الفهرس 
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Abstract
Trypanosoma evansi is a pathogenic hemoflagelate protozoan belonging to the Salivaria section. The disease progression, clinical, hematological and pathological aspects in the host can vary according to the strain virulence, the host susceptibility and the epizootic conditions. It transmits among hosts by hematophagous insects. T. evansi causes ‘surra’ which is an animal disease which spreads in various geographical areas among different domestic and wild animals. In Egypt, trypanosomiasis evansi is an important livestock disease causing significant losses in camels. For long period, T. evansi is not known to be pathogenic to humans, but the first well documented human infection with T. evansi was reported in India which was confirmed by different diagnostic methods. On invading the susceptible host, the protozoan, multiplies rapidly in the blood and later reach the CNS. The degenerative changes observed could be due to tissue anoxia, possibly caused by anaemia, immunological response or other mechanisms may also be involved. Generally, anemia is a major component of the pathology of surra and of African trypanosomosis. Indeed, anemia has been implicated in the development of most tissue degenerative changes and, consequently, the disorders reported in trypanosome-infected animals. The immune system is involved in infection control and activates different cellular mechanisms, in which cytokines play an important role. In trypanosomiasis, the lymphocytes produce IFN-γ in response to the parasitic antigens. IFN-γ activates the macrophages increasing their ability to destroy the organisms. A hallmark of Th17 cells is the production of interleukin-17A (IL-17A) (also called IL-17), a proinflammatory cytokine which plays important pathological roles in several immune-mediated diseases. The receptor for IL-17A is expressed in various tissues and by various types of cells; these cells produce diverse proinflammatory cytokines such asIL-1, IL-6 and TNF-α and chemokines in response to IL-17A stimulation which are playing important roles in the replication process of the parasite as well as in the host immune response. Nitrous oxide (NO) has important roles in immunity against different microbes, including the induction and suppression of apoptosis, and microbicidal activity. The enzyme is responsible for the generation of cytotoxic and immunoregulatory free radical NO. High levels of NO are mediated by up regulated expression of the iNOS gene in response to the activating signals, in particular to the secretion of proinflammatory cytokines by Thl cells. Production of the proinflammatory cytokines predisposes to the increased synthesis of NO. Recently, it has been demonstrated that NO is able to regulate the induction and activity of regulatory T cells (T reg) and TH17 cells , which mediates host protection through either direct parasite killing or by limiting parasite growth. This work targeted to study parasitological, heamatological, histopathological and some immunological changes occurring in the experimentally T. evansi infected mice. Sixty four mice were divided into two main groups; T. evansi infected group (Group I) and control uninfected one (Group II). Group I was subdivided according to period of the infection into 4 subgroups; I-a (sacrificed at day 3 PI), I-b (sacrificed at day 5 PI), I-c (sacrificed at day 10 PI) and I-d (sacrificed at day 20 PI), each containing 10 mice. Group II was also subdivided into 4 subgroups; II-a, II-b, II-c and II-d which were sacrificed at the same time in parallel to their counterpart subgroups of Group I. In the present study, the presence and the degree of parasitemia were estimated daily for each infected mouse by direct blood smear and Geimsa stained smear. The CBC was measured and the level of serum iron was determined. The histopathological study was performed from liver, spleen, brain, lung, kidney and heart from each mouse in both the mice groups (I and II) and stained with H&E. Immunological parameters were measured in the form detection of inducible nitric oxide synthase (iNOS) enzyme in the tissue and IL17 detection in the sera and in some tissues of the mice. T. evansi was detected in the blood of all the infected mice starting from the 2nd day PI and the level of parasitemia increased progressively to reach its peak at the 5th day PI recording 142.9±37.74 trypanosomes/HPF, and then the level of parasitemia decreased to become only 0.7±0.82 trypanosomes/HPF at the 20th day PI. All the subgroups of the T. evansi infected mice (group I) revealed significant reduction of Hb concentration, HCT % and RBCs count in comparison to the control uninfected mice subgroups, while MCV and MCHC were within their normal ranges, and all these parameters are characters of the normocytic normochromic anemia. On counting the different types of WBCs, there was leucocytosis, in all infected mice groups, which was due to the increase in the count of the lymphocytes. Also, there was significant increase in the number of neutrophils in group I. On the other hand, the numbers of monocytes and eosinophils increased in all infected mice subgroups, but without any statistically significant difference when compared with the uninfected control mice subgroups. The highest degree of anemia was coinciding with the peak of the parasitemia. There was a negative correlation between the parasitemia and some of the heamtological parameters. The level of serum iron increased significantly in all the infected mice subgroups (Group I) and the subgroup I-b showed the highest serum iron concentration which was coinciding with the peak of parasitemia. Gross examination of various tissues from the infected mice subgroups revealed splenomegaly, hepatomegaly and marked congestion of lungs. On microscopic examinations, all degrees of inflammation were detected in these tissues and most of them showed trypanosomes. The level of iNOS increased in the tissues of T. evansi infected mice as the infection progressed from the 3rd day till the end of the experiment and there was a negative correlation between the level of T. evansi in the blood (parasitemia) and iNOS expression in the different examined tissues of infected mice subgroups In this study, it was observed that IL17 increased whether in the sera or in the tissues of T. evansi infected mice and there was a significant negative correlation between the level of parasitemia and level of IL17 either in the serum or in the tissues of T. evansi infected mice.