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A very large literature, much in eastern European languages, exists on this subject; it has been expertly summarized by Honigberg (1970). A later review (Ackers, 1989) discusses more recent work and should be consulted for more details than can be accommodated here.
Clinical experience shows that repeated infections with T. vaginalis can occur and that in most cases the parasite is not rapidly cleared without treatment. A long-lasting sterile immunity clearly does not result, although the majority of women will develop modest levels of serum antibody. This response has been extensively studied in the hopes of developing a serodiagnostic test, but a combination of generally modest titres, background natural antibodies in uninfected persons and considerable antigenic diversity has meant that no such tests have been found to be useful in
practice; the immune response in males is, in general, even more feeble. Local IgA responses occur in some women but were not detected in a small study of male patients and did not seem to protect against reinfections in a primate model.
Cell-mediated immune responses in human trichomoniasis are even less well-defined, although delayed-type hypersensitivity may be detected by skin testing in a proportion of patients. The contribution, if any, of these responses to host defence is not known, although unactivated human macrophages appear to be able to kill T. vaginalis. The predominant cell type in the discharge seen in many patients is, however, the neutrophil, which the parasite appears to attract both by releasing chemotactic factors (see above) and by activating complement via the alternative pathway; these cells may then be activated by a parasite-derived factor similar to leukotriene B4. Anti-trichomonal IgG augments this response. This behaviour by the parasite seems most unwise, since neutrophils can kill T. vaginalis, apparently via bound C3b.
The ability of human complement to kill trichomonads, either directly or with the help of neutrophils, may well be one of the factors that prevent systemic dissemination by T. vaginalis—a fortunate circumstance, given the highly pathogenic nature of the organisms when artificially introduced into the skin or peritoneal cavity of mice. Freshly isolated strains differ greatly in their susceptibility to complement-mediated killing, although all seem to become uniformly sensitive after prolonged in vitro cultivation (Demes et al., 1988b). Cervical mucus contains very little complement and menstrual blood significantly lower levels than those found in serum. The presence of complement in the vagina during menstruation may account for the lower number of parasites found at that time (Demes et al., 1988a); the fact that iron increases the complement resistance of T. vaginalis (Alderete et al., 1995b) may represent a response by the parasite to a temporarily hostile environment.
Other factors that may limit the dissemination or multiplication of T. vaginalis include its predilection for squamous epithelium and, in males, the high levels of zinc present in prostatic fluid (Krieger and Rein, 1982); the modest role of specific immune responses in controlling trichomoniasis is emphasized by the general absence of
reports of more severe disease in patients with HIV/AIDS.
A particular problem in studying the immunology of trichomoniasis is that most available animal models either do not result in long-lasting, symptomatic infections or are quite unphysiolo-gical. Intravaginal infections in small laboratory animals are usually transitory and asymptomatic, although altering the vaginal milieu can improve matters (McGrory and Garber, 1992). A primate model (in Saimiri sciurius) develops realistic histopathology (Gardner et al., 1987), and infection with the bovine parasite Tritrichomonas foetus has been proposed as a guide to understanding trichomoniasis in women.
The molecular biology of T. vaginalis is not well studied or understood—this is nicely illustrated by considering the organism’s chromosome number. As with many protozoans, mitosis occurs without dissolution of the nuclear membrane and clearly visible condensed chromosomes are not seen. Thus, neither the karyotype nor the ploidy are known for certain. Very recently, two groups have published answers to this problem; unfortunately they do not wholly agree, for while both describe six different chromosomes, one finds the organism to be diploid but the other haploid.
A complex relationship exists between expression of a highly immunogenic glycoprotein (referred to as P270) on the surface of T. vaginalis and other biological properties. All strains seem to contain the gene for P270 and to synthesize the P270 protein, but in some isolates (Type I strains) P270 is exclusively cytoplasmic, while in others (Type II strains) it is also expressed on the cell surface—not continuously, however, for Type II strains alternately express P270 and the four adhesins (AP65, AP51, AP33 and AP23) described above (Alderete, 1988). The phenotype is described by the expression of P270—those cells expressing it are positive, those expressing adhesins instead are of negative phenotype. Because only negative Type II cells express adhesins, only they can bind to and kill target cells in vitro. Further complexity is provided by the observation that only negative phenotype