Changes in peripheral blood lymphocyte subpopulations and parasite-specific antibody responses in Trypanosoma evansi infection of sheep

Abstract

This paper reports on changes in the lymphocyte composition of the peripheral blood in sheep infected with Trypanosoma evansi. In addition, parasite-specific IgG1 and IgM antibody responses were monitored using a double-sandwich enzyme-linked immunosorbent assay (ELISA) technique. Eight sheep were infected with 2 x 10(6) T. evansi TREU 2143. The infection was characterised by chronicity and ended in self-cure in two of the sheep. These two sheep were designated group A, whereas the other six sheep, which remained parasitaemic until treated, were designated group B. Analysis of the peripheral blood lymphocytes (PBLs) by indirect immunofluorescence staining and flow cytometry revealed significant alterations in the numbers of T- and B-cell subsets detected in all infected sheep. In group A, whereas the numbers of CD8+ cells decreased, CD4+ cells showed marginal decreases, remaining at or above pre-infection figures and resulting in increase in the CD4:CD8 ratio. In group B, CD8+ cells showed few marginal decreases, being at or above pre-infection figures most of the time, whereas CD4+ cells decreased significantly from day 26 post infection (p.i.) such that the CD4:CD8 ratio decreased. Infection also resulted in significant increases (P < 0.001) as of day 26 p.i. in circulating B-cells in group B as shown by the numbers of sIg+, CD45R+, CD1+ and major histocompatibility complex (MHC) II+ cells. The increases, however, were moderate and biphasic in group A. T. evansi-specific IgM and IgG1 antibody isotypes were detected in all infected sheep, but their levels were significantly higher in group A than in group B (IgM P < 0.05; IgGI P < 0.01). In addition, although an initially higher level of IgM response was subsequently replaced by a higher level of IgG1 response in group A, this was never the case in group B until after drug treatment.

Isolation, cloning, and pathologic analysis of Trypanosoma evansi field isolates

“…Therefore, we cloned the field isolates of T. evansi from infected water buffaloes and performed virulence assessment tests using mice and cattle. There have been some reports about the virulence assessment of field isolates of trypanosomes using rodents or ruminant (de Menezes et al 2004; Holzmuller et al 2008; Masumu et al 2006; Onah et al 1999; Onah et al 1996). However, there have been few reports about the virulence assessment tests using both livestock and rodents.…”

Trypanosoma evansiand Surra: A Review and Perspectives on Origin, History, Distribution, Taxonomy, Morphology, Hosts, and Pathogenic Effects

“…In experimentally infected sheep, dissection of the immune components involved in T. evansi -induced immunosuppression highlighted that macrophages but not CD8(+) T cells were mainly responsible for suppression [189]. Actually, in terms of lymphocyte populations it was shown that an increase in the CD4 : CD8 ratio and IgG1 was associated with self-cure in T. evansi -infected sheep, whereas a decrease in the CD4 : CD8 ratio and IgM associated with an increase in the number of sIg+, CD45R+, CD1+, a major histocompatibility complex (MHC) II+ circulating B cells, was associated with infection and disease development [186, 190]. …”

A Non-Cytosolic Protein of Trypanosoma evansi Induces CD45-Dependent Lymphocyte Death

“…Again, upon challenge with T. congolense , the CD4+ T-cell and gamma delta T-cell populations decrease in Boran cattle (susceptible) but not in N'Dama cattle (tolerant) [8]. Similarly, among sheep infected by T. evansi , the most susceptible animals showed a significant decrease in CD4+ T-cells, whereas self-cured animals did not [9]. Recently, when recording daily changes in the mouse haemogram after infection with T. evansi , we observed a remarkable synchrony between the peak of parasitaemia and the nadir of the white blood cell count [10].…”