Recently, DNA probing and gene amplification have been used also for the diagnosis of T. vaginalis. A commercial test, based on synthetic oligonucleotide probes (Affirm VP Microbial Identification Test, developed by MicroProbe Corporation, Bothell, WA), was evaluated by Briselden and Hillier (1994). The test system, designed for use in the physician's office, had a sensitivity of 83%, a positive predictive value of 100% and a negative predictive value of 98% in a population with a 9% prevalence of T. vaginalis. DeMeo et al. (1996) also studied the Affirm VP test comparing it with microscopy of vaginal 'wet mounts' and with cultures in Diamond's medium. In that study of 615 women with signs or symptoms of vaginitis, the DNA test had a sensitivity of 90% and a specificity of 99.8%. In fact, polymerase chain reaction (PCR) analysis is sensitive enough to be used on introital specimens. Witkin et al. (1996) compared introital specimens with specimens from the endocervix and from the posterior vaginal vault in 219 pregnant women. Introital testing had a sensitivity of 95.5% and a specificity of 100%. Screening for T. vaginalis based on PCR of urine specimens only, might have a sensitivity problem. That is, among 51 women positive by vaginal wet prep or culture, 65% of urine specimens were PCR-positive (Lawing et al. 2000). By contrast, van Der Schee et al. (1999), identified trichomoniasis by PCR on vaginal swab of 10 and on urine specimen of 11 of 200 Dutch women.
Trichomonas vaginalis infects, almost exclusively, the epithelium of the lower genital tract. In women, the vagina, urethra, and Skene's glands are the main sites of infection. Some infected individuals are asymptomatic, while others may have severe local symptoms. Symptomatology may be related to trichomonas virulence factors or to host factors. Antigenic heterogeneity, phenotypic variation, cytotoxicity, proteinases, and secretion of immunogens into the culture medium are possible virulence factors of T. vaginalis (Lehker and Alderete 1990). Attachment of T. vaginalis to epithelial cells seems to be dependent upon a 30-kDa cysteine proteinase (CP30) on the surface of the protozoa (Mendoza-Lopez et al. 2000). Contact-dependent cytotoxicity relies on specific surface proteins (adhesins) which mediates the interaction of T. vaginalis with epithelial cells (Arroyo et al. 1992). Studies of the interaction between trichomonads and the epithelial layer of human amniotic membrane have demonstrated damaged and desquamated cells in areas where parasites were in direct contact with the target cells (Mirhaghani and Warton 1996). A cysteine proteinase with a molecular mass of 65kDa on the plasma membrane of T. vaginalis has recently been shown to be involved in T. vaginalis cytotoxicity (Alvarez-Sanchez et al. 2000). Cytotoxicity may also be caused by soluble factors, including free lactic or acetic acids (Pindak and Gardner 1993), and the so-called 'cell-detatching factor' (Garber et al. 1989). Cell-detatching factor is a 200-kDa glycoprotein that causes detachment of monolayer cells.
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