Classification and Species
The genus Trichomonas includes several species that inhabit the human body. They differ in localization site and pathogenicity:
- Trichomonas vaginalis (urogenital trichomonad). The primary human pathogen causing urogenital trichomoniasis (strict anthroponosis).
- Pentatrichomonas (Trichomonas) hominis (intestinal). Infects the gastrointestinal tract, causing colitis and enteritis, but primarily in immunocompromised individuals.
- Trichomonas tenax (oral). A harmless commensal of the oral cavity that does not cause disease.
Structure and Life Cycle
The life cycle of trichomonads is extremely simple: they exist only in the vegetative stage (trophozoite) and reproduce by longitudinal binary fission. Due to the absence of a cyst stage, they rapidly perish in the external environment.
Morphologically, they are pear-shaped cells measuring 8–40 by 3–14 µm. For locomotion, the parasite utilizes:
- Flagella. Five flagella located at the anterior end of the cell.
- Undulating membrane. A specialized wavy fold along the side of the cell, connected to one of the flagella and extending approximately to the middle of the body.
An internal skeletal structure, the axostyle (a dense hyaline rod), runs through the cell and projects as a spine at the posterior end. Trichomonads feed via a cell mouth (cytostome), which appears as a small slit.
Pathogenesis of Urogenital Trichomoniasis
The causative agent (T. vaginalis) is transmitted primarily sexually, and less commonly vertically (during childbirth) or via contact with contaminated fomites (moist hygiene items). The incubation period ranges from 7 to 10 days, occasionally extending up to a month.
Upon invading the urogenital tract, the trichomonad secretes invasion factors—hyaluronidase and a cell-detaching factor—which assist it in penetrating beneath the epithelium. Inflammation ensues, manifesting as urethritis, vaginitis, or prostatitis. Patients report itching, pain, and purulent-serous discharge, though the infection is frequently asymptomatic.
An important feature of T. vaginalis is its capacity for incomplete phagocytosis. The parasite engulfs other bacteria (such as gonococci or Chlamydia) but fails to digest them. Inside the trichomonad, these bacteria are shielded from antibiotics and immune cells, significantly complicating the management of coinfections.
Laboratory Diagnostics
The primary method for detecting trichomonads is microscopy. Urine sediment, prostatic secretion, or urethral discharge are used for analysis.
Two types of preparations are utilized:
- Native (live) smears. Prepared as a hanging drop with warm saline. Using phase-contrast microscopy (×40 objective), cells comparable in size to leukocytes are observed displaying characteristic flagellar and membrane motility.
- Stained smears. Stains such as methylene blue or Giemsa are applied.
In chronic cases, culture on SKDS medium, serological tests (ELISA, DFA), and PCR diagnostics are employed.
Treatment and Prevention
Antimicrobial therapy relies on nitroimidazoles, such as metronidazole, ornidazole, tinidazole, or nimorazole.
General prevention follows standard measures for sexually transmitted infections. For women, a specific prophylactic vaccine («Solcotrichovac») based on Lactobacillus acidophilus has been developed.