Pathogenesis of Trichomonas vaginitis

The pathogen of trichomoniasis vaginitis is Trichomonas vaginalis. Trichomonas hidden in the glands and vaginal folds can reproduce before and after menstruation, causing inflammation. Trichomonas vaginalis can consume or engulf the glycogen in the vaginal epithelial cells and hinder the production of lactic acid. However, due to the lack of an ideal animal model, the medical community currently has little understanding of the pathogenesis of trichomoniasis caused by Trichomonas vaginalis, which is roughly as follows:

Trichomonas vaginalis infects the human body in the form of trophozoites. When encountering an unfavorable growth environment, it becomes spherical. When inactive, it is difficult to distinguish from host cells and is often mistaken for a cyst. However, under a high-power microscope, undulating membranes and flagellar activity can be seen.

Trichomonas vaginalis adheres to vaginal epithelial cells through the lectins and cysteine ​​proteases on its surface, and directly contacts and destroys target cells through the mechanical damage of ameba-like movement and the cytotoxic effects of secreted proteases and proteinases, and induces the production of inflammatory mediators, ultimately leading to epithelial cell dissolution and shedding, and local inflammation.

Trichomonas vaginalis is bloodthirsty and alkali-resistant. It can consume and engulf glycogen in vaginal epithelial cells, use the glycogen and iron of host cells for energy metabolism, engulf lactobacilli, and hinder lactic acid production. It can induce the body to produce immune responses, including cellular immunity, humoral immunity, activate complement response, stimulate host cells to produce some cytokines, and lead to local inflammatory changes. Different strains of Trichomonas have different abilities to destroy the nucleus of isolated target cells, and different strains have different intrinsic toxicity.