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83 SEXUALLY TRANSMITTED DISEASES AND REPRODUCTIVE TRACT INFECTIONS

83 SEXUALLY TRANSMITTED DISEASES AND REPRODUCTIVE TRACT INFECTIONS
Harrison’s Manual of Medicine

83

SEXUALLY TRANSMITTED DISEASES AND REPRODUCTIVE TRACT INFECTIONS

Common STD Syndromes

Urethritis in Men

Epididymitis

Urethral Syndrome in Women

Vaginitis

Mucopurulent Cervicitis

Ulcerative Genital Lesions

Proctitis, Proctocolitis, Enterocolitis, and Enteritis
Gonococcal Infections
Chlamydial Infections

C. trachomatis Genital Infections

Lymphogranuloma Venereum
Pelvic Inflammatory Disease
Ulcerative Genital Lesions

Syphilis

Herpes Simplex Virus Infections

Chancroid

Lymphogranuloma Venereum

Donovanosis (Granuloma Inguinale)
Human Papillomavirus (HPV) Infections
Bibliography

See Table 83-1 for a list of sexually transmitted pathogens and Table 83-2 for pathogens associated with clinical syndromes.

Table 83-1 Sexually Transmitted and Sexually Transmissible Microorganisms

Table 83-2 Major STD Syndromes and Sexually Transmitted (ST) Microbial Etiologies

COMMON STD SYNDROMES
Most pts with STD syndromes are initially managed on the basis of presenting Sx.
Urethritis in Men
CLINICAL PRESENTATION   Pts usually present with a purulent or mucopurulent urethral discharge that can be expressed by milking of the urethra.
ETIOLOGY   Neisseria gonorrhoeae, Chlamydia trachomatis, Trichomonas vaginalis, herpes simplex virus (HSV), Mycoplasma genitalium, and Ureaplasma urealyticum are among the pathogens that can cause urethritis in men.
DIAGNOSIS   If milking of the urethra yields no discharge, the centrifuged sediment of the first 20–30 mL of voided urine should be examined with Gram’s stain. Urethritis is usually present if microscopy shows ³5 PMNs/1000× field. Absence of gram-negative diplococci (presumably N. gonorrhoeae) warrants a preliminary diagnosis of nongonococcal urethritis (NGU). Culture or nucleic acid detection should be performed for N. gonorrhoeae and C. trachomatis (see “Gonococcal Infections” and “Chlamydial Infections,” below).

TREATMENT
See organism-specific sections below.

EPIDIDYMITIS
CLINICAL PRESENTATION   Pts usually present with unilateral testicular pain of acute onset, intrascrotal swelling, tenderness, and fever.
ETIOLOGY   In sexually active men <35 years old, acute epididymitis is caused most frequently by C. trachomatis and less frequently by N. gonorrhoeae and is usually associated with overt or subclinical urethritis. Epididymitis in men who have practiced insertive rectal intercourse is often caused by Enterobacteriaceae.
DIAGNOSIS   Testicular torsion and tumor must be excluded. Gram’s stain and culture or nucleic acid detection should be performed as for urethritis.

TREATMENT
See organism-specific sections below.

Urethral Syndrome in Women
CLINICAL PRESENTATION   Pts present with symptomatic urethritis, primarily with dysuria and pyuria.
ETIOLOGY   N. gonorrhoeae, C. trachomatis, and HSV cause this syndrome.
DIAGNOSIS   Escherichia coli or other common uropathogens characteristically are present at counts of £102/mL in urine culture. Young age, more than one sexual partner, a new sexual partner, or coexisting mucopurulent cervicitis (MPC) suggests an STD etiology.

TREATMENT
See organism-specific sections below.

Vaginitis
CLINICAL PRESENTATION   Unsolicited reporting of abnormal vaginal discharge suggests bacterial vaginosis or trichomoniasis.
ETIOLOGY   T. vaginalis, Gardnerella vaginalis, Mycoplasma hominis, and anaerobic bacteria can be associated with vaginitis.
DIAGNOSIS AND TREATMENT   See Table 83-3.

Table 83-3 Diagnostic Features and Management of Vaginal Infection

Mucopurulent Cervicitis
CLINICAL PRESENTATION   MPC is symptomatically silent, with yellow mucopurulent discharge from the cervical os.
ETIOLOGY   N. gonorrhoeae or C. trachomatis may be involved, but 50% of cases are idiopathic.
DIAGNOSIS   The diagnosis rests on the detection of yellow mucopurulent discharge from the cervical os or of ³20 PMNs/1000× field on a Gram’s stain of cervical mucus. Culture or nucleic acid detection should be performed as for urethritis.

TREATMENT
See organism-specific sections below.

Ulcerative Genital Lesions
See “Ulcerative Genital Lesions,” below.
Proctitis, Proctocolitis, Enterocolitis, and Enteritis
CLINICAL PRESENTATION   Proctitis or proctocolitis presents as pain and mucopurulent bloody discharge. Proctitis commonly produces tenesmus and constipation, whereas proctocolitis and enterocolitis more often cause true diarrhea.
ETIOLOGY   Sexually acquired proctitis is usually due to the typical STD pathogens. Proctocolitis, enterocolitis, and enteritis can result from ingestion of typical intestinal pathogens through oral-anal exposure during sexual contact.
DIAGNOSIS   Culture or nucleic acid detection should be used to identify the pathogen.

TREATMENT
See sections on individual pathogens, below and elsewhere.

GONOCOCCAL INFECTIONS
ETIOLOGY   Gonorrhea, an infection of columnar and transitional epithelium, is caused by N. gonorrhoeae, a gram-negative diplococcus.
EPIDEMIOLOGY   The incidence of gonorrhea has decreased significantly in the U.S., although there are still ~315,000 newly reported cases each year. Gonorrhea predominantly affects young, nonwhite, unmarried, less educated members of urban populations. It is transmitted most efficiently from males to females, with a 40–60% rate of transmission to a woman after a single episode of unprotected vaginal intercourse with an infected man.
CLINICAL MANIFESTATIONS   Males   Urethritis develops 2–7 d after exposure, with symptoms of purulent urethral discharge (90–95%), dysuria, and meatal erythema; some gonococcal strains may cause less overt symptoms. Balanitis may develop in uncircumcised men. In the antibiotic era, complications due to N. gonorrhoeae (e.g., epididymitis, prostatitis, inguinal lymphadenitis) are rare.
Females   Gonococcal infection in the female involves (in descending order of frequency) the endocervix, urethra, anal canal, and pharynx. The incubation period is less well defined in women than in men; if symptoms develop, they usually do so within 10 d. Increased vaginal discharge and dysuria are the most common symptoms. Acute uncomplicated gonococcal cervicitis produces mucopurulent (yellow) endocervical discharge, causes easily induced cervical bleeding, and may coexist with C. trachomatis or the organisms causing vaginitis. Gonococcal urethritis and proctitis are common, but the urethra and the rectum are rarely the sole infected sites. Unilateral acute Bartholin’s gland inflammation frequently is due to gonorrhea. The pt’s report of dyspareunia, lower abdominal pain, or back pain makes it imperative to consider a diagnosis of pelvic inflammatory disease (PID), which complicates ~20% of cases of gonococcal cervicitis.
Anorectal Gonorrhea   Gonococcal anorectal infection can occur in females as well as males. Symptoms include anorectal pain or pruritus, tenesmus, purulent rectal discharge, and rectal bleeding. Rectal isolates of N. gonorrhoeae from homosexual men tend to be more resistant to antibiotics than other gonococcal isolates.
Pharyngeal Gonorrhea   Fellatio is a more efficient means of contracting pharyngeal gonorrhea than cunnilingus. Symptoms are usually mild or lacking, although this syndrome almost always coexists with genital infection. Transmission from the pharynx to sexual contacts is rare. Pharyngeal infection may be more common in pregnancy because of altered sexual practices.
Ocular Gonorrhea in Adults   Ocular gonococcal infection may result in a markedly swollen eyelid, chemosis, and profuse purulent discharge. Corneal ulceration and, in rare instances, perforation may occur. Prompt recognition and treatment are of paramount importance.
Disseminated Gonococcal Infection (DGI)   Two-thirds of pts with DGI are women; symptoms of bacteremia often begin during menses. Strains causing DGI tend not to cause inflammation or (consequently) symptoms at genital or pharyngeal sites. Pts present either with manifestations of gonococcemia (fever, polyarthralgias, and the appearance—usually on the distal extremities—of 3–20 papular, petechial, pustular, hemorrhagic, or necrotic skin lesions) or with purulent oligoarthritis. Initial joint manifestations are characteristically limited to tenosynovitis involving several joints asymmetrically, most commonly the knees, wrists, ankles, and elbows. Septic arthritis may ensue, often without prior fever, polyarthralgia, or skin lesions; it usually causes pain and swelling of a single joint and is indistinguishable from septic arthritis caused by other pathogens. Up to 13% of pts with DGI have complement deficiencies.
DIAGNOSIS   The presence of intracellular gram-negative diplococci on Gram’s stain of urethral or endocervical exudate is grounds for a presumptive diagnosis of urethral gonorrhea. However, Gram’s stain of the cervical os is not sensitive for the diagnosis of gonorrhea in women; rather, specimens of cervical exudate should be submitted for culture or nonculture assay. Material should be collected on a Dacron or rayon swab and cultured on Thayer-Martin selective medium in a humidified, CO2-enriched atmosphere. Acceptable specimens may be obtained with swabs of the urethra, endocervix, anorectum, and pharynx. Endocervical culture is positive in 80–90% of cases of gonorrhea in women; the yield can be increased by concomitant rectal, urethral, and pharyngeal cultures. N. gonorrhoeae is recovered from <5% of skin lesions in DGI. Isolator blood cultures may enhance the yield in suspected cases. Gonococci are frequently recovered from early joint effusions and may be recovered from effusions with >80,000 WBCs/µL.
Nucleic acid probe tests are now widely used for the detection of N. gonorrhoeae in urogenital specimens. However, using nonculture methods as the sole means of detection precludes antibiotic susceptibility testing.

TREATMENT
Table 83-4 summarizes current guidelines for the treatment of gonorrhea. Because of resistance to fluoroquinolones in several parts of Southeast Asia, these agents should not be used for gonorrhea acquired in that region. Third- generation cephalosporins remain the mainstay of therapy for uncomplicated genital, rectal, and pharyngeal gonorrhea, although symptomatic gonococcal pharyngitis is more difficult to eradicate than genital infection.

Table 83-4 Recommended Treatment for Gonococcal Infections: 1998 Guidelines of the Centers for Disease Control and Prevention

CHLAMYDIAL INFECTIONS
C. trachomatis Genital Infections
EPIDEMIOLOGY   An estimated 4 million cases of C. trachomatis genital infection occur each year; thus these infections are the most common bacterial STDs in the U.S. C. trachomatis and N. gonorrhoeae often coinfect women with cervicitis and heterosexual men with urethritis.
CLINICAL MANIFESTATIONS   Nongonococcal and Postgonococcal Urethritis   These terms refer, respectively, to symptomatic urethritis in the absence of gonococcal infection and to nongonococcal urethritis developing in men 2–3 weeks after single-dose treatment for gonococcal urethritis. C. trachomatis accounts for 20–40% of cases of NGU among heterosexual men but is a less common cause among homosexual men.
Epididymitis   C. trachomatis is the major cause of epididymitis in heterosexual men <35 years old in the U.S., accounting for 70% of cases. Men typically present with unilateral scrotal pain, fever, and epididymal tenderness or swelling. Testicular torsion should be excluded.
Reiter’s Syndrome   This syndrome consists of conjunctivitis, urethritis (in males) or cervicitis (in females), arthritis, and characteristic mucocutaneous lesions. C. trachomatis may be recovered from the urethra of up to 70% of men with nondiarrheal Reiter’s syndrome and associated urethritis.
Proctitis   Cases occur in persons of either sex who practice receptive anal intercourse. C. trachomatis strains of either the genital immunotypes or the lymphogranuloma venereum (LGV) immunotypes cause proctitis in homosexual men. Pts present with mild rectal pain, mucous discharge, tenesmus, and (occasionally) bleeding. Anoscopy in non-LGV cases reveals patchy mucosal friability and mucopurulent discharge; LGV strains produce more severe ulcerations that can be confused with HSV infection.
Mucopurulent Cervicitis   MPC, an inflammation of the columnar epithelium and subepithelium of the endocervix, is the most common major STD syndrome among women and can be a harbinger of PID. C. trachomatis is its most common cause, although N. gonorrhoeae is often responsible. Although many females with C. trachomatis infection of the cervix have no signs or symptoms, a careful speculum examination reveals MPC in 30–50% of cases.
DIAGNOSIS   The “gold standard” for diagnosis of C. trachomatis genital infections is the isolation of the organism by cell culture techniques, which are generally available only at larger medical centers and have a sensitivity of 60–80%. Since the organism is an intracellular pathogen, specimens for culture must include epithelial cells. Because of these limitations, nonculture methods have been developed. The direct immunofluorescent antibody (DFA) slide test is 70–85% sensitive. ELISA-based assays are 60–80% sensitive and 97–99% specific and are better suited for screening than DFA. PCR and ligase chain reaction are the most sensitive tests available and can be used with urine specimens rather than conventional swabs. Serologic tests are of limited usefulness.

TREATMENT
For uncomplicated genital infection, doxycycline (100 mg bid PO) or tetracycline (500 mg qid PO) can be given for 7 d. For complicated infections (e.g., epididymitis, PID), a 14-d course is recommended. Azithromycin (1 g PO in a single dose) is effective in uncomplicated chlamydial infection and has appeal when follow-up care may not be possible. Ofloxacin (300 mg bid PO for 7 d) is also effective. These agents, however, are expensive. For pregnant pts, erythromycin base (500 mg qid PO for 10–14 d) is recommended. Sexual partners should be screened and treated, whether or not they are symptomatic.

Lymphogranuloma Venereum
See under “Ulcerative Genital Lesions,” below.
PELVIC INFLAMMATORY DISEASE
ETIOLOGY   The term PID usually refers to an ascending infection involving the endometrium and/or fallopian tubes. PID is generally caused by N. gonorrhoeae, C. trachomatis, and/or organisms that can be regarded as components of an altered vaginal microflora (anaerobes, G. vaginalis, Enterobacteriaceae, group B Streptococcus, Mycoplasma spp., and Ureaplasma spp.). First episodes of PID are more likely to be caused by the sexually transmitted pathogens. Tuberculous salpingitis is an unusual but well-described syndrome.
EPIDEMIOLOGY   The annual incidence of PID in the U.S. has declined since the mid-1970s. Risk factors for the development of PID include a history of salpingitis and recent vaginal douching. The use of an IUD in nulliparous women and recent IUD insertion in any woman are also risk factors. Oral contraceptive use decreases the risk of PID. Tuberculous salpingitis is found more often in older women, with 50% of cases documented after menopause.
CLINICAL MANIFESTATIONS   Symptoms usually develop in the first half of the menstrual cycle and evolve by stage of infection, which proceeds from cervicitis (mucopurulent vaginal discharge) to endometritis (midline abdominal pain and abnormal vaginal bleeding) to salpingitis (bilateral lower abdominal and pelvic pain) to peritonitis (nausea, vomiting, and increased abdominal tenderness). Abnormal uterine bleeding precedes or coincides with abdominal pain in 40% of women with PID; symptoms of urethritis (dysuria) occur in 20%. Symptoms of proctitis (anorectal pain, tenesmus, and rectal discharge or bleeding) are seen occasionally in pts with gonococcal or chlamydial infection. Spread of infection to the upper abdomen causes perihepatitis (Fitz- Hugh–Curtis syndrome) in 3–10% of cases, with right-sided or bilateral upper quadrant abdominal tenderness and occasionally a hepatic friction rub; this syndrome is usually a complication of chlamydial PID. Appendiceal serositis (periappendicitis) can occur. On speculum examination, MPC is found in the majority of pts with either gonococcal or chlamydial PID. On bimanual examination, cervical motion tenderness, uterine fundal tenderness, and abnormal adnexal tenderness are noted. Gonococcal PID presents more acutely than chlamydial PID. IUD-associated PID tends to be relatively indolent. HIV-infected women with PID are more likely than women without HIV infection to present with tuboovarian abscess requiring hospitalization and surgical drainage.
DIAGNOSIS   Laparoscopy is the most specific method for diagnosis of PID but is generally impractical. In addition to a clinical exam consistent with the disease, findings favoring PID include fever, a palpable adnexal mass, an ESR of >15 mm/h, and >30 PMNs/high-power field on Gram’s stain of cervical mucus. Aerobic and anaerobic culture of cervical mucus and/or culdocentesis fluid should be done, with culture and amplification assays for N. gonorrhoeae and C. trachomatis. Pregnancy testing should also be performed in women of childbearing age. Endometrial biopsy with the finding of tuberculous granulomas confirms the diagnosis of tuberculous salpingitis.

TREATMENT
Two inpatient regimens have been used extensively: (1) doxycycline (100 mg IV q12h) plus cefotetan (2 g IV q12h) or cefoxitin (2 g IV q6h); and (2) clindamycin (900 mg IV q8h) plus gentamicin (1.5 mg/kg IV q8h after a loading dose of 2 mg/kg IV). Parenteral therapy should be continued until at least 48 h after the pt’s condition improves, at which time doxycycline (100 mg PO bid) should be given to complete a 14-d course. For pts treated with regimen 2, clindamycin (450 mg qid) is an alternative oral agent; its enhanced anaerobic spectrum is particularly useful in cases with tuboovarian abscess. Suggested outpatient regimens include (1) ofloxacin (400 mg PO bid) plus metronidazole (500 mg PO bid) for 14 d, or (2) ceftriaxone (a single dose of 250 mg IM) followed by doxycycline (100 mg PO bid for 14 d). Sexual partners of pts with acute PID should be evaluated for STDs and treated promptly with a regimen effective against uncomplicated gonococcal and chlamydial infection.

ULCERATIVE GENITAL LESIONS
Syphilis
ETIOLOGY   Syphilis is a chronic systemic infection caused by the spirochete Treponema pallidum.
EPIDEMIOLOGY   Nearly all cases of syphilis follow sexual contact with infectious lesions; less common modes of transmission include nonsexual personal contact, in utero exposure, and blood transfusion. A rather steady increase since 1956 in the number of new cases of infectious syphilis in the U.S. has been punctuated by four cycles of 7–10 years, each with a rapid rise and fall in incidence. Since the most recent peak in 1990, the number of cases reported annually has again declined by >80%. During the early part of the AIDS epidemic, about half of all pts with early syphilis were homosexual and bisexual men. Because of changes in sexual practices due to the epidemic, this proportion has decreased. The most recent epidemic of syphilis predominantly involved African-American heterosexual men and women and occurred largely in urban areas. The incidence of congenital syphilis parallels that of infectious syphilis in women. Fifty percent of all named contacts of index cases are infected; thus “epidemiologic” treatment of all contacts is important for syphilis control.
CLINICAL MANIFESTATIONS   Syphilis is characterized by episodes of active disease interrupted by periods of latency and conventionally is divided into stages.
Primary Syphilis   The typical primary chancre usually begins as a single painless papule that rapidly becomes eroded, usually becomes indurated, and has a characteristic cartilaginous consistency. Atypical primary lesions are common. In heterosexual men, the chancre is most often located on the penis. In homosexual men it can be found in the anal canal or rectum, in the mouth, or on the external genitalia, while in women common sites are the cervix and labia. Consequently, primary syphilis is less often recognized in women and homosexual men than in heterosexual men. Regional lymphadenopathy usually appears within 1 week of the primary lesion. The nodes are firm, nonsuppurative, and painless. The chancre generally heals within 4–6 weeks, but lymphadenopathy may persist for months.
Secondary Syphilis   Manifestations of secondary syphilis vary widely but include skin lesions, lymphadenopathy, and constitutional symptoms. The skin rash begins as pale, pink or red macules that may go unnoticed; proceeds to papules; and may progress to lesions that resemble pustules. The palms and soles are frequently involved. In 10% of pts, papules enlarge to form moist, pink or gray-white, highly infectious lesions called condylomata lata in intertriginous areas. Mucous patches, which are superficial mucosal erosions, occur in 10–15% of cases. Constitutional symptoms may precede or accompany other manifestations. Syphilitic meningitis develops in only 1–2% of cases, but protein levels or WBC counts may be elevated in the CSF in ³30%. Less common complications of secondary syphilis include hepatitis, nephropathy, GI involvement, arthritis, periostitis, and iridocyclitis.
Latent Syphilis   Positive serologic tests for syphilis in a pt with a normal CSF examination and no clinical manifestations of syphilis indicate a diagnosis of latent syphilis. Early latent syphilis refers to latency during the first year after infection, whereas late latent syphilis refers to latency that has persisted longer. Untreated latent syphilis progresses to clinically evident late syphilis in 30% of cases. Positive serologic tests rarely if ever revert to negative without treatment.
Late Syphilis (Tertiary Stage)
1.   Neurosyphilis: The spectrum of symptomatic neurosyphilis includes meningeal syphilis (usually occurring within the first year), meningovascular syphilis (5–10 years after infection), general paresis (20 years), and tabes dorsalis (25–30 years). Symptoms of meningeal syphilis include headache, nausea, vomiting, neck stiffness, cranial nerve palsies, seizures, and changes in mental status. Meningovascular syphilis presents most commonly as a stroke syndrome in the middle cerebral artery distribution, often preceded by a subacute encephalitic syndrome (headaches, vertigo, insomnia, psychological abnormalities). General paresis (corresponding to the mnemonic “paresis”) includes abnormalities of the personality, affect, reflexes (hyperactive), eye (Argyll Robertson pupils), sensorium, intellect, and speech. Tabes dorsalis presents as symptoms and signs of demyelination of the posterior columns, dorsal roots, and dorsal root ganglia (e.g., ataxic wide-based gait; footslap; paresthesia; bladder disturbances; impotence; areflexia; and loss of position, deep pain, and temperature sensations). Trophic joint degeneration (Charcot’s joints) results from loss of pain sensation. The small, irregular Argyll Robertson pupil, a feature of both general paresis and tabes dorsalis, reacts to accommodation but not to light.
2.   Cardiovascular syphilis: Cardiovascular manifestations occur in ~10% of pts with untreated late latent disease and include aortitis, aortic regurgitation, saccular aneurysm (particularly in the ascending and transverse segments of the aortic arch), and coronary ostial stenosis. Symptoms appear 10–40 years after infection. Syphilitic aneurysms do not lead to dissection.
3.   Gummas: Gummas are granulomatous inflammatory lesions that range from microscopic size to several centimeters in diameter. The most commonly involved sites are skin, bones, mouth, upper respiratory tract, larynx, liver, and stomach. The rapid healing of gummas after penicillin treatment may be diagnostically helpful.
DIAGNOSIS   Syphilis is most often diagnosed serologically. Nontreponemal tests, including the VDRL and the RPR, are used for initial screening and serum antibody quantitation and usually become negative with treatment. Specific treponemal tests, including the FTA-ABS and MHA-TP, confirm syphilis (when positive), identify false-positive nontreponemal tests (when negative), and remain positive even after therapy. False-positive nontreponemal tests occur in a variety of conditions, but titers in these instances rarely exceed 1:8. Dark- field examination is used to evaluate suspicious moist cutaneous lesions. DFA is used for identification of the organism in fixed smears. PCR-based techniques are being developed. Evaluation for neurosyphilis by lumbar puncture (LP) is recommended for pts with neurologic signs, untreated syphilis of unknown or >1 year’s duration, treatment failure, a serum VDRL or RPR titer of >1:32, or anticipated nonpenicillin therapy. In addition, LP should be considered for pts whose VDRL or RPR tests remain positive 1 year after treatment. Because standard agents for the treatment of early syphilis fail to reach treponemicidal levels in the CSF, some experts advise LP in secondary and early latent syphilis, especially for HIV-infected pts. The most common CSF findings are pleocytosis and an elevated protein level. The CSF VDRL is a highly specific but relatively insensitive diagnostic test. An unabsorbed FTA test on CSF is more sensitive but less specific. A negative unabsorbed FTA test on CSF rules out neurosyphilis. All pts with newly diagnosed syphilis should undergo HIV testing. Conversely, pts with newly diagnosed HIV infection should be tested for syphilis. There is no evidence that the sensitivity of serologic testing for syphilis differs in HIV-infected pts. Some authorities recommend CSF evaluation for all HIV- infected pts with syphilis. Serologic testing after treatment is important in all pts, particularly those also infected with HIV.

TREATMENT
(See Table 83-5) Therapy for syphilis should be administered according to the stage of the disease, regardless of pregnancy status. The Jarisch-Herxheimer reaction to treatment for syphilis and certain other spirochetal infections consists of fever, chills, myalgias, headache, tachycardia, increased respiratory rate, increased circulating neutrophil count, and vasodilatation with mild hypotension. This reaction is self-limited and of undefined pathogenesis. It occurs in ~50% of pts treated for primary syphilis, 90% treated for secondary syphilis, and 25% treated for early latent syphilis. The onset usually comes within 2 h of the initiation of treatment, with resolution in 12–24 h. In neurosyphilis, the reaction is more delayed, peaking after about 12–14 h. The response of early syphilis to treatment should be determined by monitoring the quantitative VDRL or RPR titer 1, 3, 6, and 12 months after treatment (more frequently in HIV-infected pts). If the titer fails to fall by fourfold, if it rises, or if symptoms persist or recur, the pt should be re-treated and LP should be considered to rule out neurosyphilis. After treatment for neurosyphilis, CSF cell counts should be determined every 3–6 months for 3 years or until findings normalize.

Table 83-5 Recommendations for the Treatment of Syphilisa

Herpes Simplex Virus Infections
CLINICAL MANIFESTATIONS   Fever, headache, malaise, and myalgias, along with the local symptoms of pain, itching, dysuria, vaginal and urethral discharge, and tender inguinal lymphadenopathy, characterize primary genital infection with HSV. Lesions include vesicles, pustules, or painful erythematous ulcers. More than 80% of women have cervical or urethral involvement in first-episode infection. Recurrence rates within 12 months are ~90% for HSV-2 and ~55% for HSV-1. HSV-1 and HSV-2 can cause rectal and perianal infections.
DIAGNOSIS   The diagnosis can be made clinically with support from a positive Tzanck preparation showing multinucleated giant cells. The definitive diagnosis is made by isolation of the virus in tissue culture.

TREATMENT
See Table 102-1

Chancroid
EPIDEMIOLOGY   Chancroid, genital ulceration and inguinal adenitis caused by Haemophilus ducreyi, occurs throughout the world and is a significant health problem in developing countries. Although less common in the U.S., its incidence has increased dramatically in recent years.
CLINICAL MANIFESTATIONS   After an incubation period of 7 d, a papule appears, develops into a pustule, and then ulcerates, resulting in a painful, sharply circumscribed genital ulcer with minimal inflammation that bleeds easily. Ulcers are occasionally multiple. About half of pts develop enlarged, tender inguinal lymph nodes that become fluctuant and may rupture.
DIAGNOSIS   An accurate diagnosis of chancroid relies on cultures of H. ducreyi from the lesion. Selective, nutritionally rich medium is necessary. Gram’s stain may show a predominance of characteristic gram-negative coccobacilli.

TREATMENT
Effective regimens include ceftriaxone, 250 mg IM as a single dose; azithromycin, 1g PO as a single dose; erythromycin, 500 mg PO qid for 7 d; and ciprofloxacin, 500 mg PO bid for 3 d.

Lymphogranuloma Venereum
ETIOLOGY   LGV is a sexually transmitted infection caused by the L serovars of C. trachomatis.
CLINICAL MANIFESTATIONS   A primary genital lesion is noted in fewer than one-third of heterosexual men with LGV and in only a few women with this infection. When present, this lesion is small and painless and usually heals in a few days without scarring. Primary anal or rectal infection can develop after receptive anal intercourse; in women, it may also arise via contiguous perineal spread of infected vaginal secretions. Lymphadenitis results from spread from the primary site to regional nodes. The inguinal syndrome is the most common presentation in heterosexual men and is characterized by painful inguinal adenopathy beginning 2–6 weeks after exposure. In two-thirds of cases, the adenopathy is unilateral. Lymph nodes become matted, fluctuant, and suppurative. The overlying skin becomes inflamed, and draining fistulas may develop. Constitutional symptoms are common. LGV proctitis may present as anorectal pain; mucopurulent, bloody rectal discharge; and tenesmus. Symptoms accompanying regional lymphadenopathy include fever, chills, headache, meningismus, anorexia, myalgias, and arthralgias. Systemic complications are infrequent but may include arthritis with sterile effusion, aseptic meningitis, meningoencephalitis, conjunctivitis, hepatitis, and erythema nodosum.
DIAGNOSIS   LGV strains can be isolated from lymph nodes or the rectum and rarely from the urethra or cervix. Serologic testing is more useful diagnostically for LGV than for other C. trachomatis infections.

TREATMENT
Fluctuant buboes should be aspirated through normal-appearing skin. The recommended antibiotic is tetracycline (500 mg qid PO) for a minimum of 14 d.

Donovanosis (Granuloma Inguinale)
EPIDEMIOLOGY   Donovanosis, of which the bacterial agent is Calymmatobacterium granulomatis, is a rare cause of genital ulcers in the U.S.
CLINICAL MANIFESTATIONS   Most lesions appear within 4 weeks of sexual exposure. The disease begins as a papule that ulcerates and develops into a usually painless, clean, friable, granulomatous lesion. Labial swelling, phimosis, and paraphimosis are common. Oral lesions are unusual but have been described.
DIAGNOSIS   The diagnosis is best made by examination of impression smears prepared from specimens obtained by punch biopsy of granulation tissue from the periphery of a lesion. The specimen is subjected to Giemsa, Leishman’s, or Wright’s staining. Donovan bodies appear as rounded coccobacilli of 1 by 2 µm lying within cystic spaces in the cytoplasm of large mononuclear cells. A serologic test has been developed.

TREATMENT
Commonly used antibiotics include tetracycline (500 mg PO q6h), doxycycline (100 mg PO q12h), TMP-SMZ (160/800 mg PO q12h), erythromycin (500 mg PO q6h), azithromycin (1 g PO weekly), and chloramphenicol (500 mg PO q6h). Treatment is usually continued until the lesion has healed completely (3–5 weeks).

HUMAN PAPILLOMAVIRUS (HPV) INFECTIONS
ETIOLOGY AND EPIDEMIOLOGY   HPVs are nonenveloped viruses of the Papovaviridae family that infect the epithelium of the skin or mucous membranes.
CLINICAL MANIFESTATIONS   The incubation period of HPV infection is usually 3–4 months, with a range of 1 month to 2 years. Anogenital warts (condylomata acuminata) are sexually transmitted, beige to brown, exophytic, hyperkeratotic papules that occur on skin and mucosal surfaces of external genitalia and perianal areas. Some of the >80 HPV types are strongly associated with cancer of the cervix, penis, anus, vagina, and vulva. HPV types 6 and 11 are most commonly associated with condylomata acuminata, whereas types 16, 18, and 31 are most frequently detected in dysplasias and carcinomas of the genital tract.
DIAGNOSIS   Most visible genital warts can be diagnosed clinically. Colposcopy is invaluable in assessing vaginal and cervical lesions. Papanicolaou smears from cervical specimens may reveal cytologic evidence of HPV. Histologic examination of biopsy specimens is useful for persistent or atypical lesions. PCR can be used to detect HPV nucleic acids and to identify specific virus types. Serologic techniques are not widely available.

TREATMENT
Available modes of treatment are not completely effective, and some have significant side effects. Moreover, lesions may resolve spontaneously. Frequently used therapies include cryosurgery, application of caustic agents, electrodesiccation, surgical excision, and laser ablation. Topical 5-fluorouracil has also been used. Various interferon preparations have been employed with modest success; a topically applied interferon inducer, imiquimod, is also of benefit.

Bibliography

For a more detailed discussion, see Holmes KK: Sexually Transmitted Diseases: Overview and Clinical Approach, Chap. 132, p. 839; Holmes KK, Brunham RC: Pelvic Inflammatory Disease, Chap. 133, p. 848; Ram S, Rice PA: Gonococcal Infections, Chap. 147, p. 931; Murphy TF: Haemophilus Infections, Chap. 149, p. 939; Kasper DL, Barlam TF: Infections Due to the HACEK Group and Miscellaneous Gram-Negative Bacteria, Chap. 150, p. 942; Hart G: Donovanosis, Chap. 164, p. 1004; Lukehart SA: Syphilis, Chap. 172, p. 1044; Stamm WE: Chlamydial Infections, Chap. 179, p. 1075; Corey L: Herpes Simplex Viruses, Chap. 182, p. 1100; and Reichman RC: Human Papillomaviruses, Chap. 188, p. 1118, in HPIM-15.

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