Variations in the carbohydrate expression pattern and in lesions of the uterine horns of BALB/c mice infected with different Tritrichomonas foetus isolates.

Bovine tritrichomonosis, a sexually transmitted disease caused by the protozoan Tritrichomonas foetus, is characterized by producing reproductive alterations in cattle. Carbohydrates on the surface of the uterine epithelium are involved in the process of adhesion and colonization of the protozoan. The murine model has proved to be an inexpensive, practical and representative alternative to study the lesions produced in the natural host. For this work, during the first stage, 6-8 week old female BALB/c mice were inoculated with 24 different T. foetus isolates in order to classify them according to their pathogenicity. Then, seven isolates were selected and processed with lectin histochemistry to determine if the differences in pathogenicity corresponded to the changes found in the uterine carbohydrate expression pattern. In this work, we demonstrate the differences in the expression of the carbohydrate pattern between infected and uninfected mice. In addition, within the group of infected mice, differences were found in the degree of pathogenicity of the isolates, thus evidencing their biological variability.

Lectin binding pattern in the uterus of pregnant mice infected with Tritrichomonas foetus.

Bovine genital tritrichomonosis is caused by the protozoon Tritrichomonas foetus and leads to embryonic death and abortion. The complexity of handling bovine experimental systems has led to the development of alternative models. The infection has been reproduced in pregnant BALB/c mice. In the pathogenesis of the disease, adhesion of the protozoon to host cell surface glycoproteins is important. Labelling with soya bean agglutinin (SBA) and peanut agglutinin (PNA) lectins increases in the luminal and glandular uterine epithelium of non-pregnant infected mice. The aim of the present study was to determine whether these changes also occur in pregnant infected BALB/c mice. Female BALB/c mice were inoculated intravaginally with T. foetus and, 15 ± 3 days post infection, were paired with males overnight. Infected and control mice were sacrificed 6, 8 and 10 days later. Samples of uterus were labelled with a panel of biotinylated lectins. Infected mice showed increased binding of PNA and SBA. There was also increased binding of concanavalin (Con-A) by luminal epithelium and Ricinus communis agglutinin (RCA-1) by glandular epithelium at day 6 post coitum. These changes may be due to the production of enzymes by T. foetus, which could act to enhance adhesion and colonization and thus favour infection.

Histological and lectin binding changes in the genital tract of mice infected with Tritrichomonas foetus.

An experimental murine model of bovine genital tritrichomonosis is described. Female mice were inoculated per vaginam with Tritrichomonas foetus and a sample of the study population was killed every 3 days up to 60 days post-infection. Microscopical changes in the reproductive organs were assessed and immunohistochemistry was used to detect T. foetus within these tissues. Lectin histochemistry was used to determine changes in the expression of carbohydrates within the reproductive mucosa. A range of microscopical changes were detected in the uterine endometrium by 10 days post-inoculation and these were associated with the presence of the protozoan. The endometrial changes included endometritis and ulceration, mucosal atrophy and glandular metaplasia, and were similar to those reported in naturally infected cows. Changes in lectin binding were recognized first in the vagina where there was increased binding of Ulex europaeus agglutinin-1 (UEA-1) which was maximal on day 16 post-inoculation. Within the uterus, there was increased binding of soy bean agglutinin (SBA) which was maximal on day 19 post-inoculation, and of peanut agglutinin (PNA) which was maximal on day 16 post-inoculation. These changes in carbohydrate expression parallel the infection kinetics, since they appeared first in the vagina and later in the uterus. The changes may reflect either a host reaction against the infection or the production of enzymes by T. foetus, which act to enhance adhesion and colonization of the genital organs by the organism. The kinetics and pathogenesis of this murine infection are similar to those of the natural bovine disease, suggesting that this model system may be valuable for further studies of this disease.

Interaction of Tritrichomonas foetus with the reproductive tract of experimentally infected female BALB/c mice: ultrastructural evaluation.

The interaction of Tritrichomonas foetus with its host is a complex process that involves colonisation, attachment and persistence. The goal of the present study was to describe the interaction of T. foetus with the genital tract using a model of non-oestrogenised female BALB/c mice which had been intravaginally infected with a suspension of T. foetus during oestrus. Animals were sacrificed after 10 weeks and the uteri fixed and processed for light and electron microscopy. Ultrastructural analysis showed that the attached protozoa interacted with the mucosa through a somal projection. With an amorphous secretion at the protozoa-host cell interface. There was no direct contact between the protozoal plasma membrane and the epithelial cell membrane. Our results demonstrated the participation of an active phagocytosis and the destruction of T. foetus by eosinophils.