Organism Source Vulva Vagina Cervix Corpus Adnexa

Herpesvirus STD Herpetic ulcers

Molluscum contagiosum STD Molluscum lesions

HPV STD Genital warts, intrapeithelial neoplasia, invasive carcinoma

Chlamydia trachomatis STD Follicular cervicitis, endometritis, salpingo-oophoritis

Neisseria gonorrhoeae STD Skene gland adenitis Vaginitis in children Acute cervicitis Acute endometritis and

salpingitis

Candida Endogenous Vulvovaginitis

Trichomonas STD Cervicovaginitis

HPV, human papillomavirus; STD, sexually transmitted disease.

risk is highest if the infection is active during delivery and particularly if it is a primary (initial) infection in the mother.[14]

Mycotic and yeast (Candida) infections are common; about 10% of women are thought to be carriers of vulvovaginal fungi. Diabetes mellitus, oral contraceptives, and pregnancy may

enhance the development of infection, which manifests as small white surface patches similar to monilial lesions elsewhere. It is accompanied by leukorrhea and pruritus. The diagnosis is

made by finding the organism in wet mounts of the lesions.

Trichomonas vaginalis is a large, flagellated ovoid protozoan that can be readily identified in wet mounts of vaginal discharge in infected patients ( Fig. 22-4 ). Infections may occur at any

age and are seen in about 15% of women in sexually transmitted disease clinics.[15] They are associated with a purulent vaginal discharge and discomfort; the underlying vaginal and

cervical mucosa typically has a characteristic fiery red appearance, called strawberry cervix. On histologic examination, the inflammatory reaction is usually limited to the mucosa and

immediately subjacent lamina propria.

Figure 22-4Flagellated trophozoites of Trichomonas vaginalis.

Figure 22-5 A, Acute salpingo-oophoritis, with tubo-ovarian abscess. The fallopian tube and ovaries have coalesced into an inflammatory mass adherent to the uterus. (Compare with

Figure 22-1 .) B, Chronic salpingitis with fusion of the tubal plicae and inflammatory cell infiltrates.

Figure 22-6Inflammatory vulvar disorders. Lichen sclerosus (upper panel). Lichen simplex chronicus (lower panel). The main features of the lesions are indicated in the figures.

Figure 22-7Lichen sclerosus, exhibiting the white parchment-like patches of the skin of the vulva and labial atrophy.

Figure 22-8 A, Numerous condylomas of the vulva encircling the introitus. (Courtesy of Dr. Alex Ferenczy, McGill University, Montreal, Quebec.) B, Histopathology of condyloma

acuminatum showing acanthosis, hyperkeratosis, and cytoplasmic vacuolation (koilocytosis, center).

Figure 22-9 A, Histopathology of classic (HPV positive) vulvar intraepithelial neoplasia with diffuse cellular atypia, nuclear crowding, and increased mitotic index. B, differentiated (HPV

negative) VIN, showing maturation, hyperkeratosis and basal cell atypia (arrow).

Figure 22-10 A, Poorly differentiated vulvar carcinoma associated with human papillomaviruses (HPV). B, Well-differentiated keratinizing vulvar carcinoma, typically HPV negative.

Figure 22-11 A, Verrucous carcinoma of the vulva. B, Basal cell carcinoma of the vulva.

Figure 22-12Paget disease of the vulva with a cluster of large clear tumor cells within the squamous epithelium.

Figure 22-13 A, Malignant melanoma involving the vaginal introitus and labia minora. B, Histology of invasive melanoma with melanin production (inset).

Figure 22-14Clear cell adenocarcinoma of the vagina showing vacuolated tumor cells in clusters and glandlike structures.

Figure 22-15Sarcoma botryoides (embryonal rhabdomyosarcoma) of the vagina appearing as a polypoid mass protruding from the vagina. (Courtesy of Dr. Michael Donovan, Children's

Hospital, Boston, MA.)

Date: 2016-04-22; view: 935