Protozoan and Fungal Infections

Candida Albicans

Among the 500 species of yeast that have been isolated from humans, 90% are pathogenic, and 50% cause genital infections. Approximately 90% of candidal species detected in vaginal secretions are C. albicans. Of the remaining 10% non-albicans species, C. glabrata (Torulopsis) is the next most common. Vulvocandidiasis (VVC) caused by the albicans and non-albicans species are identical with the non-albicans species more resistant to therapy. It is estimated that 75% of women will have one episode of VVC, with 40 to 45% having a recurrence, and about 5% will have retractable infection. Although sexual transmission of C. albicans occurs, the role of such transmission in promoting infection among sexually active women is unclear.

Pathogenesis
The pathogenic mechanism of Candida infection has yet to be defined. Colonization occurs mainly from perianal areas. Although the number of organisms is not related to production of disease, other factors are related to establishment of infection, including host factors, disease states (eg, diabetes mellitus, AIDS), medications, oral contraception, and degree of the organism’s adherence to vaginal epithelia.

Clinical Syndromes, Diagnosis, and Treatment
These topics are reviewed in

Table 3-16. Although it is nonspecific, the most common symptom related to infection is vulvovaginal itching with or without vaginal discharge.

Trichomonas Vaginalis

Trichomonads are flagellated protozoans with three species linked to disease in humans: Trichomonas tenax (mouth): Pentatrichomonas hominis (intestine), and Trichomonas vaginalis (genital organs of men and women). T. vaginalis has been shown to be sexually transmitted.

Pathogenesis
The pathogenesis of disease in humans is not completely understood. T. vaginalis is known to attach to epithelial cells. The response to infection varies from little or no reaction (carrier state) to an acute inflammatory response marked by the presence of numerous polymorphonuclear leukocytes. It is known that half of all asymptomatic carriers of T. vaginalis become symptomatic within 6 months. Development of disease appears to be related to the menstrual period, pubertal development, vaginal pH, environmental microbiological flora, and gender.

Clinical Syndromes
Syndromes associated with the organism include vaginitis and cervicitis in women and urethritis in both men and women. In women, genitourinary symptoms include vaginal discharge, dyspareunia, pruritus, lower abdominal pain, dysuria, and frequency. On examination, the vulva is often erythematous, and copious vaginal discharge may be present. On speculum examination, the vaginal walls appear granular in over half the cases. Although a discharge is common, the “classical” frothy yellow-green discharge occurs in only 12% and has been described in other causes of vaginitis. The “strawberry cervix” (punctate hemorrhages on the exocervix), which was erroneously considered pathognomonic for T. vaginalis cervicitis, occurs in only 2% of the infections. In men, the infection is usually self-limited, and most men are asymptomatic or present with features of nongonococcal urethritis (

Table 3-16). Infrequently, epididymitis or proctitis may develop.

Diagnosis and Treatment
The diagnosis of Trichomonas vaginitis is made in the presence of vulvovaginal symptoms, a vaginal pH over 5.0, and identification of organisms on wet mount, Pap cytology, or direct culture. Detection of the organism depends on their number in the inoculum for both wet mount and culture and on the ability to maintain the specimen at body temperature and examine the wet mount immediately to preserve motility of the organism. The wet mount and Pap smear detect only about 60% of infections, with the Pap smear having the disadvantage of a 31% false-positive rate. Culture techniques (Diamond’s media) and direct monoclonal antibody techniques detect 82 to 95% of infections. There is a commercially available culture technique (Trich In-Pouch). An overview of the diagnostic assessment is outlined in

Figs. 3-6 and 3-7, and treatment is described in

Table 3-16.

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Provided by ArmMed Media
Revision date: June 14, 2011
Last revised: by Andrew G. Epstein, M.D.