Trichomonas vaginalis

Author: MBLOGSTU

Introduction

Trichomonas vaginalis is the causative agent of trichomoniasis—a common cause of vaginitis. Although it is a readily diagnosed and treatable sexually transmitted disease (STD), trichomoniasis is not a reportable infection and has received relatively little emphasis from public health STD control programs.

More recently, the high prevalence of the disease and its association with adverse pregnancy outcomes and an increased risk for human immunodeficiency virus (HIV) infection have underscored the need for greater control efforts.

The clinical presentation ranges from severe inflammation with a frothy, malodorous discharge to an asymptomatic carrier state. This disease also has significant medical, social, and economic implications. In pregnant women, infection predisposes to premature rupture of the placental membranes, premature labor, and low-birth-weight infants. Other complications linked to trichomoniasis include cervical cancer, atypical pelvic inflammatory disease, and infertility. Additionally, like other STDs, T. vaginalis infection can increase an individual’s susceptibility to HIV.

Other Species

Other trichomonads include Trichomonas tenax (found in the oral gingival and tracheobronchial sites) and Pentatrichomonas hominis (isolated from the intestinal tract). These species are considered nonpathogenic and occur infrequently in humans.

Each human trichomonad displays a specific tropism for its site of infection. Tritrichomonas foetus, a nonhuman parasite, is the trichomonad most similar to T. vaginalis. Aside from possessing three anterior flagella (versus four in T. vaginalis), there are few morphological differences. T. foetus causes bovine trichomoniasis and exhibits cytotoxicity toward mammalian cells, adherence to host cells, and the production of various hydrolases. The host response in the reproductive tract to T. foetus—marked by a mononuclear infiltration—is in many ways similar to that observed in T. vaginalis infection.

Epidemiology

Humans are the only natural host of T. vaginalis, and trichomoniasis is an extremely common infection worldwide. The World Health Organization estimates that this infection accounts for almost half of all curable STDs globally.

Studies in African populations have reported vaginal trichomoniasis prevalence rates between 11% and 25%, with one study (Laga et al.) noting an incidence of 38% over a four‐month exposure in HIV-infected women in Zaire.

Trichomoniasis is commonly associated with other STDs (notably gonorrhea) and serves as a marker of high-risk sexual behavior. In many cases, women with trichomoniasis also have bacterial vaginosis. Unlike other STDs that more commonly affect adolescents and young adults, T. vaginalis infection is distributed more evenly among sexually active women, thereby reinforcing its potential use as a marker for risky sexual behavior. Although survival on fomites has been documented, transmission of T. vaginalis is thought to occur almost exclusively through sexual contact.

Morphology

T. vaginalis is the most widely studied among the trichomonads. This urogenital pathogen is variable in size and shape, with an average length of 10 μm and width of 7 μm. In axenic culture, the organism tends to appear pear-shaped or oval; however, when attached to vaginal epithelial cells, it often assumes a more amoeboid form.

It is a flagellated protozoan with five flagella—four at its anterior end and a fifth incorporated into an undulating membrane supported by a slender, noncontractile costa. This arrangement confers to the parasite its characteristic quivering motility. The nucleus is located at the anterior portion, enclosed by a porous nuclear envelope, and a slender, hyaline, rod-like structure called an axostyle extends from the nucleus, bisecting the cell longitudinally.

Life Cycle

The life cycle of T. vaginalis is relatively simple compared to other protozoan parasites. Transmission occurs directly between sexual partners via the motile trophozoite. Unlike many protozoans, T. vaginalis does not form a cyst in nature, although pseudocyst forms can be observed in vitro under adverse conditions.

Pathogenesis

The cell surface of T. vaginalis plays a pivotal role in adhesion, host–parasite interactions, and nutrient acquisition. The surface is a complex mosaic of adhesins, receptors for host extracellular matrix proteins, and carbohydrate moieties that together facilitate ligand-receptor binding.

Adherence and Adhesins

Adhesion to vaginal epithelial cells is a critical early step in pathogenesis and is dependent on factors such as time, temperature, and pH. T. vaginalis demonstrates a preference for parasitizing vaginal epithelial cells. This process is mediated by four key adhesion proteins—AP65, AP51, AP33, and AP23—which interact with host receptors in a specific ligand-receptor manner. In addition, contact-initiated ameboid transformation, marked by pseudopodia formation and upregulation of adhesin synthesis, suggests the involvement of a complex signal transduction system. Adhesion also appears to rely on the activity of cysteine proteinases.

Hemolysis

Given that the vaginal mucosa is a suboptimal nutritional environment and that T. vaginalis cannot synthesize lipids, erythrocytes become an important source of fatty acids for the parasite. Hemolysis occurs in three stages:

• A specific ligand-receptor interaction permits attachment to the erythrocyte.
• The parasite then releases perforin-like proteins (possibly cysteine proteinases) that form pores in the erythrocyte membrane.
• Finally, T. vaginalis detaches, causing cell lysis.

Proteinases

Cysteine proteinases (CPs) are implicated in both lysing erythrocytes during hemolysis and mediating adherence to epithelial cells. In addition, these enzymes can degrade host immunoglobulins G and A (IgG and IgA) found in the vagina.

Interaction with Vaginal Flora

Infected women often exhibit a rise in vaginal pH accompanied by a reduction or complete loss of Lactobacillus acidophilus and a corresponding increase in anaerobic bacteria. T. vaginalis has been observed to phagocytize bacteria (including possibly lactobacilli), and secreted products—such as cysteine proteinases—may directly destroy beneficial lactobacilli.

Clinical Manifestations

The clinical spectrum of trichomoniasis in women ranges from an asymptomatic carrier state to overt vaginitis. Approximately one third of asymptomatic cases eventually develop symptoms within six months. The parasite primarily infects the squamous epithelium of the genital tract and typically persists longer in females than in males.

Acute Infection: Presents with diffuse vulvitis characterized by copious leukorrhea. The discharge is usually frothy, yellow or green, and mucopurulent. Small punctate hemorrhagic spots on the vaginal and cervical mucosa create the “strawberry” appearance—which is observed in roughly 2% of cases—and symptoms are cyclic, worsening around menses.

Chronic Infection: Symptoms are generally milder, with pruritus and dyspareunia. The vaginal secretion tends to be scanty and mucus-mixed. Of epidemiologic importance, many asymptomatic carriers (up to 25–50%) maintain a normal vaginal pH (3.8–4.2) and flora yet may later develop symptoms.

In addition to vaginitis, trichomoniasis is sometimes associated with infection of the Bartholin’s glands, adnexitis, pyosalpinx, endometritis, infertility, low birth weight, and cervical erosion. The infection also increases the risk of HIV transmission.

In men, the infection is predominantly asymptomatic. When symptoms do occur, urogenital trichomoniasis in men can be classified as: an asymptomatic carrier state; acute trichomoniasis marked by profuse purulent urethritis; or a mild symptomatic condition clinically indistinguishable from other forms of nongonococcal urethritis.

Diagnosis

Clinical Presentation: The classic symptoms include a yellowish-green frothy discharge, pruritus, dysuria, dyspareunia, and the “strawberry” cervix (punctate hemorrhagic lesions). However, because these features are seen only in a minority of cases—only about 2% display a “strawberry” cervix and 12% a frothy discharge—clinical diagnosis alone is often unreliable.

In a study by Fouts and Kraus (1980), relying solely on these classic features would fail to diagnose 88% of infected women and falsely label 29% of uninfected women as positive.

Microscopic Examination: Diagnosis has traditionally depended on observing motile protozoa in vaginal or cervical secretions under a microscope. The sensitivity of the wet-mount preparation ranges from 38% to 82% due to potential loss of motility after the specimen cools.

Culture Methods: The broth culture method, considered the “gold standard,” is straightforward to interpret and can detect as few as 300 to 500 trichomonads per milliliter. Moreover, Diamond’s media and McCoy cell cultures are even more sensitive, detecting T. vaginalis at concentrations as low as 3 organisms per milliliter.

Antibody-Based Techniques: Various serologic methods (including agglutination, complement fixation, indirect hemagglutination, gel diffusion, fluorescent antibody, and enzyme-linked immunosorbent assays) have been used to demonstrate antitrichomonal antibodies. Direct antigen detection using monoclonal antibodies holds promise as a rapid diagnostic tool.

DNA Techniques: Recombinant DNA methods, such as PCR, are increasingly utilized to improve both specificity and sensitivity. These techniques are particularly valuable for detecting nonviable organisms and for samples that have undergone fixation or partial degradation.

Treatment

Treatment of trichomoniasis typically involves the use of a nitroimidazole derivative. Additional treatment options include topical agents such as clotrimazole, povidone-iodine, and nonoxynol-9.