SEXUALLY TRANSMITTED DISEASES docx

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 course occur mor

se-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 course, cunnilingus, anilingus, fellatio, and mouth or genital to

inter-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 Thischapter 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

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 mitted by sexual contact (.70%), by parenteral exposure to infected

trans-blood or body fluids, or by transplacental passage of the virus from

mother to fetus The highest-risk groups for HIV infection are 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

ho-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 course occur more commonly than do breaks in penile skin.Although anti-HIV antibodies develop within 12 weeks of ex-

inter-posure, 45%–90% of persons infected with HIV will develop toms of an acute infection similar to mononucleosis within a few months They experience weight loss, fever, night sweats, pharyn-

symp-gitis, lymphadenopathy, and an erythematous maculopapular rash.Most of these symptoms resolve within a few weeks, although thepatients remain infectious despite being asymptomatic Some will

progress to develop symptoms of AIDS-related complex (ARC), with early immunosuppression (decreased CD4 lymphocytes).ARC is usually marked by generalized lymphadenopathy, weightloss, diarrhea, malabsorption, and wasting Some patients experi-

ence further immunosuppression and develop AIDS (any of the

symptoms of acute sepsis, opportunistic infections, Kaposi’s coma, cognitive difficulties, or depression) Once AIDS has beendiagnosed, mortality is
90% 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

sar-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 bricated with nonoxynol 9 is the most effective method of limitingthe risk of infection If a woman is HIV positive, she should becounseled (1) not to donate blood, plasma, tissue, or organs; (2) toavoid pregnancy; (3) to maintain a monogamous relationship;

lu-and (4) to assiduously use condoms lubricated with nonoxynol 9during any sexual contact

HIV antibody testing begins with the enzyme-linked munosorbent assay (ELISA), which has a
95% sensitivity and a

im-
99% 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 vided) should be encouraged for women in the following cate-

pro-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 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 fection, but the chance of the fetus acquiring the virus is 20%–50%.

in-The neonate may be infected during labor and delivery by 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

mater-be misdiagnosed if HIV serologic testing is not performed WhenHIV infection is diagnosed during pregnancy, treatment should bedelayed because of the teratogenic potential of the medicationsused The pregnant HIV-infected woman should be screened forother STDs, along with evaluation for opportunistic infection Abaseline serologic study for CMV and toxoplasmosis, TB skin test-ing, and chest radiograph are recommended Recently AZT and otherchemotherapeutic agents have been found to decrease maternal–fetaland neonatal transmission of HIV When caring for HIV positivemothers, 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 partum and postpartum interval includes protection of health careworkers by using universal infection control guidelines (e.g.,water-repellent gowns, gloves, masks, goggles for potential splashsituations, wall or bulb suctioning) Scalp electrodes and fetalscalp blood samples should be avoided (potential entry site forHIV if fetus is not already infected) Circumcision should not bedone if the neonate is HIV positive Because anti-HIV IgG anti-body passes through the placenta, the infant may be seropositivewithout being infected Abnormal facial features have been de-scribed in some HIV-positive newborns, but this is not common

peri-If neonatal/pediatric AIDS develops, the course of the disease ismuch more rapid than in adults, with death in months rather thanyears.

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 primaryinvolves 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 thelower 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
90% In uppergenital tract infections (salpingitis, peritonitis) proven by laparo-scopically obtained culture, only ⬃50% 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 (Chapter20) 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 thalmitis may result from autoinoculation

oph-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 testingbecause 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), orspectinomycin 2 g IM (single dose for patients with cephalosporinintolerance) 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 performedwithin 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 IVq8h Patients with allergy to beta-lactamase drugs may be treatedwith spectromycin 2 g IM q12h If sensitivity testing confirms thatthe organism is penicillin-sensitive, ampicillin 1 g q6h may begiven Whichever regimen is chosen, therapy should be continuedfor 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 Althoughthey 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), signsand symptoms tend to be localized to the infected area (e.g., eye orgenital tract) without deep tissue invasion

CERVICITIS

C trachomatis cervical and tubal infections occur in women of young age (2–3 times higher in women 20 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 dial infection, and the cervix shows hypertrophic inflammation (mu-

chlamy-copurulent cervicitis) The infection may be asymptomatic in 15%

of nonpregnant, sexually active women

Speci-Tissue culture is required for culture of C trachomatis, and because

of the high cost, limited availability, and 2–6 day delay, it is usedinfrequently 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 ganisms may be present simultaneously

can-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 associatedproblems

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 tubalepithelium

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 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,

cer-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,500 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 dominal cramps may occur late in this disease Late complications

ab-include vulvar elephantiasis.

The diagnosis is confirmed by tissue culture and serotype termination, but complement fixation for Chlamydia with titer

de-1:16 is presumptive, as is a rising titer (
1:64 is diagnostic) munofluorescent testing is available The differential diagnosis forthe cutaneous lesions includes granuloma inguinale, tuberculosis,syphilis, chancroid, vulvar cancer, genital herpes, and Hodgkin’sdisease With systemic symptoms, meningitis, arthritis, peritonitis,and pleurisy must be considered

Im-Treatment for lymphogranuloma venereum includes

doxycy-cline 100 mg PO bid for 21 days Persistent disease requires a ond course Alternative drugs include tetracycline, erythromycin, orsulfisoxizole, each at 500 mg PO qid for 21 days After the disease

sec-is under control, surgery may be necessary (e.g., partial tomy) Abscesses should not be excised but treated by aspiration.Anal strictures should be dilated weekly A diversionary colostomymay be required for severe anal stricture.

vulvec-SYPHILIS

Syphilis is a disease caused by the spirochete Treponema pallidum,

which is transmitted by direct contact with an infectious moist sion These organisms can pass through intact mucous membranes

le-or abraded skin le-or may be acquired transplacentally A single ual encounter with an infected partner carries ⬃10% 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.

sex-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 italia, cervix, or vagina or any area of skin or mucous membrane

gen-of the body but is gen-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 performedweekly for 6 weeks or until positive (usually reactive 1–4 weeksafter 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 munofluorescent studies Other mucous patches may be present, aswell as patchy alopecia, hepatitis, or nephritis Generalized lym-

im-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 curs in one third of patients.

oc-Tertiary syphilis is marked by the presence of destructive 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%

le-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 18 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 theprimary or latent stages The incidence of stillbirth and prematuredelivery is increased with syphilis Hydramnios may be present Theplacenta is involved; it has a waxy, hydropic appearance Infectionlate in pregnancy results in fetal or neonatal infection in 40%–50%.Congenital syphilis occurs in the fetus or newborn whose motherhas 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 secondarysyphilis sometime after birth

Classically, the newborn with congenital syphilis may be dergrown, with wrinkled facies because of reduced subcutaneous fat The skin may have a brownish (café-au-lait) tint The most

un-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 patientsmay 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 nervoussystem may be apparent at birth, or defects may develop later inuntreated cases Any infant with the stigmata of syphilis should beplaced in isolation until a definitive diagnosis can be made and ap-propriate treatment given

Because serologic testing evaluates IgG antibodies that aretransplacentally acquired, the baby will be positive if the mother ispositive Effective neonatal treatment is shown by progressivelyfalling titers over weeks to months

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 thetreponemes in a biopsy specimen Because the organisms are

demonstrable for only a short time, diagnosis usually relies on tory and serologic testing.

his-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, tion, drug addiction, old age, and pregnancy itself The titer seenwith false-positive tests usually is low However, any positive testshould be investigated by an antitreponemal antibody test The mostwidely performed antitreponemal antibody test is the fluorescenttreponemal antibody absorption (FTA-ABS) test The test remainspositive regardless of therapy Thus, titers are not determined

vaccina-DIFFERENTIAL DIAGNOSIS

The differential diagnosis for primary syphilis includes chancroid,

granuloma inguinale, lymphogranuloma venereum, herpes, noma, scabies, trauma, lichen planus, psoriasis, drug eruption,aphthosis, mycotic infection, Reiter’s syndrome, and Bowen’sdisease

carci-The differential diagnosis for secondary syphilis includes

pityr-iasis rosea, psorpityr-iasis, lichen planus, tinea versicolor, drug eruption,

“id” eruptions, perleche, parasitic infection, iritis, neuroretinitis,condylomata accuminata, acute exanthems, infectious mononucle-osis, alopecia, and sarcoidosis

Contacts and patients with early syphilis (primary, secondary,and latent 1 year) should be treated with one of the followingregimens: (1) benzathine penicillin G 2.4 million units IM, (2)tetracycline hydrochloride 500 mg PO qid or doxycycline 100 mgbid for 14 days (for penicillin allergy but not during pregnancy),

or (3) erythromycin (stearate, ethylsuccinate, or base) 500 mg POqid for 15 days (30 g total) for penicillin allergy and if unable totake tetracycline A short-lived (24 h) febrile reaction occurs in50%–75% of those receiving penicillin therapy, presumably due

to a release of toxic treponemal products The fever, which occurs

4–12 h after injection, is a Jarisch-Herxheimer reaction.

Congenital syphilis is treated with benzathine penicillin G50,000 units/kg IM if the infant is asymptomatic and there is noevidence of neurosyphilis Symptomatic congenital syphilis orneurosyphilis is treated with aqueous crystalline penicillin G50,000 units/kg/day IV, divided in two doses for 10 days or aque-ous procaine penicillin G 50,000 units/kg daily for 10 days

CHANCROID

Chancroid (soft chancre) is caused by the gram-negative rod Haemophilus ducreyi and is uncommon in the United States (1500cases/year) This infection begins in females as a papule or vesico-

pustular lesion on the perineum, cervix, or vagina 3–5 days after exposure The lesion progresses over 48–72 h to a very tender saucer-shaped ragged ulcer Several ulcers may develop in a clus-

ter The heavy discharge produced by the ulcer(s) is foul-smelling

and infectious Over 50% of patients develop painful inguinal lymphadenitis that may become necrotic and drain spontaneously.

Aspiration of pus from a bubo may yield the organism Syphilis must

be ruled out, although the differential diagnosis also includes herpessimplex, lymphogranuloma venereum, and granuloma inguinale.Treatment includes sitz baths, soap and water plus antibiotics

The therapeutic regimen will vary depending on sensitivity of the pathogen Ceftriaxone 250 mg IM qd, erythromycin 500 mg PO

qid, and trimethoprim (160 mg)/sulfamethoxazole (800 mg) PO bidhave been effective Treatment should continue for a minimum of

10 days until the ulcer(s) and lymph nodes are healed Abscessednodes should be aspirated rather than incised and drained

GRANULOMA INGUINALE

Granuloma inguinale is caused by Calymmatobacterium matis A characteristic finding in the lesions is the Donovan body

granulo-(bacteria encapsulated in mononuclear leukocytes) It is almostnever seen in the United States (⬃100 cases/year) but is common

in India, Brazil, and the West Indies The incubation period is 1–12 weeks Granuloma inguinale may be spread by repeated sexual or

nonsexual contact

The disease usually is localized to the vulva and inguinal areabut may involve the cervix, uterus, ovary, or mouth It begins as anasymptomatic papule or nodule that ulcerates to form a red, gran-ular area with sharp borders The ulcer drains a foul-smelling dis-

charge Healing is extremely slow, but there are few local or

sys-temic manifestations Satellite ulcers may coalesce into one largeulcer Buboes may occur late in the disease Pain may be present ifthe urethra or anus is involved

Late complications include dyspareunia if the introitus

con-stricts from chronic disease The differential diagnosis includes cinoma, chancroid, lymphogranuloma venereum, and syphilis Thediagnosis is confirmed by finding Donovan bodies in a biopsy spec-imen or smear using Wright, Giemsa, or a silver stain

car-The drug of choice for treatment of granuloma inguinale is

tetra-cycline 500 mg qid for a minimum 21 days Other choices includeerythromycin 500 mg qid for 14–21 days, doxycycline 100 mg bidfor 21 days, or sulfamethoxazole 1 g bid for 21 days

act incidence of upper genital tract infection is unclear, over 10%

of U.S women of reproductive age have received treatment for anupper genital tract infection A functional classification of pelvic in-fections is shown in Table 24-1

Organisms may disseminate to and throughout the pelvis in any

of five ways

● Intraluminal Nonpuerperal acute pelvic inflammatory

dis-ease nearly always (⬃99%) follows a progression of trance of pathogens through the cervix into the uterinecavity Infection then spreads to the uterine tubes, with puseventually entering the peritoneal cavity from the ostia.Organisms known to spread by this mechanism include

en-N gonorrhoeae, C trachomatis, Streptococcus agalactiae, cytomegalovirus, and herpes simplex virus Three fourths of

women with acute PID have concomitant endometritis,whereas⬃40% of those with mucopurulent cervicitis and

50% of those with positive C trachomatis or N gonorrhoeae

endocervical cultures have concomitant endometritis The

endometritis phase is generally asymptomatic, often brief, and occurs at the end of a menses.

● Lymphatic Puerperal infections (including abortion) and

IUD-related infections are disseminated through the

lym-phatic system, as are nonpuerperal Mycoplasma infections.

● Hematogenous Hematogenous dissemination of pelvic

dis-ease is limited to certain disdis-eases (e.g., tuberculosis) and isuncommon in the United States

● Intraperitoneal Intraabdominal infections (e.g.,

appendici-tis, diverticulitis) as well as intraabdominal accidents (e.g.,perforated viscus or ulcer) may lead to an infectious processinvolving the internal genital system

Cesarean section (common)

Vaginal (less common)

Postgynecologic procedure infection

Acute PID after diagnostic instrumentation

Abortion-related infections

Postabortal cellulitis

Incomplete septic abortion

Cuff cellulitis and parametritis

Vaginal cuff abscess