[Evaluation of a direct serologic card agglutination test for the diagnosis of camel trypanosomiasis caused by Trypanosoma evansi]. / Evaluation d'un test sérologique d'agglutination directe sur carte dans le diagnostic de la trypanosomose caméline à Trypanosoma evansi.

The results of a novel direct serological card agglutination test for the diagnosis of camel trypanosomosis due to Trypanosoma evansi (CATT/T. evansi) were compared with those obtained by direct detection of parasites in a study using 1,093 sera from camels raised in northern Mali. A good correlation was revealed between the percentage of positive results obtained by CATT and the presence of trypanosomes (89%), as well as a good coincidence between the percentage of positive results obtained by CATT and low haematocrit values (packed cell volume). CATT revealed a global serological prevalence of 30.6%, whereas trypanosomes were found in only 5.85% of the corresponding animals. CATT/T. evansi is a quick and easy-to-read test, which merits further evaluation in camel-rearing countries.

Only the serum-resistant bloodstream forms of Trypanosoma brucei rhodesiense express the serum resistance associated (SRA) protein.

The Trypanosoma brucei species consists of three subspecies. T. b. rhodesiense and T. b. gambiense are human infective forms, while T. b. brucei is lysed upon exposure to the cytotoxic factor in normal human serum. T. b. rhodesiense can however occur as a serum-resistant (R) and as a serum-sensitive form (S). In a study of the molecular basis of serum resistance in T. b. rhodesiense it was shown that in the cloned ETaR1-repertoire only the serum-resistant variants express specific transcripts, encoding a protein with VSG-characteristics. When a serial of freshly isolated T. b. rhodesiense isolates was tested, the presence of the R-transcripts in the serum-resistant populations was confirmed. The absence of the serum resistance associated (SRA) mRNAs in several isolates from T. b. brucei and especially T. b. gambiense (including an a-typical one), indicates that more than one mechanism might be involved in the phenomenon of serum resistance in the T. brucei group. Neither T. evansi, nor T. equiperdum expresses the SRA-transcripts. Interestingly, the transcription of the R-specific transcripts is not maintained during the life cycle of T. b. rhodesiense; in the procyclic forms the SRA-mRNAs are no longer present.

Mechanisms underlying trypanosome-elicited immunosuppression.

T-cell proliferative responses of lymph node cells are profoundly suppressed during experimental infections of mice with Trypanosoma brucei. The active suppression of lymph node T-cell proliferative responses is attributed to the coexistence of at least two unlinked suppressive mechanisms that block different T-cell regulatory steps and operate through different effector mechanisms. The generation of prostaglandin-producing macrophages is entirely responsible for the suppression of IL-2 production whereas the induction of a prostaglandin-independent suppressive mechanism accounts for the suppression of the expression of IL-2 receptors (IL-2R). Both mechanisms are mediated by the cells that co-purify which macrophages. Despite an impairment at the level of T-cell proliferation, lymph node cells from T. brucei infected animals produce substantial amounts of interferon-gamma (IFN-gamma) and this lymphokine participates in the down-regulation of IL-2R expression. T-brucei-pulsed macrophage cell lines acquire concomitantly the potential to suppress T-cell proliferative responses and to stimulate CD8+ T-cells to secrete IFN-gamma. The sensibilization of CD8+ T cells by T. brucei-pulsed macrophages might be mediated by TNF-alpha. Collectively, these results indicate that the uptake of T. brucei by macrophages, either in vivo or in vitro, results in the generation of suppressive cells that annihilate T-cell proliferative responses. Furthermore, at least two cytokines (i.e., TNF-alpha and IFN-gamma) are released during these interactions. Besides playing a role in the pathway of T-cell immunosuppression, TNF-alpha and IFN-gamma could also contribute to immunopathological features that occur during trypanosome infections.

Infectivity of Trypanosoma (Trypanozoon) brucei gambiense for baboons (Papio hamadryas, Papio papio).

In order to study sensitivity or resistance of T.b. gambiense to baboon serum, two species of baboons, P. hamadryas and P. papio were inoculated with T.b. gambiense clone LiTat 1.1. Both species were receptive to infection but, parasitological and immunological parameters showed that P. papio was more trypanotolerant than P. hamadryas. The VAT-specific trypanolysis test and the ELISA, using MoAb for circulating antigen detection may be appropriate for the diagnosis of human trypanosomiasis due to T.b. gambiense.

Detection of circulating trypanosomal antigens in Trypanosoma evansi-infected animals using a T. brucei group-specific monoclonal antibody.

An antigen-detection enzyme immunoassay based on a T. brucei group-specific monoclonal antibody was used for the detection of circulating antigens in several animal species experimentally infected with T. evansi stocks from Sudan, Indonesia, Thailand and South America. Circulating antigens were detected as early as 6 days after infection, and they persisted throughout the observation period of up to 60 days postinfection. In an analysis of sera from naturally infected water buffaloes from Thailand, the test identified all the animals with positive parasitological findings, and 3 additional cases that had not been diagnosed by parasitological techniques. In an analysis of sera from pigs on a farm in Thailand suspected of a T. evansi outbreak, the assay detected "antigenaemia" in 66.7% of the animals, with antigen titres ranging from 1:2 to 1.512.