Behavior and Pathogenicity of Tritrichomonas foetus in Chick Liver Cell Cultures*

Abstract

SYNOPSIS. Clones of Tritrichomonas foetus, referred to as strains KV‐1, DK‐2, and UT‐1, which were judged by subcutaneous mouse assay to differ in pathogenicity, had different effects on trypsin‐dispersed liver cell cultures prepared from 3 lines (Light Brown Leghorn, Massachusetts Brown, Massachusetts Low Growth) of chicks. The general pattern of parasite‐cell interaction was similar in all cell cultures, but the intensity of certain responses of the cultures to trichomonads, reflected best in the levels of macrophage activity, depended on the line of chicks. The mild UT‐1 strain was readily engulfed and digested by the macrophages, caused very little damage to the epithelial cells and fibroblasts, and had a minimal inhibitory effect on the division rate of the latter. Many abnormal changes were seen, however, in the cytoplasm and nucleil of fibroblasts and epithelial cells in cultures exposed to strains of high (KV‐1) and intermediate (DK‐2) pathogenicity or to cell‐free filtrates of rich active cultures (henceforth referred to as filtrates) of these strains. The changes included retraction of cytoplasm which caused cell‐free spaces to appear in the sheets of fibroblasts and around the epithelial islands; the islands became detached from the surrounding fibroblast sheets and tended to form multilayered cell mounds. The flagellates and filtrates of KV‐1 strain greatly inhibited fibroblast division, and similar, but less pronounced, inhibitory effects were exerted by DK‐2 strain and its filtrates. Trichomonads of all 3 strains did not attach themselves to fibroblasts and epithelial cells. Thus the abnormal changes in cultures infected with KV‐1 and DK‐2 parasites apparently were caused by some toxic substances produced by the trichomonads, which had to be responsible also for the identical changes in cultures exposed to filtrates of these strains. KV‐1 and DK‐2 strains inhibited the phagocytic activity of the macrophages in the early stages of infection, the former causing stronger and longer lasting inhibition. Trichomonads of KV‐1 strain multiplied actively within the phagocytes which developed degenerative changes and ultimately burst, releasing healthy parasites into the medium. DK‐2 flagellates, altho incapable of dividing inside the macrophages, usually were not digested and caused degeneration of the cells which contained them.

Presence of laminin-binding proteins in trichomonads and their role in adhesion.

“…Attachment to cells leads to monolayer disruption and cytotoxicity (39)(40)(41)(42), a phenomenon not observed for nonpathogenic trichomonads (37,41). Few, if any, molecules involved in this process have been characterized so far (44).…”

Construction and bootstrap analysis of DNA fingerprinting-based phylogenetic trees with the freeware program FreeTree: application to trichomonad parasites.

“…The methods of molecular taxonomy can be divided into two groups : single-locus methods and multilocus methods. The result of any single-locus method, such as DNA sequencing, microsatellite analysis or singlestranded conformational polymorphism (SSCP) analysis, is the so-called ' gene tree ', the topology of (1986) ; 'Forsgren & Forssman (1979) ; (Meingassner & Thurner (1979) ; ) Kulda et al (1999) ; * Kulda & Honigberg (1969) ; "! Culberson et al (1986) ; "" Kulda et al (1974).…”

Tritrichomonas foetus: a scanning electron microscopy study of erythrocyte adhesion associated with hemolytic activity

“…8 and 13) may represent a very efficient mechanism for the parasite to make contact with the erythrocyte surface. Furthermore, the movement of the four flagella found in T. foetus is of importance not only to the locomotion of the parasite into liquid media, but also to the induction of liquid currents that become parasites able to easily uptake nutrients from the surrounding medium [20]. Likewise, Figure 10 shows the anterior and posterior flagella, and even the axostyle, probably involved in the capture of the erythrocyte.…”

“…Although extensively studied, the mechanisms of the pathogenicity of T. foetus have not yet been well defined. The pathogenicity of T. foetus has been previously reported, employing growth characteristics [20], mouse inoculation [13] and in vitro experiments using epithelial cells to investigate pathogenic trichomonad-host cell interaction relationships [31,32]. The hemolytic activities of different species of Trichomonadida, including Trichomonas vaginalis [6,7,16,19,27], T. gallinae [10,11,33] Tritrichomonas foetus [8,9] and Tritrichomonas suis [8], have been studied using in vitro methods.…”