Ch35.pdf

CHAPTER

Sexually Transmitted

Diseases

INFECTIONS OF

THE EXTERNAL GENITALIA

Infections of the External Genitalia

Human Papillomavirus (Condylomata Acuminata)

Genital Herpes

Chancroid

Lymphogranuloma Venereum

Vaginal Infections

Candidiasis

Trichomoniasis

Bacterial Vaginosis (Nonspeciﬁc Vaginitis)

Vaginal-Urogenital-Systemic Infections

Chlamydial Infections

Gonorrhea

Syphilis

Some STDs primarily affect the mucocutaneous tissues of the

external genitalia. These include human papillomavirus infec-

tion, genital herpes, chancroid, granuloma inguinale, and lym-

phogranuloma venereum (LGV).

Human Papillomavirus

(Condylomata Acuminata)

Condylomata acuminata, or genital warts , are caused by the

human papillomavirus (HPV). Although recognized for cen-

turies, HPV-induced genital warts have become one of the

fastest-growing STDs of the past decade. The Centers for

Disease Control and Prevention (CDC) estimates that 20 mil-

lion Americans carry the virus and that as many as 5.5 million

new cases are diagnosed each year. 1 The current prevalence of

HPV is difﬁcult to determine because it is not a reportable dis-

ease in all states.

A 1998 American Medical Association consensus confer-

ence on external genital warts identiﬁed four speciﬁc types of

warts: condyloma acuminata (cauliﬂower-shaped lesions that

tend to appear on moist skin surfaces such as the vaginal in-

troitus or anus); keratotic warts (display a thick, horny layer; de-

velop on dry, fully keratinized skin such as the penis, scrotum,

or labia majora); papular warts (smooth surface; typically de-

velop on fully keratinized skin); and ﬂat warts (macular, some-

times faintly raised, usually invisible to the naked eye; occur on

either fully or partially keratinized skin). Biopsy may be re-

quired to differentiate warts from other hyperkeratotic or pre-

cancerous lesions. 2

A relation between HPV and genital ( i.e. , cervix, vulva, and

penis) neoplasms has become increasingly apparent since the

early 1980s. One hundred types of HPV have been identified,

more than 30 of which affect the anogenital area. Types 6 and

11 are found in most external genital warts but usually are

benign, with only a low potential for dysplasia. Persons with

visible genital warts may be infected simultaneously with

multiple HPV types. Other HPV types of the anogenital region

( e.g. , types 16, 18, 31, 33, and 35) have been strongly asso-

ciated with cervical neoplasia. 3 HPV type 16 is present in 50%

T he incidence and types of sexually transmitted diseases

(STDs), as reported in the professional literature and

public health statistics, are increasing. However, the in-

cidence of disease is based on clinical reports, and many STDs

are not reportable or not reported. The agents of transmission

include bacteria, chlamydiae, viruses, fungi, protozoa, para-

sites, and unidentiﬁed microorganisms. Portals of entry in-

clude the mouth, genitalia, urinary meatus, rectum, and skin.

All STDs are more common in persons who have more than

one sexual partner, and it is not uncommon for a person to be

concurrently infected with more than one type of STD.

This chapter discusses the manifestations of STDs in men

and women in terms of infections of the external genitalia,

vaginal infections, and infections that have systemic effects and

genitourinary manifestations. Human immunodeﬁciency virus

(HIV) infection is presented in Chapter 10.

627

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Unit Nine: Alterations in the Male and Female Reproductive Systems

who has had an abnormal Pap smear. Microscopic examina-

tion of a wet-mount slide preparation and cultures are used to

exclude associated vaginitis. Acetic acid soaks may be used be-

fore inspecting the vulva under magniﬁcation, and specimens

for biopsy can be taken from questionable areas. Colposcopic

examination of the cervix and vagina may be advised as a follow-

up measure when there is an abnormal Pap smear or when

HPV lesions are identiﬁed on the vulva. Evaluation and treat-

ment of sexual partners may be suggested, although this may be

difﬁcult considering that warts often do not become clinically

apparent for several years after exposure.

The recent development and controlled trial of a vaccine to

protect against HPV type 16 may eventually reduce the risk of

cervical cancer associated with this strain of HPV. 4 However,

currently there is no treatment to eradicate the virus once a per-

son has become infected. Thus, treatment goals are aimed at

elimination of symptomatic warts, surveillance for malignancy

and premalignant changes, and education and counseling to

decrease psychosocial distress. 6 Prevention of HPV transmission

through condom use has not been adequately demonstrated.

The CDC recommends several pharmacologic agents for

symptomatic removal of visible genital warts, including patient-

applied therapies (podoﬁlox and imiquimod) and provider-

administered therapies (podophyllin and trichloroacetic acid). 3

Podophyllin, a topical cytotoxic agent, has long been used for

the treatment of visible external growths. Trichloroacetic acid is

a weak destructive agent that produces an initial burning in the

affected area, followed in several days by a sloughing of the

superﬁcial tissue. Imiquimod cream is a new type of therapeu-

tic agent that stimulates the body’s immune system ( i.e. , pro-

duction of interferon-

KEY CONCEPTS

SEXUALLY TRANSMITTED DISEASE

Sexually transmitted diseases (STDs) are spread by

sexual contact and involve both male and female

partners. Portals of entry include the mouth, geni-

talia, urinary meatus, rectum, and skin. All STDs are

more common in persons who have more than one

sexual partner, and it is not uncommon for a person

to be concurrently infected with more than one

type of STD.

■

In general, STDs due to bacterial pathogens can be

successfully treated and the pathogen eliminated by

antimicrobial therapy. However, many of these

pathogens are developing antibiotic resistance.

■

STDs due to viral pathogens, such as the human

papillomavirus (HPV) and genital herpes simplex

virus infections (HSV-1 and HSV-2), are not elimi-

nated by current treatment modalities and persist

with risk of recurrence (HSV infections) or increased

cancer risk (HPV).

■

Untreated, STDs such as chlamydial infection and

gonorrhea can spread to involve the internal genital

organs with risk of complications and infertility.

■

Intrauterine or perinatally transmitted STDs can have

potentially fatal or severely debilitating effects on a

fetus or an infant.

■

and other cytokines).

Genital warts also may removed using cryotherapy, laser

surgery, or electrocautery. Because it can penetrate deeper than

other forms of therapy, cryotherapy ( i.e. , freezing therapy)

often is the treatment of choice for cervical HPV lesions. Laser

surgery can be used to remove large or widespread lesions of

the cervix, vagina, or vulva, or lesions that have failed to re-

spond to other ﬁrst-line methods of treatment. Electrosurgical

treatment has become more widespread for these types of le-

sions because it is more readily available in outpatient settings

and is much less expensive than laser.

of cervical cancers and in 25% of low-grade cervical intraepi-

thelial neoplasias 4 (see Chapter 34). However, only a subset

of women with HPV go on to develop cancer, suggesting that

there may be variants of even the most virulent HPV, type 16,

with differing oncogenic potential. Cofactors that may in-

crease the risk for cancer include smoking, immunosuppres-

sion, and exposure to hormonal alteration ( e.g. , pregnancy,

oral contraceptives). 5 The association with premalignant and

malignant changes has increased the concern about diagnosis

and treatment of this viral infection.

HPV infection begins with viral inoculation into a strati-

fied squamous epithelium, where infection stimulates the re-

plication of the squamous epithelium, producing the various

HPV-proliferative lesions. The incubation period for HPV-

induced genital warts ranges from 6 weeks to 8 months. Sub-

clinical infection occurs more frequently than visible genital

warts among men and women. Infection often is indirectly di-

agnosed on the cervix by Papanicolaou testing (Pap smear),

colposcopy, or biopsy. Both spontaneous resolution and in-

fection with new HPV types are common. Although reinfection

from sexual partners has been considered as a reason for the

high prevalence of this disease, it is now thought that reinfec-

tion with the same HPV type is infrequent. Instead, it is thought

that HPV may be a lifelong infection.

Genital condylomas should be considered in any woman

who presents with the primary complaint of vulvar pruritus or

Genital Herpes

Herpesviruses are large, encapsulated viruses that have a double-

stranded genome. There are nine types of herpesviruses, be-

longing to three groups, that cause infections in humans:

(1) neurotropic

-group viruses, including herpes simplex virus

type 1 (HSV-1; usually associated with cold sores) and HSV-2

(usually associated with genital herpes); (2) varicella-zoster

virus (causes chickenpox and shingles); and (3) lympho-

tropic

-group viruses, including cytomegalovirus (causes cyto-

megalic inclusion disease), Epstein-Barr virus (causes infec-

tious mononucleosis and Burkitt’s lymphoma), and human

herpesvirus type 8 (the apparent cause of Kaposi’s sarcoma). 7

Genital herpes is caused by the herpes simplex virus. Be-

cause herpesvirus infection is not reportable in all states, reli-

able data on its true incidence (estimated number of new cases

every year) and prevalence (estimated number of people cur-

rently infected) are lacking. From the late 1970s to early 1990s,

genital herpes prevalence increased 30%. Incidence rates have

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Chapter 35: Sexually Transmitted Diseases

been relatively stable since 1990, with an estimated 1 million

new cases occurring each year. Recent estimates in the United

States indicate 50 million people (one in ﬁve adolescents or

adults) are infected with genital herpes. 3 Women have a greater

mucosal surface area exposed in the genital area and therefore

are at greater risk of acquiring the infection.

HSV-1 and HSV-2 are genetically similar, both cause a sim-

ilar set of primary and recurrent infections, and both can cause

genital lesions. Both viruses replicate in the skin and mucous

membranes at the site of infection (oropharynx or genitalia),

where they cause vesicular lesions of the epidermis and infect

the neurons that innervate the area. HSV-1 and HSV-2 are

neurotropic viruses, meaning that they grow in neurons and

share the biologic property of latency. Latency refers to the abil-

ity to maintain disease potential in the absence of clinical signs

and symptoms. In genital herpes, the virus ascends through the

peripheral nerves to the sacral dorsal root ganglia (Fig. 35-1).

The virus can remain dormant in the dorsal root ganglia, or it

can reactivate, in which case the viral particles are transported

back down the nerve root to the skin, where they multiply and

cause a lesion to develop. During the dormant or latent period,

the virus replicates in a different manner so that the immune

system or available treatments have no effect on it. It is not

known what reactivates the virus. It may be that the body’s de-

fense mechanisms are altered. Numerous studies have shown

that host responses to infection inﬂuence initial development

of the disease, severity of infection, development and mainte-

nance of latency, and the frequency of HSV recurrences.

HSV is transmitted by contact with infectious lesions or se-

cretions. HSV-1 is transmitted by oral secretions, and infections

frequently occur in childhood, with most persons (50% to

90%) being infected by adulthood. 8 HSV-1 may be spread to

the genital area by autoinoculation after poor hand washing or

through oral intercourse. HSV-2 usually is transmitted by sex-

ual contact but can be passed to an infant during childbirth if

the virus is actively being shed from the genital tract. Most cases

of HSV-2 infection are subclinical, manifesting as truly asymp-

tomatic or symptomatic but unrecognized infections. These

subclinical infections can occur in people who have never had

a symptomatic outbreak or between recognized clinical recur-

rences. Up to 70% of genital herpes cases are spread through

asymptomatic shedding by people who do not realize they

have the infection. 3 This “unknown” transmission of the virus

to sex partners explains why this infection has reached epide-

mic proportions throughout the world.

The incubation period for HSV is 2 to 10 days. Genital HSV

infection may manifest as a primary, nonprimary, or recurrent

infection. Primary infections are infections that occur in a person

who is seronegative for antibody to HSV-1 or HSV-2. Initial

nonprimary infections refer to the ﬁrst clinical episode in a per-

son who is seropositive for antibodies to the opposite HSV type

(usually genital herpes in someone seropositive to HSV-1).

Recurrent infections refer to the second or subsequent outbreak

caused by the same virus type. HSV-2 is responsible for more

than 90% of recurrent genital herpes infections. 6

The initial symptoms of primary genital herpes infections

include tingling, itching, and pain in the genital area, followed

by eruption of small pustules and vesicles. These lesions rup-

ture on approximately the ﬁfth day to form wet ulcers that are

excruciatingly painful to touch and can be associated with

dysuria, dyspareunia, and urine retention. Involvement of the

cervix and urethra is seen in more than 80% of women with

primary infections. 9 In men, the infection can cause urethritis

and lesions of the penis and scrotum. Rectal and perianal in-

fections are possible with anal contact. Systemic symptoms as-

sociated with primary infections include fever, headache,

malaise, muscle ache, and lymphadenopathy. Primary infec-

tions may be debilitating enough to require hospitalization,

particularly in women.

Untreated primary infections typically are self-limited and

last for approximately 2 to 4 weeks. The symptoms usually

worsen for the first 10 to 12 days. This period is followed by

a 10- to 12-day interval during which the lesions crust over

and gradually heal. Nonprimary episodes of genital herpes

manifest with less severe symptoms that usually are of shorter

duration and have fewer systemic manifestations. Except for

the greater tendency of HSV-2 to recur, the clinical manifes-

tations of HSV-2 and genital HSV-1 are similar. Recurrent

HSV infection results from reactivation of the virus stored in

the dorsal root ganglia of the infected dermatomes. An out-

break may be preceded by a prodrome of itching, burning, or

tingling at the site of future lesions. Because immune lym-

phocytes have already developed from the primary infection,

recurrent episodes have fewer lesions, fewer systemic symp-

toms, less pain, and a shorter duration (7 to 10 days). The fre-

quency and severity of recurrences vary from person to person.

Numerous factors, including emotional stress, lack of sleep,

overexertion, other infections, vigorous or prolonged coitus,

and premenstrual or menstrual distress have been identiﬁed as

triggering mechanisms.

Diagnosis of genital herpes is based on the symptoms, ap-

pearance of the lesions, and identification of the virus from

cultures taken from the lesions. The likelihood of obtaining a

positive culture decreases with each day that has elapsed after

a lesion develops. The chance of obtaining a positive culture

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Unit Nine: Alterations in the Male and Female Reproductive Systems

Lymphogranuloma Venereum

Lymphogranuloma venereum (LGV) is an acute and chronic

venereal disease caused by Chlamydia trachomatis types L1, L2,

and P3. The disease, although found worldwide, has a low in-

cidence outside the tropics. Most cases reported in the United

States are in men.

The lesions of LGV can incubate for a few days to several

weeks and thereafter cause small, painless papules or vesicles

that may go undetected. An important characteristic of the

disease is the early (1 to 4 weeks later) development of large,

tender, and sometimes fluctuant inguinal lymph nodes called

buboes . There may be flulike symptoms with joint pain, rash,

weight loss, pneumonitis, tachycardia, splenomegaly, and

proctitis. In later stages of the disease, a small percentage of

affected persons develop elephantiasis of the external geni-

talia, caused by lymphatic obstruction or fibrous strictures of

the rectum or urethra from inﬂammation and scarring. Ure-

thral involvement may cause pyuria and dysuria. Cervicitis is a

common manifestation of primary LGV and could extend to

perimetritis or salpingitis, which are known to occur in other

chlamydial infections. 5 Anorectal structures may be compro-

mised to the point of incontinence. Complications of LGV may

be minor or extensive, involving compromise of whole systems

or progression to a cancerous state.

Diagnosis usually is accomplished by means of a comple-

ment ﬁxation test for LGV-speciﬁc Chlamydia antibodies. High

titers for this antibody differentiate this group from other chla-

mydial subgroups. Treatment involves 3 weeks of doxycycline

or erythromycin. 3 Surgery may be required to correct sequelae

such as strictures or ﬁstulas or to drain ﬂuctuant lymph nodes.

from a crusted lesion is slight, and patients suspected of having

genital herpes should be instructed to have a culture within

48 hours of development of new lesions. Type speciﬁc (HSV-1

and HSV-2) serologic tests are available for determining past

infection. Because almost all HSV-2 infections are sexually

acquired, the presence of type-speciﬁc HSV-2 antibodies usu-

ally indicates anogenital infection; whereas the presence of

HSV-1 antibodies does not distinguish between anogenital

and orolabial infections. The CDC recommends that serologic

assays for HSV-2 be available for persons who request them

but does not recommend they be used for screening of the gen-

eral population. 3

There is no known cure for genital herpes, and the methods

of treatment are largely symptomatic. The antiviral drugs acy-

clovir, valacyclovir, and famciclovir have become the corner-

stone for management of genital herpes. By interfering with viral

DNA replication, these drugs decrease the frequency of recur-

rences, shorten the duration of active lesions, reduce the num-

ber of new lesions formed, and decrease viral shedding with pri-

mary infections. Good hygiene is essential to prevent secondary

HSV infection. Fastidious hand washing is recommended to

avoid hand-to-eye spread of the infection. HSV infection of the

eye is the most common cause of corneal blindness in the

United States. To prevent spread of the disease, intimate con-

tact should be avoided until lesions are completely healed.

Approximately 30% to 50% of infants born vaginally to

mothers experiencing a primary HSV infection at the time of

delivery will be infected, compared with only 1% of those born

to women with recurrent infection. 3 The risk of mortality in

HSV-infected neonates ranges from 15% to 57%, and a signif-

icant number of survivors have signiﬁcant sequelae. 10 Active in-

fection during labor may necessitate cesarean delivery.

In summary, STDs that primarily affect the external geni-

talia include HPV (condyloma acuminata), genital herpes

(HSV-2), chancroid, and lymphogranuloma venereum. The

lesions of these infections occur on the external genitalia of

male and female sexual partners. Of concern is the relation

between HPV and genital neoplasms. Genital herpes is caused

by a neurotropic virus (HSV-2) that ascends through the peri-

pheral nerves to reside in the sacral dorsal root ganglia. The

herpesvirus can be reactivated, producing recurrent lesions in

genital structures that are supplied by the peripheral nerves of

the affected ganglia. There is no permanent cure for herpes

infections. Chancroid and lymphogranuloma venereum pro-

duce external genital lesions with various degrees of inguinal

lymph node involvement.

Chancroid

Chancroid ( i.e. , soft chancre) is a disease of the external gen-

italia and lymph nodes. The causative organism is the gram-

negative bacterium Haemophilus ducreyi , which causes acute

ulcerative lesions with profuse discharge. This disease has be-

come uncommon in the United States, with only 143 reported

cases in 1999. 1 It typically occurs in discrete outbreaks, rather

than as an endemic disease in this country. It is more prevalent

in Southeast Asia, the West Indies, and North Africa. A highly in-

fectious disease, chancroid usually is transmitted by sexual in-

tercourse or through skin and mucous membrane abrasions.

Autoinoculation may lead to multiple chancres.

Lesions begin as macules, progress to pustules, and then

rupture. This painful ulcer has a necrotic base and jagged edges.

In contrast, the syphilitic chancre is nontender and indurated.

Subsequent discharge can lead to further infection of self or

others. On physical examination, lesions and regional lymph-

adenopathy ( i.e. , buboes) may be found. Secondary infec-

tion may cause signiﬁcant tissue destruction. Diagnosis usually

is made clinically but may be conﬁrmed through culture.

Gram’s stain rarely is used today because it is insensitive and

nonspeciﬁc. Polymerase chain reaction (PCR) methods may

soon be available commercially for deﬁnitive identiﬁcation of

H. ducreyi . The organism has shown resistance to treatment

with sulfamethoxazole alone and to tetracycline. The CDC rec-

ommends treatment with azithromycin, erythromycin, cipro-

ﬂoxacin, or ceftriaxone. 3

VAGINAL INFECTIONS

Candidiasis, trichomoniasis, and bacterial vaginosis are vagi-

nal infections that can be sexually transmitted. Although these

infections can be transmitted sexually, the male partner usually

is asymptomatic.

Candidiasis

Also called yeast infection, thrush , and moniliasis , candidiasis is

the second leading cause of vulvovaginitis in the United States.

Approximately 75% of reproductive-age women in the United

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Chapter 35: Sexually Transmitted Diseases

States experience one episode in their lifetime; 40% to 45% ex-

perience two or more infections. 5

The causative organism is Candida, a genus of yeastlike

fungi. The species most commonly identiﬁed is Candida albi-

cans , but other candidal species, such as Candida glabrata and

Candida tropicalis , have caused symptoms. Although vulvovagi-

nal candidiasis usually is not transmitted sexually, it is included

in the CDC STD treatment guidelines because it often is diag-

nosed in women being evaluated for STDs. 3 The possibility of

sexual transmission has been recognized for many years; how-

ever, candidiasis requires a favorable environment for growth.

The gastrointestinal tract also serves as a reservoir for this

organism, and candidiasis can develop through autoinocula-

tion in women who are not sexually active. Although studies

have documented the presence of Candida on the penis of male

partners of women with vulvovaginal candidiasis, few men

develop balanoposthitis that requires treatment.

Causes for the overgrowth of C. albicans include antibiotic

therapy, which suppresses the normal protective bacterial

flora; high hormone levels associated with pregnancy or the

use of oral contraceptives, which cause an increase in vaginal

glycogen stores; and diabetes mellitus or HIV infection be-

cause they compromise the immune system. In obese persons,

Candida may grow in skin folds underneath the breast tissue,

the abdominal ﬂap, and the inguinal folds. Vulvar pruritus ac-

companied by irritation, dysuria, dyspareunia, erythema, and

an odorless, thick, cheesy vaginal discharge are the predomi-

nant symptoms of the infection. Accurate diagnosis is made by

identification of budding yeast filaments ( i.e. , hyphae) or

spores on a wet-mount slide using 20% potassium hydroxide

(Fig. 35-2). The pH of the discharge, which is checked with lit-

mus paper, typically is less than 4.5. When the wet-mount

technique is negative but the clinical manifestations are indi-

cative of candidiasis, a culture may be necessary.

Antifungal agents such as clotrimazole, miconazole, buto-

conazole, and terconazole, in various forms, are effective in

treating candidiasis. These drugs, with the exception of ter-

conazole, are available without prescription for use by women

who have had a previously conﬁrmed diagnosis of candidiasis.

Oral ﬂuconazole has been shown to be as safe and effective as

the standard intravaginal regimens. 3 Tepid sodium bicarbonate

baths, clothing that allows adequate ventilation, and the ap-

plication of cornstarch to dry the area may increase comfort

during treatment. Chronic vulvovaginal candidiasis, deﬁned as

four or more mycologically conﬁrmed episodes within 1 year,

affects approximately 5% of women and is difﬁcult to manage.

Subsequent prophylaxis (maintenance therapy) often is re-

quired for the long-term management of this problem. 11

Trichomoniasis

An anaerobic protozoan that can be transmitted sexually, Tri-

chomonas vaginalis is shaped like a turnip and has three or four

anterior ﬂagella (see Fig. 35-2). Trichomonads can reside in the

paraurethral glands of both sexes. Males harbor the organism

in the urethra and prostate and are asymptomatic. Although

10% to 25% of women are asymptomatic, trichomoniasis is a

common cause of vaginitis when some imbalance allows the

protozoan to proliferate. Five million cases of trichomoniasis

were diagnosed in 1999. 1 This extracellular parasite feeds on

the vaginal mucosa and ingests bacteria and leukocytes. The in-

fection causes a copious, frothy, malodorous, green or yellow

discharge. There commonly is erythema and edema of the

affected mucosa, with occasional itching and irritation. Some-

times, small hemorrhagic areas, called strawberry spots , appear

on the cervix.

Diagnosis is made microscopically by identification of the

protozoan on a wet-mount slide preparation. The pH of the

discharge usually is greater than 6.0. Special culture media

are available for diagnosis but are costly and not needed for

diagnosis.

Because the organism resides in urogenital structures other

than the vagina, systemic treatment is recommended. The treat-

ment of choice is oral metronidazole (Flagyl), a medication

that is effective against anaerobic protozoans. 3 Metronidazole

is chemically similar to disulﬁram (Antabuse), a drug used in

the treatment of alcohol addiction that causes nausea, vomit-

ing, ﬂushing of the skin, headache, palpitations, and lowering

of the blood pressure when alcohol is ingested. Alcohol should

be avoided during and for 24 to 48 hours after treatment.

Gastrointestinal disturbances and a metallic taste in the mouth

are potential adverse effects of the drug. Metronidazole has not

been proven safe for use during pregnancy and is used only

after the ﬁrst trimester for fear of potential teratogenic effects.

Sexual partners should be treated to avoid reinfection, and ab-

stinence is recommended until the full course of therapy is

completed.

Bacterial Vaginosis (Nonspeciﬁc Vaginitis)

Bacterial vaginosis is a vaginal infection that produces a char-

acteristic ﬁshy- or ammonia-smelling discharge yet fails to pro-

duce an inﬂammatory response that is characteristic of most

infections.

Bacterial vaginosis represents an upheaval in the complex

vaginal bacterial flora with disappearance of the normal lacto-

bacillus species in the vagina and an overgrowth of other or-

ganisms, including Gardnerella vaginalis and resident anaerobic

vaginal bacterial . 12 It has been suggested that the presence of

anaerobes, which produce ammonia or amines from amino

■ FIGURE 35-2 ■ Organisms that cause vaginal infections. ( A ) Can-

dida albicans (blastospores and pseudohyphae). ( B, C ) Trichomonas

vaginalis.

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