Morbidity associated with trichomonal vaginitis may be related to BV. Patients with trichomonas vaginitis are at increased risk for postoperative cuff cellulitis following hysterectomy (8). Pregnant women with trichomonas vaginitis are at increased risk for premature rupture of the membranes and preterm delivery. Because of the sexually transmitted nature of trichomonas vaginitis, women with this infection should be tested for other sexually transmitted diseases (STDs), particularly Neisseria gonorrhoeae and Chlamydia trachomatis. Serologic testing for syphilis and HIV infection should be considered.
Treatment The treatment of trichomonal vaginitis can be summarized as follows: 1.
Metronidazole is the drug of choice for treatment of vaginal trichomoniasis. Both a single-dose (2 g orally) and a multidose (500 mg twice daily for 7 days) regimen are highly effective and have cure rates of about 95%.
2.
The sexual partner should be treated.
3.
Metronidazole gel, although effective for the treatment of BV, should not be used for the treatment of vaginal trichomoniasis.
4.
Women who do not respond to initial therapy should be treated again with metronidazole, 500 mg, twice daily for 7 days. If repeated treatment is not effective, the patient should be treated with a single 2-g dose of metronidazole once daily for 5 days or tinidazole, 2 g, in a single dose for 5 days.
5.
Patients who do not respond to repeated treatment with metronidazole or tinidazole and for whom the possibility of reinfection is excluded should be referred for expert consultation. In these uncommon refractory cases, an important part of management is to obtain cultures of the parasite to determine its susceptibility to metronidazole and tinidazole.
An estimated 75% of women experience at least one episode of vulvovaginal candidiasis during their lifetimes (19). Nearly 45% of women will experience two or more episodes (20). Few are plagued with a chronic, recurrent infection. Candida albicans is responsible for 85% to 90% of vaginal yeast infections. Other species of Candida, such as C. glabrata and
C.
tropicalis, can cause vulvovaginal symptoms and tend to be resistant to therapy. Candida are dimorphic fungi existing as blastospores, which are responsible for transmission and asymptomatic colonization, and as mycelia, which result from blastospore germination and enhance colonization and facilitate tissue invasion. The extensive areas of pruritus and inﬂammation often associated with minimal invasion of the lower genital tract epithelial cells suggest that an extracellular toxin or enzyme may play a role in the pathogenesis of this disease. A hypersensitivity phenomenon may be responsible for the irritative symptoms associated with VVC, especially for patients with chronic, recurrent disease. Patients with symptomatic disease usually have an increased concentration of these micro-organisms (>104 per mL) compared with asymptomatic patients (<103 per mL) (21).
Factors that predispose women to the development of symptomatic VVC include antibiotic use, pregnancy, and diabetes (22–25). Pregnancy and diabetes are associated with a qualitative decrease in cell-mediated immunity, leading to a higher incidence of candidiasis.
Table 18.1 Classification of Vulvovaginal Candidiasis
From Sobel JD, Faro S, Force RW, et al. Vulvovaginal candidiasis: epidemiologic, diagnostic, and therapeutic considerations. Am J Obstet Gynecol 1998;178:203–211.
It is helpful to categorize women with VVC as having either uncomplicated or complicated disease (Table 18.1)