Bow chicka bovine: sexually transmitted Tritrichomonas foetus infections in cattle

By LS

Sexually transmitted diseases in humans are something I would venture most of the adult population have experience with- if not through personal experience but through some rudimentary biology lecture on the various microbes that are prone to infecting humans following sexual contact. What may be less familiar to most people, however, are sexually transmitted diseases in cattle. One such organism that infects cows is Tritrichomonas foetus, a parasitic protozoa and the causative agent of bovine trichomonosis. Infection is characterized by spontaneous abortion and infertility. The parasite therefore represents a major threat to economic concerns of the cattle industries in the US and in Latin America and to the health of cows everywhere.

Tritrichomonas foetus is an extracellular parasite with a simple life cycle that consists mostly of a trophozoite stage (1). Trophozoites are tear drop shaped cells with a single membrane bound nucleus (2). They are able to move via the four flagella that extend from a complex on the organism’s anterior end. Three of these flagella extend freely from the anterior while the fourth extends backwards towards the posterior end (2). Trophozoites do not have a mitochondria (3) and survive best in low oxygen environments.

Under stressful conditions, Tritrichomonas foetus adopts a spherical form and internalizes its flagella (3). This psuedocyst form lacks a true cyst wall (3) and because it lacks flagella, cannot move (1). Though the role of the psuedocyst in the parasitic lifestyle is not well understood, it is thought that it exists to protect individuals from unfavorable environmental conditions, as encystment can be induced by environmental  stressors such as extreme cooling (3). However, psuedocysts are able to adhere to host cell surfaces better than trophozoites are and their adhesion is uninterrupted by treatment with antimicrobial drugs (1). It has therefore been proposed that psuedocysts may have a more active role in the Tritrichomonas foetus lifecycle than previously thought.

Infection by the parasite is localized to tissues of the reproductive system. Bulls act as asymptomatic carriers of the disease and do not experience any adverse effects or lowered fertility for being infected. Trophozoites do not invade the epithelial tissues of bulls but are present in discharge from the lining epithelial tissues of the penis, foreskin and urethra (2) and contaminate sperm. Interestingly, the age at which a bull becomes infected is a major determinant for whether or not the bull becomes a transient or chronic carrier. Experimental infection of previously uninfected bulls found that chronic infection was established frequently in bulls aged 3-7 and almost never following experimental infection of bulls aged 1-2 (2).This is not thought to be due to differences in health between older and younger bulls but is instead due to anatomical features: as bulls age epithelial crypts (indentations lined by epithelial cells) on the penis and prepuce deepen (2), creating a more favorable, lower oxygen environment for the microbe. While infection in bulls shows no clinical symptoms, it is still important because of the ability of an infected bull to spread the infection to females. Some experiments have shown that excreted products produced by T. foetus decrease the sperm motility (4). However, sperm viability is not affected(4).

Female cows acquire T. foetus infections through mating with an infected male. Trophozoites attach to epithelial cells lining the vaginal canal, uterus, and oviduct. Parasite attachment to host cells is mediated by four main surface proteins (1) though not much work has been done to characterize these proteins beyond their initial identification. Additionally, T. foetus produces soluble cytotoxins that may also play a role in establishing initial infection: a purified cysteine protease from T. foetus as well as live parasite were able to cause apoptosis in cultures of bovine vaginal epithelial cells (BVECs) (5). In cows, infection with T. foetus can interfere with egg fertilization and embryonic development (2). Spontaneous abortions in affected cows usually occur between 50 and 70 days gestation. Exact mechanisms through which this occurs have not been determined but it is likely related to the parasite’s cytotoxicity towards host cells and subsequent tissue damage and inflammation. Tritrichomonas foetus is able to cross the placenta and infect the developing embryo (6). In fact, the organism got its name because it was first identified in studies of aborted fetal calves (2). T. foetus is also able to colonize the deeper reproductive tract (such as the oviduct), resulting in tissue damage and long term infertility (6). Aside from tissue damage and infertility, overt clinical symptoms are rare. Infections are usually transient though the length of their duration can vary widely (2). Exposure does not confer long term immunity (2). In a small proportion of cases, the initial infection becomes chronic. These individuals act as reservoirs of infection and create challenges when attempting to prevent future outbreaks within herds.

Given that overt clinical symptoms are subtle in cows or non-existent in bulls, diagnosing an infection with T. foetus is difficult. It is usually done when the parasite, present in preputial or vaginal secretions, or occasionally amniotic fluid, is identified morphologically under a microscope upon direct examination of these fluids. There is no treatment for T. foetus and control methods center on preventing spread of the infection. Infected bulls are often slaughtered. Additionally, herds may be divided into infected and uninfected groups, with infected individuals being prevented from mingling with the rest of the herd. Artificial insemination has shown promise as another way to prevent the disease, as it is spread only through sexual contact. However, controlling further outbreaks after members of a herd are infected are difficult and costly. Tritrichomonas foetus therefore remains a threat to the economic health of the cattle industry, in addition to threatening the reproductive health of cows everywhere.

  

1. R. M. Mariante, L. C. Lopes, M. Benchimol, Tritrichomonas foetus pseudocysts adhere to vaginal epithelial cells in a contact-dependent manner., Parasitol. Res. 92, 303–12 (2004).
2. D. O. Rae, J. E. Crews, Tritrichomonas foetus., Vet. Clin. North Am. Food Anim. Pract. 22, 595–611 (2006).
3. A. Pereira-Neves, L. F. Nascimento, M. Benchimol, Cytotoxic effects exerted by Tritrichomonas foetus pseudocysts., Protist 163, 529–43 (2012).
4. C. M. Ribeiro et al., Tritrichomonas fetus extracellular products decrease progressive motility of bull sperm., Theriogenology 73, 64–70 (2010).
5. B. N. Singh et al., Tritrichomonas foetus induces apoptotic cell death in bovine vaginal epithelial cells., Infect. Immun. 72, 4151–8 (2004).
6. M. Benchimol, A. B. Dias, R. Fontes, Interaction of Tritrichomonas foetus and the bovine oviduct in an organ culture model., Vet. Parasitol. 140, 244–50 (2006).