Download Other Infections of the Vulva

BENIGN DISORDERS OF THE
VULVA
Rukset Attar, MD, PhD
Department of
Obstetrics and Gynecology





Originates from ectoderm
erithematous, ulcerative, proliferative and
hyperkeratotic lesions
Examined after application of 3-5% acetic acide
or 1% toluidin blue
Colposcopy is time consuming
Biopsy from multiple sites with Keyes biopsy
forceps
Benign Lesions of the Vulva

Inflamatory




Dermatities ( contact, seboreic-intertrigo, psoriasis,
candidasis, tinea, infections of the major and minor
vestibular glands)
Viral diseases ( HSV, HPV, Herpes Zoster,
Molluscum contagiosum)
Ulcerative lesions ( Crohn, Behcet, venerial diseases,
nonspes lesions-hydradenitis, folliculitis,etc)
Traumatic


hematomas
lacerations

White



Depigmentation-vitiligo or leukoderma
Hypercheratotic lesions( inflamatory,benign
neoplasms)
Vulvar dystrophies (Lichen sclerosus, squamous cell
hyperplasia-hyperplastic dystrophy,mixt)
Benign Lesions of the Vulva

Benign neoplasms
Benign cystic tumors (Epidermal cysts, sebaceous
cysts, apocrine sweat gland cysts, Skene duct cyst,
urethral diverticulum, inguinal hernia, Gartner's duct
cyst, Bartholin's duct cyst and abscess)
 Benign solid tumors (Acrochordon, pigmented nevi,
leiomyoma, fibroma, lipoma, neurofibromas, granular
cell myoblastoma)
 Vascular and lymphatic disease (Varicosities,
hematoma, edema, granuloma pyogenicum,
hemangioma, lymphangioma)



Vulvar manifestation of systemic disease
(Leukemia, dermatologic disorders
(disseminated lupus erythematosus, pemphigus
vulgaris)
Infestations of the vulva (Pediculosis pubis,
scabies, enterobiasis)
Vascular and lymphatic disease






varicosities
hematoma
edema
granuloma pyogenicum(a variant of a capillary
hemangioma. It usually is single, raised, and dull red. Its
size seldom exceeds 3 cm. Pyogenic granuloma is
important because it tends to bleed easily if traumatized.
Wide excisional biopsy is indicated to alleviate
symptoms and to rule out a malignant melanoma)
hemangioma
lymphangioma
Vulvar manifestation of systemic disease



leukemia
dermatologic disorders (disseminated lupus
erythematosus, pemphigus vulgaris, contact dermatitis,
psoriasis)
obesity
 Acanthosis nigricans is a benign hyperpigmented
lesion characterized by papillomatous hypertrophy. It
may be associated with an underlying
adenocarcinoma.
 Intertrigo is an inflammatory reaction involving the
genitocrural folds or the skin under the abdominal
panniculus. It is common in obese patients and
results from persistent moistness of the skin surfaces.
Vulvar manifestation of systemic disease


Diabetes Mellitus
 Diabetic vulvitis. It is caused by a chronic
vulvovaginal candidiasis
 Necrotizing fasciitis is seen most commonly in
diabetics. It is an uncommon, acute, rapidly
spreading, frequently fatal polymicrobial infection of
the superficial fascia and subcutaneous fascia. It may
be seen following a surgical procedure such as an
episiotomy or after minor trauma. It presents as an
extremely painful, tender, and indurated region with
central necrosis and peripheral purplish erythema.
Treatment requires surgical debridement and
systemic antibiotics.
Behçet's syndrome
Viral Infections




Herpes genitalis
HPV
Herpes Zoster
Molluscum Contagiosum
Herpes Zoster



A painful eruption of groups of vesicles is distributed
over an area of skin corresponding to the course of 1 or
more peripheral sensory nerves.
The causative agent is varicella-zoster virus.
The lesion is commonly unilateral and not infrequently
attacks 1 buttock, 1 thigh, or 1 side of the vulva.
Molluscum Contagiosum





These benign epithelial poxvirus-induced tumors are
dome-shaped, often umbilicated, and vary in size up to 1
cm.
The lesions often are multiple and are mildly contagious.
The microscopic appearance is characterized by
numerous inclusion bodies (molluscum bodies) in the
cytoplasm of the cells.
Each lesion can be treated by desiccation, freezing, or
curettage and chemical cauterization of the base.
Topical imiquimod( aldara ) can be used as alternative
therapy
Infestations of the Vulva

Pediculosis Pubis
 The crab louse (Phthirus pubis) is transmitted through
sexual contact or from shared infected bedding or
clothing.
 intense pubic and anogenital itching.
 minute pale-brown insects and their ova may be seen
attached to terminal hair shafts.
 treatment consists of permethrin 1% cream, lindane
1% shampoo, or pyrethrins with piperonyl butoxide.
 Lindane is not recommended for pregnant or lactating
women or for children younger than 2 years.
 Treat all contacts and sterilize clothing that has been
in contact with the infested area.
Infestations of the Vulva

Scabies
 Sarcoptes scabiei
 itching and excoriation of the skin surfaces in the
vicinity of minute skin burrows where parasites have
deposited ova.
 The itch mite is transmitted, often directly, from
infected persons.
 The patient should take a hot soapy bath, scrubbing
the burrows and encrusted areas thoroughly.
 Treatment consists of permethrin cream (5%), which
should be applied to the entire body from the neck
down, with particular attention to the hands, wrists,
axillae, breasts, and anogenital region. It should be
washed off after 8–14 hours.
Infestations of the Vulva




Alternatively, lindane (1%) in the lotion or cream form
can be applied in a thin layer to all areas of the body
and washed off after 8 hours.
All potentially infected clothing or bedding should be
washed or dry-cleaned.
All contacts or persons in the family must be treated
in the same way to prevent reinfection.
Therapy should be repeated in 10–14 days if new
lesions develop.
Infestations of the Vulva

Enterobiasis (Pinworm, Seatworm)
 Apply ammoniated mercury ointment to the perianal
region twice daily for relief of itching.
 Pinworms succumb to systemic treatment with
pyrantel pamoate, mebendazole, or pyrvinium
pamoate
Mycotic Infections of the Vulva

Fungal Dermatitis (Dermatophytoses)
 Tinea cruris is a superficial fungal infection of the
genitocrural area that is more common in men than in
women.
 The most common organisms are Trichophyton
mentagrophytes and Trichophyton rubrum.
 The initial lesions usually are located on the upper
inner thighs and are well circumscribed,
erythematous, dry, scaly areas that coalesce.
 Scratching causes lichenification and a gross
appearance similar to neurodermatitis.
Mycotic Infections of the Vulva




The diagnosis depends on microscopic examination
(as for Candida)
Culture on Sabouraud's medium confirms the
diagnosis.
Treatment with 1% haloprogin, tolnaftate, or a similar
agent is effective.
Topical imidazole preparation at twice-daily
application for 2–3 weeks also is highly effective
Other Infections of the Vulva

Impetigo







is caused by the hemolytic S aureus or streptococci.
The disease is autoinoculable and spreads quickly to
other parts of the body, including the vulva.
Thin-walled vesicles and bullae develop that display
reddened edges and crusted surfaces after rupture.
The disease is common in children, particularly on the
face, hands, and vulva.
The patient must be isolated and the blebs incised or
crusts removed aseptically.
Neomycin or bacitracin should be applied twice daily
for 1 week.
Bathing with an antibacterial soap is recommended.
Other Infections of the Vulva

Furunculosis





Vulvar folliculitis is caused by a staphylococcal
infection of hair follicles.
Furunculosis occurs if the infection spreads into the
perifollicular tissues, producing a localized cellulitis.
Minor infections can be treated by applications of
topical antibiotic lotions.
Deeper infections can be brought to a head with hot
soaks, after which the pustules should be incised and
drained.
Appropriate systemic antibiotics are warranted when
extensive furunculosis is present.
Other Infections of the Vulva

Erysipelas
 Erysipelas is a rapidly spreading erythematous lesion
of the skin caused by invasion of the superficial
lymphatics by β-hemolytic streptococci.
 is extremely rare and is most commonly seen after
trauma to the vulva or a surgical procedure.
 Systemic symptoms of chills, fever, and malaise
 Vesicles and bullae may appear, and erythematous
streaks leading to the regional lymph nodes are
typical.
 The patient should be given systemic (preferably
parenteral) penicillin or tetracycline orally in large
doses
Other Infections of the Vulva

Hidradenitis
 Hidradenitis suppurativa is a refractory process of the
apocrine sweat glands, usually associated with
staphylococci or streptococci.
 Treatment early in the disease consists of drainage
and administration of antibiotics based on organism
sensitivity testing.
 Long-term therapy with isotretinoin may be
considered.
 Antiandrogen therapy with cyproterone acetate or
ethinyl estradiol may be an alternate but highly
effective treatment.
Other Infections of the Vulva




Severe chronic infections may not respond to medical
therapy, and the involved skin and subcutaneous tissues
must be removed down to the deep fascia.
This may necessitate a filet and curettage or a complete
vulvectomy.
The area generally will not heal after a primary closure;
therefore, the wound must be left open and allowed to
heal by secondary intention, or a split-thickness graft
may be placed.
Squamous cell carcinoma is rarely associated with
hidradenitis suppurativa.
Other Infections of the Vulva

Tuberculosis (Vulvovaginal Lupus Vulgaris)
 is manifested by chronic, minimally painful, exudative
"sores" that are tender, reddish, raised, moderately
firm, and nodular, with central "apple jelly"-like
contents
 wet compresses of aluminum acetate solution
(Burow's solution) are helpful.
 systemic antituberculosis therapy should be given.
Vulvar Nonneoplastic Epithelial Disorders


Vulvar dystrophies was previously used to define the
nonneoplastic epithelial disorders of the vulva.
As characterized by the International Society for the
Study of Vulvovaginal Disease (ISSVD), these lesions
include
 lichen sclerosus (previously lichen sclerosus et
atrophicus),
 squamous cell hyperplasia (previously hyperplastic
dystrophy), and
 mixt
Vulvar Nonneoplastic Epithelial Disorders




These lesions present classically with intense pruritus
with or without pain and vulvar epithelial changes.
Differentiating from among these disorders and ruling
out an underlying malignant process require
histopathologic diagnosis.
The risk of an underlying malignancy is less than 5%.
Patients must be reexamined periodically, and one
should not hesitate to take additional biopsy
specimens.
Vulvar Nonneoplastic Epithelial Disorders

Lichen sclerosus
 Thin, white, wrinkled tissue, with a cigarette-paper
appearance
 Clobetasol propionate(dermovate) 0.05% twice daily
for 3 months
 2% testosterone cream twice daily for 3 months
 1.25% topical progesterone twice daily for 3 months 9
esp for children-discontinue for 1 year at puberty and
menapaosal women)
 Intralesional triamcinolone injection5 mg in 2 ml or 10
mg in 1 ml injection 0.1 ml at diff sites with 22 gauge
spinal needle
 surgery
Vulvar Nonneoplastic Epithelial Disorders

Squamous cell hyperplasia
 Circumscribed, single or multifocal
 Raised white lesion on vulva or adjacent tissue
(generally of labia majora and clitoris)
 Medium-potency topical steroids twice daily (
kenocort-A, locacortene)- not eff then high-potency
topical steroids(dermovate) twice daily when
satisfactory relief established then hydrocortisone
 With benadryl at bedtime and white cotton gloves
 Intralesional triamcinolone injection5 mg in 2 ml or 10
mg in 1 ml injection 0.1 ml at diff sites with 22 gauge
spinal needle
 surgery
Vulvar Nonneoplastic Epithelial Disorders

Lichen simplex chronicus
 Thickened white epithelium on vulva
 Generally unilateral and localized
 Medium-potency topical steroids twice a daily
Benign Cystic Tumors

Epidermal Cyst
 epithelial cells-may result from traumatic suturing of
skin fragments during closure of the vulvar mucosa
and skin after trauma or episiotomy.
 most epidermal cysts arise from occlusion of
pilosebaceous ducts.
 These cysts usually are small, solitary, and
asymptomatic.
Benign Cystic Tumors

Sebaceous Cysts
 develops when the sebaceous gland's duct becomes
occluded and accumulation of the sebaceous material
occurs.
 are frequently multiple and almost always involve the
labia majora.
 are generally asymptomatic; however, acutely
infected cysts may require incision and drainage.
Benign Cystic Tumors

Apocrine Sweat Gland Cysts
 Occlusion of the ducts with keratin results in an
extremely pruritic, microcystic disease called FoxFordyce disease.
 Chronic infection in the apocrine glands, usually with
staphylococci or streptococci, results in multiple
painful subcutaneous abscesses and draining
sinuses. This condition is called hidradenitis
suppurativa, which is generally treated with a broadspectrum antibiotic.
 Hidradenoma and syringoma are included in a
diverse group of benign cystic or solid tumors of
apocrine sweat gland origin present as small
subcutaneous and asymptomatic tumors.
Benign Cystic Tumors

Bartholin's Duct Cyst and Abscess
 Obstruction of the main duct of Bartholin's gland
results in retention of secretions and cystic dilatation.
 Infection is an important cause of obstruction;
however, other causes include inspissated mucus
and congenital narrowing of the duct.
 Secondary infection may result in recurrent abscess
formation.
 The gland and duct are located deep in the posterior
third of each labium majus. Enlargement in the
postmenopausal patient may represent a malignant
process (although the incidence is < 1%), and biopsy
should be considered
Benign Cystic Tumors

Other
 Skene duct cyst
 urethral diverticulum
 An inguinal hernia
 Occlusion of a persistent processus vaginalis (canal
of Nuck) may cause a cystic tumor or hydrocele.
 Dilatation of the mesonephric duct vestiges produces
lateral vaginal wall cysts, Gartner's duct cyst.
 Supernumerary mammary tissue that persists in the
labia majora may form a cystic or solid tumor or even
an adenocarcinoma; engorgement of such tissue in
the pregnant patient can be symptomatic.
Benign Solid Tumors

Acrochordon
 An acrochordon is a flesh-colored, soft polypoid tumor
of the vulvar skin that has been called a fibroepithelial
polyp or simply a skin tag.
 The tumor does not become malignant and is of no
clinical importance, unless it becomes traumatized,
causing bleeding.
 Simple excision biopsy in the office is ordinarily
adequate therapy.
Benign Solid Tumors



Pigmented Nevus
Leiomyoma, Fibroma, and Lipoma
Neurofibroma - may be solitary, solid tumors of the vulva
or associated with generalized neurofibromatosis
(Recklinghausen's disease)-They arise from the neural
sheath and usually are small lesions of no consequence
Benign Solid Tumors

Granular Cell Myoblastoma (Schwannoma)-is usually a
solitary, painless, slow-growing, infiltrating but benign
tumor of neural sheath origin, most commonly found in
the tongue or integument, although approximately 7%
involve the vulva. The usual picture consists of small
subcutaneous nodules 1–4 cm in diameter. With
increasing size, they erode through the surface and
result in ulcerations that may be confused with cancer.
The margins of the tumor are indistinct, and wide local
excision is necessary to completely excise the cells
extending into contiguous tissues. The area of resection
must be periodically re-examined and secondary
excision performed promptly if recurrence is suspected
Vulvar Pain Syndrome





Vulvar pain in the absence of relevant, visible physical
findings is termed vulvodynia.
The patient suffering from vulvodynia describes her
symptoms as burning, rawness, irritation, dryness, and
hyperpathia (pain provoked by very light touch).
Approximately 16% of the female population has
experienced vulvodynia and approximately 1.5%
currently suffer from the disorder.
Vulvodynia has been classified into generalized
vulvodynia (provoked or unprovoked) and localized
vulvodynia (provoked and unprovoked).
a detailed history and examination are important to help
determine the etiology and to direct the diagnosis and
treatment.
Vulvar Pain Syndrome-Etiology




Infections
 Bartholin's gland abscess, vulvovaginal candidiasis,
herpes, herpes zoster, human papillomavirus,
molluscum contagiosum, trichomoniasis
Trauma
 Sexual assault, prior vaginal deliveries, hymenectomy
Systemic Illness
 Behçet's disease, Crohn's disease, Sjögren's
syndrome, systemic lupus erythematosus
Neoplasia
 Vulvar intraepithelial neoplasia and invasive
squamous cell carcinoma
Vulvar Pain Syndrome-Etiology



Allergens/toxic medications
 Soaps, sprays, douches, antiseptics, suppositories,
creams, laser treatment, podophyllin, trichloroacetic
acid, 5-fluorouracil
Dermatologic conditions
 Allergic and contact dermatitis, eczema, hidradenitis
suppurativa, lichen planus, lichen sclerosus,
pemphigoid, pemphigus, psoriasis, squamous cell
hyperplasia
Urinary tract syndromes
 Interstitial cystitis and urethral syndrome
Vulvar Pain Syndrome-Etiology
 Neurologic
 Referred pain from urethra, vagina, and bladder;
 dysesthesias secondary to herpes zoster, spinal disk
problems;
 specific neuralgias (pudendal, genitofemoral)
 Psychological
 Sexual/physical abuse history
Localized Provoked Vulvodynia





was formerly known as vulvar vestibulitis/clitorodynia.
The vestibule is the nonpigmented, nonkeratinized
squamous epithelium of the vulva between the labia
minora and the hymen
generally affects women in their 20s and 30s who
complain of introital dyspareunia.
present as persistent vaginal discharge and burning.
is characterized by 3 criteria:
 introital pain on vestibular or vaginal entry (entry
dyspareunia),
 vestibular erythema or inflammation of the vestibule,
commonly involving the posterior fourchette, and
 vestibular tenderness—pressure from a cotton-tipped
applicator at the vestibule reproduces the pain.
Localized Provoked Vulvodynia


Patients should be instructed on proper vulvar hygiene
(cotton underwear, keeping area dry, avoidance of
constrictive garments and irritating agents).
The initial conservative approach to therapy includes
topical estradiol with twice-daily application, 5% lidocaine
ointment daily, calcium citrate 400 mg 3 times daily to
decrease the urinary oxalate crystal concentration, oral
antifungal therapy using fluconazole 150 mg weekly, and
pelvic floor therapy with biofeedback.
Localized Provoked Vulvodynia


The injectable forms of therapy include intralesional
interferon injection to treat possible HPV, trigger point
injections with long-acting injectable anesthetics, and
injection of botulism toxin to treat vaginismus as the
source of vulvodynia.
The surgical treatment of localized provoked vulvodynia
in the form of vulvar vestibulectomy with vaginal
advancement is most effective (70% success rate) in
patients who have been refractory to more conservative
therapies.
Generalized Unprovoked Vulvodynia






was formerly known as pudendal neuralgia.
Its etiology is unknown.
The pain involves a larger surface area than that of
localized vulvodynia.
The average patient is in her 40s.
The typical patient complains of intermittent or constant
burning sensation with periods of unexplained relief
and/or flares. The diagnosis is made by exclusion.
Infections and dermatosis should be ruled out.
Generalized Unprovoked Vulvodynia


A test for allodynia and hyperalgesia using a cottontipped swab should be performed.
It is believed to be a neuropathic pain, but other organic
causes, including pudendal nerve entrapment, pudendal
nerve injury due to child birth, referred pain from
ruptured disk, neuropathic viruses such as herpes
simplex or varicella-zoster, and neurologic disease such
as multiple sclerosis, are possible.
Generalized Unprovoked Vulvodynia




Treatment of generalized unprovoked vulvodynia is
mostly unsuccessful.
The patient should be counseled on elimination of
irritants and on self-care.
Topical local anesthetics, tricyclic antidepressants, or
anticonvulsants such as gabapentin can be tried.
If the patient is refractory to such treatment, acupuncture
or referral to a pain center may be attempted.
BENIGN DISORDERS OF VAGINA
AND VULVOVAGINITIS
Rukset Attar, MD, PhD
Department of
Obstetrics and Gynecology
Benign Disorders of Vagina



Vulvovaginitis
Benign cysts
Congenital anomalies
 Mullerian anomalies
 Hymenal Septum
 Hymen imperforatus
Causes of Vulvovaginitis

Infectious
 Vulvovaginal candidiasis
 Bacterial vaginosis
 Bacterial infections
 Trichomoniasis
 Viral infections
 Desquamative inflammatory vaginitis (clindamycin
responsive)
 Secondary bacterial infection associated with foreign
body
 Atrophic vaginitis
 Parasitic
Causes of Vulvovaginitis

Noninfectious
 Atrophic vaginitis
 Allergic vaginitis
 Foreign body
 Desquamative inflammatory vaginitis (steroid
responsive)
 Collagen vascular disease
 Behçet's syndrome
 Pemphigus syndromes
Candidiasis




75% of women will experience an episode of
vulvovaginal candidiasis.
Candida albicans is the most common Candida species
causing symptomatic candidiasis in approximately 90%
of cases
C albicans frequently inhabits the mouth, throat, large
intestine, and vagina normally.
Clinical infection may be associated with a systemic
disorder (diabetes mellitus, human immunodeficiency
virus [HIV], obesity), pregnancy, medication (antibiotics,
corticosteroids, oral contraceptives), and chronic
debilitation.
Candidiasis




presents with intense vulvar pruritus; a white curdlike,
cheesy vaginal discharge; and vulvar erythema. A
burning sensation
Diagnosis is based on demonstration of candidal mycelia
and a normal vaginal pH 4.5.
Identification of C albicans requires finding filamentous
forms (pseudohyphae) of the organism when vaginal
secretions are mixed with 10% KOH solution.
The gold standard for its diagnosis is a vaginal culture.
Candidiasis




Chemicals and dyes
 1% Gentian violet (once per week)
 Boric acid
Polyenes—
 Nystatin-have been largely replaced by imidazoles.
Imidazole
 clotrimazole and oral agents such as ketoconazole
(mostly used as topical agents and are effective
against C albicans.
 A single 150-mg oral dose of fluconazole
Inclusion of a topical steroid
Bacterial infections





Gardnerella vaginalis
Neisseria gonorrhoeae
Chlamydia
Mycoplasma hominis
Ureaplasma urealyticum.
Bacterial Vaginosis




The most common cause of symptomatic bacterial
infection in reproductive-age women.
In bacterial vaginosis the normal vaginal flora is altered.
The concentration of the hydrogen peroxide–producing
lactobacilli is decreased
There is overgrowth of Gardnerella vaginalis, Mobiluncus
spp., anaerobic gram-negative rods (Prevotella spp.,
Porphyromonas spp., Bacteroides spp.), and
Peptostreptococcus spp
Bacterial Vaginosis




Presents as a "fishy" vaginal discharge, which is more
noticeable following unprotected intercourse.
The patient complains of a malodorous, nonirritating
discharge, and examination reveals homogeneous, graywhite secretions with a pH of 5.0–5.5.
A transient "fishy" odor can be released on application of
10% KOH to the vaginal secretions on a glass slide.
A wet mount of the vaginal secretions using normal
saline under microscopy demonstrates the characteristic
clue cells, decreased lactobacilli, and few white blood
cells.
Bacterial Vaginosis



Gram stain reveals a large number of small gramnegative bacilli and a relative absence of lactobacilli.
Gram stain provides a more sensitive (93%) and specific
(70%) diagnosis than does wet mount.
Treatment in nonpregnant women include
 metronidazole 500 mg orally twice daily for 7 days,
metronidazole gel 0.75% (1 full applicator, 5 g)
intravaginally once or twice daily for 5 days, or
 clindamycin cream 2% (1 full applicator, 5 g)
intravaginally at bedtime for 7 days.
 Alternative regimens include metronidazole 2 g orally
in a single dose, clindamycin 300 mg orally twice daily
for 7 days, or clindamycin ovules 100 g intravaginally
once at bedtime for 3 days.
Bacterial Vaginosis


Pregnant women, the recommended treatment
 metronidazole 250 mg orally 3 times daily for 7 days.
 Alternatively, clindamycin 300 mg orally twice daily for
7 days can be given.
Possible management strategies for recurrent vaginosis
includes use of condoms, longer treatment periods,
prophylactic maintenance therapy, oral or vaginal
application of yogurt containing lactobacillus acidophilus,
intravaginal planting of other exogenous lactobacilli, and
hydrogen peroxide douches.
Neisseria Gonorrhoeae





Up to 85% of women are asymptomatic
In acute disease, patients present with a copious
mucopurulent discharge, and Gram's stain reveals gramnegative diplococci within leukocytes.
However, diagnosis should be confirmed with a culture
or with nucleic acid amplification.
The specimen is collected from the endocervix.
Cultures may also be taken from the urethra, rectum,
and mouth.
Neisseria Gonorrhoeae



An estimated 15–20% of women with lower tract disease
will develop upper tract disease presenting with
salpingitis, tubo-ovarian abscess, and peritonitis.
Ectopic pregnancy and infertility may result.
If active infection is present during delivery, the newborn
may develop conjunctivitis by contamination during
vaginal delivery
Neisseria Gonorrhoeae



Treatment of uncomplicated gonococcal infections of the
cervix consists of ceftriaxone 125 mg IM in a single
dose. Cefixime 400 mg orally in a single dose,
ciprofloxacin 500 mg orally in a single dose, ofloxacin
400 mg orally in a single dose, or levofloxacin 250 mg
orally in a single dose are other recommended regimens.
Spectinomycin 2 g IM in a single dose can be given to
patients sensitive to cephalosporins and quinolones.
Treatment of Chlamydia trachomatis infection should be
considered
Chlamydia Trachomatis


present with a mucopurulent cervicitis, dysuria, and/or
postcoital bleeding
can also cause an ascending infection, salpingitis, in 20–
40% of untreated patients. More than 50% of upper tract
infections may be caused by C trachomatis, leading to
tubal occlusion, ectopic pregnancy, or infertility. C
trachomatis also can cause neonatal conjunctivitis if
untreated and atypical cytologic findings on
Papanicolaou smear. C trachomatis may present as
lymphogranuloma venereum (LGV), which most
commonly affects the vulvar tissues. Retroperitoneal
lymphadenopathy may be present
Chlamydia Trachomatis





Can be identified by culture (50–90% sensitivity), a direct
fluorescent antibody (50–80% sensitivity) and enzyme
immunoassay (40–60% sensitivity), or most recently
using nucleic acid amplification tests (polymerase chain
reaction or ligase chain reaction, 60–100% sensitivity)
Azithromycin 1 g orally in a single dose or doxycycline
100 mg orally twice daily for 7 days.
Erythromycin base 500 mg orally 4 times daily for 7
days,
Ofloxacin 300 mg orally twice daily, or
Levofloxacin 50 mg once daily for 7 days are alternative
regimens. Doxycycline, levofloxacin, and ofloxacin
should be avoided in pregnancy and during lactation.
M Hominis and U Urealyticum


May cause infertility, spontaneous abortion, postpartum
fever, nongonococcal urethritis in men, and possibly
salpingitis and pelvic abscess.
The most effective treatment is doxycycline 100 mg
orally twice daily for 10 days.
Trichomonas Vaginitis





Trichomonas vaginalis is a unicellular flagellate
protozoan
T vaginalis organisms are larger than polymorphonuclear
leukocytes but smaller than mature epithelial cells.
T vaginalis infects the lower urinary tract in both women
and men
A persistent vaginal discharge is the principal symptom
with or without secondary vulvar pruritus.
The discharge is profuse, extremely frothy, greenish, and
at times foul-smelling.
Trichomonas Vaginitis




The pH of the vagina usually exceeds 5.0.
The labia minora may become edematous and tender.
Urinary symptoms may occur; however, burning with
urination is most often associated with severe vulvitis.
Examination of the vaginal epithelium and cervix shows
generalized vaginal erythema with multiple small
petechiae, the so-called strawberry spots, which may be
confused with epithelial punctation.
Trichomonas Vaginitis




Wet mount with normal saline reveals an increase in
polymorphonuclear cells and characteristic motile
flagellates in 50–70% of culture-confirmed cases (Fig
37–3).
Papanicolaou smears have a sensitivity of approximately
60% and may yield false-positive results.
Culture is the gold standard, providing 95% sensitivity
and 100% specificity.
DNA probes and monoclonal antibodies may assist with
accurate diagnosis.
Trichomonas Vaginitis



Metronidazole is the only Food and Drug Administration
(FDA)-approved treatment in the United States, with cure
rates of approximately 90–95%. A single-dose regimen
of 2 g may assure compliance.
Other regimens include a 500-mg tablet orally twice daily
for 7 days.
In resistant cases, which most likely are related to
reinfection, oral metronidazole can be repeated after 4–6
weeks if the presence of trichomonads has been
confirmed and the white blood cell count and differential
are normal.
Viral Infections

The viruses that affect the vulva and vagina are
 Herpesvirus (herpes simplex, varicella-zoster, and
cytomegalovirus)
 Poxvirus (molluscum contagiosum) and
 Papovavirus types
Herpesvirus






Infection occurs through direct contact with secretions or
mucosal surfaces contaminated with the virus.
The virus enters the skin through cracks or other lesions
but can enter through an intact mucosa.
The virus initially replicates in the dermis and epidermis.
Incubation time is 2–7 days.
Prodromal symptoms of tingling, burning, or itching may
occur shortly before vesicular eruptions appear.
The vesicles erode rapidly, resulting in painful ulcers
distributed in small patches, or they may involve most of
the vulvar surfaces
Herpesvirus





Bilateral inguinal adenopathy may be present.
Dysuria or other urinary symptoms may develop,
including urinary retention.
Approximately one-third of patients demonstrate
systemic manifestations such as fever, malaise,
headaches, and myalgia.
In other cases the primary infection is asymptomatic.
Lesions may persist for 2–6 weeks with no subsequent
scarring
Herpesvirus





Approximately 85% of patients develop immunoglobulin
(Ig)M antibodies to type II virus within 21 days of
exposure.
Serologic tests are best used to determine whether the
patient has been infected in the past.
A 4-fold or higher increase in neutralizing complement
fixation antibody titers between acute and convalescent
sera may be useful to document a primary infection.
Only 5% of patients with recurrent infection demonstrate
a 4-fold or higher rise in antibody titer.
New type-specific serologic tests for herpes simplex
virus are available.
Herpesvirus




The incidence of neonatal simplex virus infection ranges
from 1 in 5000 to 1 in 20,000 live births.
Infection in the newborn is associated with a 60%
mortality rate, and at least half of the survivors have
significant neurologic and/or ocular sequelae.
The risk of infection to an infant born vaginally in a
mother with active primary genital infection is 40–50%;
for recurrent infection the risk is 5%.
Suppressive antiviral therapy may be initiated at 36
weeks to decrease the need for cesarean section
Human Papillomavirus





is responsible for condyloma acuminata of the vagina,
cervix, vulva, perineum, and perianal areas as well as for
dysplasia and cancer.
Condylomatous vaginitis causes a rough vaginal surface,
demonstrating white projections from the pink vaginal
mucosa.
Vaginal discharge and pruritus are the most common
symptom with florid condylomas.
Postcoital bleeding may occur.
No specific symptoms are related to the other types of
condylomas.
Human Papillomavirus

Treatment
 Bichloroacetic acid (BCA) or trichloroacetic acid
(TCA), 50–80% solution, Xylocaine 1% gel can be
applied around the wart to prevent damage to
adjacent skin. Repeat weekly as necessary.
 Podophyllin 10–25% in tincture of benzoin
 Cryosurgery,
 electrosurgery,
 simple surgical excision,
 laser vaporization
 Podofilox 0.5% solution or gel
 Imiquimod 5% cream (topically active immune
enhancer that stimulates production of interferon and
other cytokines)
Atrophic Vaginitis




Prepubertal, lactating, and postmenopausal women lack
the vaginal effects of estrogen production.
The pH of the vagina is abnormally high, and the
normally acidogenic flora of the vagina may be replaced
by mixed flora.
The vaginal epithelium is thinned and more susceptible
to infection and trauma.
Although most patients are asymptomatic, many
postmenopausal women report vaginal dryness,
spotting, presence of a serosanguineous or watery
discharge, and/or dyspareunia.
Atrophic Vaginitis




Treatment includes intravaginal application of estrogen
cream. Approximately one-third of the vaginal estrogen
is systemically absorbed; therefore, this treatment may
be contraindicated in women with a history of breast or
endometrial cancer.
The estradiol vaginal ring, which is changed every 90
days, may provide a more preferable route of
administration for some women, or
Estradiol hemihydrate (Vagifem) 1 tablet intravaginally
daily for 2 weeks and then 2 times per week for at least
3–6 months may be less messy.
Systemic estrogen therapy should be considered if there
are no contraindications.
Foreign Bodies



Treatment involves removal of the foreign body.
Rarely, antibiotics are required for ulcerations or cellulitis
of the vulva or vagina.
Dryness or ulceration of the vagina secondary to use of
menstrual tampons is transient and heals spontaneously.
Desquamative Inflammatory Vaginitis





The cause is unknown.
Patients complain of a profuse purulent vaginal
discharge, vaginal burning or irritation, dyspareunia, and
occasional spotting.
The process is patchy and usually localized to the upper
half of the vagina.
The purulent discharge contains many immature
epithelial and pus cells without any identifiable cause.
Vaginal erythema is present and synechiae may develop
in the upper vagina, causing partial occlusion
Desquamative Inflammatory Vaginitis

Treatment often is unsatisfactory but has included local
application of estrogen, antibiotics (particularly
clindamycin cream 2% 5 g intravaginally daily for 7
days), and corticosteroids.
Noninfectious Vaginitis




Chemical vaginitis secondary to multiple irritating
offenders, including topical irritants (sanitary supplies,
spermicides, feminine hygiene supplies, soaps,
perfumes), allergens (latex, antimycotic creams), and
possibly excessive sexual activity can cause pruritus,
irritation, burning, and vaginal discharge.
The etiology may be confused with vulvovaginal
candidiasis.
The offending agent should be removed for treatment.
A short course of corticosteroid treatment may be used
along with sodium bicarbonate sitz baths and topical
vegetable oils.
Cervical Mucorrhea or Vaginal Epithelial
Discharge




Cervicitis due to cervical polyps or cervical or vaginal
cancer can cause a mucopurulent discharge and
bleeding.
Excessive cervical ectropion may cause excessive
discharge of cervical mucus from normal endocervical
cells.
Vaginal adenosis (the presence of the metaplastic
cervical or endometrial epithelium within the vaginal
wall) may cause the same type of clear, mucoid-type
discharge with no associated symptoms.
Excessive desquamation of the vaginal epithelium may
produce a diffuse gray-white pasty vaginal discharge,
which may be confused with candidiasis
Cervical Mucorrhea or Vaginal Epithelial
Discharge




Vaginal pH is normal.
Microscopic evaluation shows normal bacterial flora,
mature vaginal squamae, and no increase in the number
of leukocytes.
Excessive but normal vaginal discharge should be
treated with reassurance and, if required at times, with
cryosurgery or carbon dioxide treatment of the cervix.
Continuous use of a tampon should be avoided.
Parasitic Infection




Pinworms (Enterobius vermicularis) and Entamoeba
histolytica
Trophozoites of E histolytica may be demonstrated on
wet-mount preparations or occasionally on a
Papanicolaou smear.
The parasite is generally detected by pressing a strip of
adhesive cellulose tape to the perineum.
The tape is then adhered to a slide, allowing the doublewalled ova to be identified under the microscope.