOGRANULOMA VENEREUM The L serotypes of C. trachomatis cause lymphogranuloma venereum, which usually occurs in tropical or subtropical areas (including the southern United States). The incubation period is 7–21 days, and men are affected 6 times more often than women. In the United States, Ͻ500 cases/year are reported, and most occur in men. Lymphogranuloma venereum begins with a vesicopustular erup- tion that progresses to very painful inguinal and vulvar ulceration, lymphedema, and secondary bacterial invasion. Clinically, a de- pression between the groups of inguinal nodes and the genitocrural fold produces the appearance of a double genital crural fold (the groove sign). There is a reddish to purplish blue, hard induration that occurs 10–30 days after exposure. Anorectal lymphedema causes painful defecation and blood-streaked stools. Later in the disease, progressive rectal strictures form, which may even prevent defecation. Vaginal strictures may cause distortion and narrowing, with resultant dyspareunia. Headache, arthralgia, chills, and ab- dominal cramps may occur late in this disease. Late complications include vulvar elephantiasis. The diagnosis is confirmed by tissue culture and serotype de- termination, but complement fixation for Chlamydia with titer Ն1:16 is presumptive, as is a rising titer (Ͼ1:64 is diagnostic). Im- munofluorescent testing is available. The differential diagnosis for the cutaneous lesions includes granuloma inguinale, tuberculosis, syphilis, chancroid, vulvar cancer, genital herpes, and Hodgkin’s disease. With systemic symptoms, meningitis, arthritis, peritonitis, and pleurisy must be considered. Treatment for lymphogranuloma venereum includes doxycy- cline 100 mg PO bid for 21 days. Persistent disease requires a sec- ond course. Alternative drugs include tetracycline, erythromycin, or sulfisoxizole, each at 500 mg PO qid for 21 days. After the disease CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 687 BENSON & PERNOLL’S 688 HANDBOOK OF OBSTETRICS AND GYNECOLOGY is under control, surgery may be necessary (e.g., partial vulvec- tomy). Abscesses should not be excised but treated by aspiration. Anal strictures should be dilated weekly. A diversionary colostomy may be required for severe anal stricture. SYPHILIS Syphilis is a disease caused by the spirochete Treponema pallidum, which is transmitted by direct contact with an infectious moist le- sion. These organisms can pass through intact mucous membranes or abraded skin or may be acquired transplacentally. A single sex- ual encounter with an infected partner carries ϳ10% chance of ac- quiring syphilis. Untreated, the disease progresses from primary to secondary to latent and, finally, to tertiary syphilis. Congenital syphilis has its own course and symptoms. There are .280,000 new cases of syphilis in the United States each year. The primary lesion of syphilis is the hard chancre, an indurated, firm, painless papule or ulcer with raised borders, which appears 10 days to 3 months (average is 3 weeks) after the treponemes have entered the body. The chancre may be located on the external gen- italia, cervix, or vagina or any area of skin or mucous membrane of the body but is often not noted in women. The primary lesion persists for 1–5 weeks and is followed in most by spontaneous heal- ing. Any lesion suspected of being a chancre should be subjected to darkfield examination, seeking treponemes, because culture is not available. Serologic tests for syphilis should be performed weekly for 6 weeks or until positive (usually reactive 1–4 weeks after the chancre appears). The generalized cutaneous eruption (macular, maculopapular, papular, or pustular) of secondary syphilis appears 2 weeks to 6 months after the primary lesion. The rash is a diffuse, bilateral, sym- metric papulosquamous eruption that may involve the palms and soles. Perineal lesions (moist papules, condyloma latum) are pres- ent and positive for treponemes on darkfield examination or im- munofluorescent studies. Other mucous patches may be present, as well as patchy alopecia, hepatitis, or nephritis. Generalized lym- phadenopathy is typical. The secondary lesions last 2–6 weeks and heal spontaneously. Serologic tests are almost always positive at this stage. Latent syphilis is untreated syphilis after secondary symptoms have subsided. These patients remain infectious for 1–2 years and may have relapses resembling the secondary stage. Latency may be lifelong or end with the development of tertiary syphilis, which oc- curs in one third of patients. Tertiary syphilis is marked by the presence of destructive le- sions of skin, bone (gummas), cardiovascular system (e.g., aortic aneurysm or insufficiency), or nervous system disorders (e.g., meningitis, tabes dorsalis, paresis). Tertiary syphilis is fatal in 25% of those affected. Although the maternal course of syphilis is unaltered by preg- nancy, it is frequently not recognized unless detected by serologic screening. The treponemes may pass transplacentally throughout pregnancy, but if the disease is discovered and treated Ͻ18 weeks gestation, the fetus appears to suffer few sequelae. After 18 weeks, the classic signs of congenital syphilis occur in the fetus. The risk of fetal infection is greater during the secondary stage than during the primary or latent stages. The incidence of stillbirth and premature delivery is increased with syphilis. Hydramnios may be present. The placenta is involved; it has a waxy, hydropic appearance. Infection late in pregnancy results in fetal or neonatal infection in 40%–50%. Congenital syphilis occurs in the fetus or newborn whose mother has untreated syphilis. Depending on time of acquisition of infection, there may be signs of intrauterine infection (e.g., he- patosplenomegaly, radiographic changes in bone, anemia, jaundice, lymphadenitis, and meningitis) or the baby may appear unaffected, only to develop signs and symptoms equivalent to secondary syphilis sometime after birth. Classically, the newborn with congenital syphilis may be un- dergrown, with wrinkled facies because of reduced subcutaneous fat. The skin may have a brownish (café-au-lait) tint. The most common lesion of early congenital syphilis in the newborn is a bullous rash, so-called syphilitic pemphigus. Large blebs may appear over the palms and soles and, occasionally, in all other areas. Seropurulent fluid from the lesions swarms with treponemes. Mucositis identical with that of secondary syphilis in older patients may be noted in the mouth and upper respiratory passages of the newborn. The nasal discharge (syphilitic snuffles) is very infectious because it contains large numbers of T. pallidum. The bones usually show signs of osteochronditis, and on x-ray, an irregular epiphyseal juncture (Guerin’s line) is characteristic. Abnormalities of the eyes and other organs or the central nervous system may be apparent at birth, or defects may develop later in untreated cases. Any infant with the stigmata of syphilis should be placed in isolation until a definitive diagnosis can be made and ap- propriate treatment given. Because serologic testing evaluates IgG antibodies that are transplacentally acquired, the baby will be positive if the mother is positive. Effective neonatal treatment is shown by progressively falling titers over weeks to months. CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 689 BENSON & PERNOLL’S 690 HANDBOOK OF OBSTETRICS AND GYNECOLOGY LABORATORY FINDINGS Visualization of the treponemal organisms requires the presence of a moist cutaneous lesion for darkfield examination (fresh smear), immunofluorescent staining (dried smear), or silver staining for the treponemes in a biopsy specimen. Because the organisms are demonstrable for only a short time, diagnosis usually relies on his- tory and serologic testing. Screening for syphilis is accomplished primarily by nonspecific nontreponemal antibody testing (e.g., VDRL, RPR). All pregnant women should be tested at the first visit. High-risk patients should be screened at 28–32 weeks gestation and at delivery. These tests become positive 3–6 weeks after infection. The titers are high in secondary syphilis and fall to low titers or even become negative in late syphilis. Titers that have a 4-fold drop or are falling in early syphilis indicate adequate treatment. False-positive tests may be associated with collagen disease, in- fectious mononucleosis, malaria, leprosy, febrile illnesses, vaccina- tion, drug addiction, old age, and pregnancy itself. The titer seen with false-positive tests usually is low. However, any positive test should be investigated by an antitreponemal antibody test. The most widely performed antitreponemal antibody test is the fluorescent treponemal antibody absorption (FTA-ABS) test. The test remains positive regardless of therapy. Thus, titers are not determined. DIFFERENTIAL DIAGNOSIS The differential diagnosis for primary syphilis includes chancroid, granuloma inguinale, lymphogranuloma venereum, herpes, carci- noma, scabies, trauma, lichen planus, psoriasis, drug eruption, aphthosis, mycotic infection, Reiter’s syndrome, and Bowen’s disease. The differential diagnosis for secondary syphilis includes pityr- iasis rosea, psoriasis, lichen planus, tinea versicolor, drug eruption, “id” eruptions, perleche, parasitic infection, iritis, neuroretinitis, condylomata accuminata, acute exanthems, infectious mononucle- osis, alopecia, and sarcoidosis. TREATMENT Treatment should be initiated if exposure has occurred even if evi- dence of disease is not present. During pregnancy, it is better to treat any suspicion of disease rather than risk congenital syphilis. [...]... especially in those who may want in vitro fertilization, when the uterus should remain * Centers for Disease Control and Prevention: 1998 guidelines for treatment of sexually transmitted diseases MMWR 1998;47(RR-1):82–84 CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 699 Treatment is reasonable on an outpatient basis for the majority of mild PID (ϳ75% of cases) The patient must not be pregnant and must not appear... from the ostia Organisms known to spread by this mechanism include N gonorrhoeae, C trachomatis, Streptococcus agalactiae, cytomegalovirus, and herpes simplex virus Three fourths of CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 693 TABLE 24-1 FUNCTIONAL CLASSIFICATION OF PELVIC INFECTIONS Pelvic inflammatory disease (PID) Limited (salpingitis) Pelvic abscess (cul-de-sac or tuboovarian) Puerperal infections... trachomatis is found in up to 30% of cases The aerobes and anaerobes found in PID usually are normal vaginal and gastrointestinal flora The anaerobes (e.g., Bacteroides, Peptostreptococcus, CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 695 Peptococcus) predominate in abscesses Common aerobes include Escherichia coli, group B Streptococcus, Streptococcus faecalis, and coagulase-negative Staphlococcus Mycoplasma hominis... purulent discharge Movement of the cervix or uterus is exquisitely painful The adnexa are tender to palpation The criteria for diagnosis of salpingitis are summarized in Table 24-2 CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 697 TABLE 24-2 CRITERIA FOR DIAGNOSIS OF SALPINGITIS Abdominal direct tenderness, with or without rebound tenderness Tenderness with motion of cervix and uterus Adnexal tenderness 14444424444443...CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 691 Contacts and patients with early syphilis (primary, secondary, and latent Ͻ1 year) should be treated with one of the following regimens: (1) benzathine penicillin G 2.4 million... prognosis for fertility is guarded, the overall prognosis is good if the abscess is localized and is treated early If rupture into the peritoneum occurs, the prognosis is serious CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 701 Tuboovarian Abscess (TOA) Although tuboovarian abscess may occur after an initial episode of acute salpingitis, it most often is associated with recurrent adnexal infections (Fig... abdomen should be entered through a midline incision The pus encountered should be sent for aerobic and anaerobic culture The entire abdomen should be explored, and all abscesses should CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 703 be drained Thorough irrigation with suction is necessary Normally, TAH and BSO are performed, but therapy must be individualized Supracervical hysterectomy may be necessary to shorten... (e.g., povidone-iodine, hexochlorophene) for several days Preoperative insertion of antibacterial vaginal creams or suppositories (especially if vaginitis or cervicitis is present) CHAPTER 24 SEXUALLY TRANSMITTED DISEASES ● ● ● ● ● 705 Meticulous operative hemostasis without strangulation of tissues Use of nonreactive suture material Suction drainage at sites of suboptimal hemostasis (with vaginal surgical... abortion) and IUD-related infections are disseminated through the lymphatic system, as are nonpuerperal Mycoplasma infections Hematogenous Hematogenous dissemination of pelvic disease is limited to certain diseases (e.g., tuberculosis) and is uncommon in the United States Intraperitoneal Intraabdominal infections (e.g., appendicitis, diverticulitis) as well as intraabdominal accidents (e.g., perforated viscus... are about 1 million cases of acute PID a year in the United States, and the total cost is estimated to exceed $7 billion per year Over a quarter of PID cases require hospitalization PID affects 1%–2% of sexually active females yearly and is more frequent in young women (75% of those affected are Ͻ25 years) In the United States, PID annually results in 2.5 million physician visits, nearly 270,000 inpatient . cervicitis). The infection may be asymptomatic in 15% of nonpregnant, sexually active women. CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 685 BENSON & PERNOLL’S 686 HANDBOOK OF OBSTETRICS AND GYNECOLOGY LABORATORY. first reported to cause disease in 1981. In the United States, AIDS is now the fifth 24 SEXUALLY TRANSMITTED DISEASES CHAPTER Copyright 2001 The McGraw-Hill Companies. Click Here for Terms of Use. BENSON. have been de- scribed in some HIV-positive newborns, but this is not common. CHAPTER 24 SEXUALLY TRANSMITTED DISEASES 683 BENSON & PERNOLL’S 684 HANDBOOK OF OBSTETRICS AND GYNECOLOGY If neonatal/pediatric