Trypanosoma evansi: Ca(2+) ATPase activity and lipid peroxidation in skeletal muscle from rats experimentally infected

The aim of this study was to evaluate Ca²⁺ ATPase activity and the lipid peroxidation in muscles from rats experimentally infected by Trypanosoma evansi and its roles in the muscle pathogenesis in trypanosomosis. Thirty-six rats were divided in two groups. Group A was infected with an isolate from T. evansi and group B was used as a negative control. Group A was divided into three subgroups (A1, A2 and A3), three animals each group, as well as group B (B1, B2 and B3). The collection of samples were performed at days 5 (A1 and B1), 15 (A2 and B2) and 30 (A3 and B3) post-infection (PI) with the purpose of comparison between healthy and infected rats in the course of the disease. The Ca²⁺ ATPase enzyme activity was determined in skeletal muscle samples. Muscle tissue lipid peroxidation was determined by TBARS levels, and histopathologically it was investigated a possible damage to the muscle tissue of rats infected with T. evansi. It was observed a significant decrease of Ca²⁺ ATPase activity in infected rats compared to not-infected. This enzymatic inhibition was observed at days 5, 15 and 30 PI. A significant increase was observed for TBARS levels in the muscles of infected rats at days 5, 15 and 30 PI. It was not identified any histological alterations for gastrocnemius in rats infected by T. evansi at days 5 and 15 PI. Nevertheless, at day 30 PI it was verified inflammatory infiltrate with mononuclear cells between muscle fibers in three infected rats (50%). T. evansi infections in rats showed a negative correlation between Ca²⁺ ATPase and TBARS levels. Based on these results we suggest that the leg weakness and muscle injuries common in infected animals with T. evansi may be related to a reduced activity of Ca²⁺ ATPase and oxidative stress.     

Trypanosoma evansi: Adenosine deaminase activity in the brain of infected rats

The study was undertaken to evaluate changes in the activity of adenosine deaminase (ADA) in brains of rats infected by Trypanosoma evansi. Each rat was intraperitoneally infected with 10⁶ trypomastigotes either suspended in fresh (group A; n = 13) and cryopreserved blood (group B; n = 13). Thirteen animals were used as control (group C). ADA activity was estimated in the cerebellum, cerebral cortex, striatum and hippocampus. No differences (P > 0.05) in ADA activity were observed in the cerebellum between infected and non-infected animals. Significant (P < 0.05) reductions in ADA activity occurred in cerebral cortex in acutely (day 4 post-infection; PI) and chronically (day 20 PI) infected rats. ADA activity was significantly (P < 0.05) decreased in the hippocampus in acutely infected rats, but significantly (P < 0.05) increased in the chronically infected rats. Significant (P < 0.05) reductions in ADA activity occurred in the striatum of chronically infected rats. Parasites could be found in peripheral blood and brain tissue through microscopic examination and PCR assay, respectively, in acutely and chronically infected rats. The reduction of ADA activity in the brain was associated with high levels of parasitemia and anemia in acute infections. Alterations in ADA activity of the brain in T. evansi-infected rats may have implications for pathogenesis of the disease.     

Trypanosoma evansi: Activities of adenine nucleotide degradation enzymes in cerebral cortex of infected rats

This study aimed to evaluate the activities of the ectoenzymes NTPDase and 5′-nucleotidase in synaptosomes from cerebral cortex of rats experimentally infected with Trypanosoma evansi. The animals were divided in four groups (n = 10) according to the time and degree of parasitemia (groups A, B, C and D). The animals from group A were euthanized on day 3 (low parasitemia), group B on day 5 (high parasitemia) and group C on day 15 (low parasitemia). Group D consisted of healthy rats (not-infected, n = 15) and were divided in three periods (n = 5) in order to compare with the infected groups. After euthanasia, cerebral cortex was removed for the preparation of synaptosomes and enzymatic assays. Group A showed no changes in enzymatic activities compared with control. The hydrolysis of ATP, ADP and AMP by the enzymes NTPDase and 5′-nucleotidase were increased (P < 0.05) in group B (38%, 140% and 61%, respectively) when compared with control. In the group C it was observed a decreased (22%) hydrolysis of ATP when compared with control group. The activities of NTPDase and 5′-nucleotidase in synaptosomes alters the acute phase of the disease when the number of circulating parasites is high, thus the change observed is probably due to the parasitemia.     

Influence of Toxoplasma gondii Acute Infection on Cholinesterase Activities of Wistar Rats

Several studies have shown the mechanisms and importance of immune responses against Toxoplasma gondii infection and the notable role of cholinesterases in inflammatory reactions. However, the association between those factors has not yet been investigated. Therefore, the aim of this study was to evaluate the acetylcholinesterase (AChE) activity in blood and lymphocytes and the activity of butyrylcholinesterase (BChE) in serum of rats experimentally infected with T. gondii during the acute phase of infection. For that, an in vivo study was performed with evaluations of AChE and BChE activities on days 5 and 10 post-infection (PI). The activity of AChE in blood was increased on day 5 PI, while in lymphocytes its activity was enhanced on days 5 and 10 PI (P<0.05). No significant difference was observed between groups regarding to the activity of BChE in serum. A positive (P<0.01) correlation was observed between AChE activity and number of lymphocytes. The role of AChE as an inflammatory marker is well known in different pathologies; thus, our results lead to the hypothesis that AChE has an important role in modulation of early immune responses against T. gondii infection.     

Trypanosoma evansi: Cholinesterase activity in acutely infected Wistar rats

The aim of this study was to evaluate cholinesterase activity during the early acute phase of Trypanosoma evansi infection in rats. Fifteen male Wistar rats were randomly distributed into three groups (n = 5 animals per group): two trypanosome-infected groups (T3 and T5) and uninfected controls (C). The animals were inoculated intraperitoneally with 10⁶ trypanosomes. The blood was collected by cardiac puncture on the 3rd (T3) or 5th day post-infection (T5 and C). Cerebrum and cerebellum were removed for the evaluation of acetylcholinesterase (AChE) activity. AChE activity was also evaluated in whole blood and butyrylcholinesterase activity (BUChE) in plasma samples. Parasitemia were progressive increase and parasites were observed in the peripheral blood of all infected animals one day post-inoculation. AChE activity was not altered in cerebrum and cerebellum tissues. AChE activity in blood significantly decreased in the T3 and T5 groups (26.63 and 25.86 mU/l mol Hb) compared with the control (37.84 mU/l mol Hb). In addition BUChE activity in plasma was lower in the T3 (7.01 μmol BTC hydrolyzed/h/mL) than the T5 and C groups (9.84 and 12.00 μmol BTC hydrolyzed/h/mL). This study therefore, shows that reductions in the activity of cholinesterase occur in acute infection by T. evansi in rats and this demonstrates an important change occurring in animals infected by the protozoan and may indicate a potential role the enzymes play in the mechanism of disease.     

Trypanosoma evansi: concentration of 3-nitrotyrosine in the brain of infected rats

Nitric oxide (NO) is involved in many physiological processes, such as blood pressure control, neurotransmission, inhibition of platelet and neutrophil adherence, and the ability to kill tumor cells and parasites. The indirect determination of NO can be made by detection of 3-nitrotyrosine (3-NT) residues. The aim of this study was to measure the concentration of 3-NT in the brain of rats experimentally infected with Trypanosoma evansi. Twenty-four were inoculated intraperitoneally with cryopreserved blood containing 1 × 10⁶ trypomastigotes per animal. Twenty-four animals were used as negative controls and received 0.2 mL of saline by the same route. The experimental groups (group C and T) were established according to the time after infection and the degree of parasitemia as follows: four control subgroups (C3, C5, C10 and C20) with six non-inoculated animals each and four test subgroups (T3, T5, T10 and T20) with six animals infected with T. evansi in each group. The animals were anesthetized with isoflurane and subsequently euthanized at the days 3 (C3, T3), 5 (C5, T5), 10 (C10, T10) and 20 (C20, T20) post-infection (PI). The brain was removed and dissected into cerebellum, cerebral cortex, striatum and hippocampus. Concentration of 3-NT in the brain was determined by Slot blot technique. At the day 3 PI no changes were observed in the concentration of 3-NT among the groups. There was a significant reduction (p < 0.05) of 3-NT concentration in the striatum and cerebellum at the days 5 and 10 PI, respectively. At the day 20 PI a significant increase (p < 0.05) of 3-NT was observed in the cerebellum, cerebral cortex and hippocampus from the infected animals. Therefore, T. evansi infection caused changes in the concentrations of 3-NT in the central nervous system (CNS), which may be related to clinical signs and infection management.     

Pre-treatment with curcumin modulates acetylcholinesterase activity and proinflammatory cytokines in rats infected with Trypanosoma evansi

The potent activity against Trypanosomes and health beneficial effects of curcumin (Cur) has been demonstrated in various experimental models. In this study, we evaluated the in vivo effect of Cur as trypanocide and as potential anti-inflammatory agent, through the evaluation of immunomodulatory mechanisms in rats infected with Trypanosoma evansi. Daily oral Cur was administered at doses of 0, 20 or 60 mg/kg as preventive treatment (30 and 15 days pre infection) and as treatment (post infection). The treatment of the groups continued until the day of euthanasia. Fifteen days after inoculation, parasitemia, plasma proinflammatory cytokines (IFN-γ, TNF-α, IL-1, IL-6), anti-inflammatory cytokines (IL-10) and blood acetylcholinesterase activity (AChE) were analyzed. Pretreatment with Cur reduced parasitemia and lethality. Cur inhibited AChE activity and improved immunological response by cytokines proinflammatory, fundamental during T. evansi infection. We found that Cur is not so important as an antitrypanosomal activity but as immunomodulator agent. These findings reveal that the preventive use of Cur stimulates anti-inflammatory mechanisms, reducing an excessive inflammatory response.     

Cytokines in rats experimentally infected with Trypanosoma evansi

The aim of this study was to measure the levels of interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), interleukin 1 (IL-1) and interleukin 6 (IL-6) in the serum of rats experimentally infected with Trypanosoma evansi and to correlate these levels with hematological parameters. Initially, 48 rats (group T) were intraperitoneally inoculated with cryopreserved blood containing 1 × 10⁶ trypomastigotes per animal. Twenty-eight animals (group C) were used as negative controls and received 0.2 mL of saline by the same route. The experimental groups were formed according to the time after infection and the degree of parasitemia as follows: four control subgroups (C3, C5, C10 and C20) with seven non-inoculated animals each and four test subgroups (T3, T5, T10 and T20) with 10 animals each inoculated with T. evansi. The blood samples were collected by cardiac puncture at days 3 (C3, T3), 5 (C5, T5), 10 (C10, T10) and 20 (C20, T20) post-infection (PI) to perform the complete blood count and the determination of IFN-γ, TNF-α, IL-1 and IL-6 levels using an ELISA quantitative sandwich. Infected rats showed normocytic normochromic anemia during the experimental period. T. evansi infection in rats caused a serum increase (P < 0.01) of IFN-γ, TNF-α, IL-1 and IL-6 levels at days 3, 5, 10 and 20 PI compared to the controls. The multiple linear regressions showed a reduction of 24% in the hematocrit as a consequence of the increased IFN-γ, TNF-α and IL-1. Therefore, we conclude that the infection caused by T. evansi causes an increase in the pro-inflammatory cytokines. These results suggest a synergism among IL-1, TNF-α and IFN-γ contributing to the development of anemia. This increase is associated with the regulation of immune responses against the parasite.     

Neospora caninum: Activity of cholinesterases during the acute and chronic phases of an experimental infection in gerbils

Neosporosis is an infectious disease primarily of dogs and cattle which has been found in many countries around the world. Neospora caninum causes an important immune response (cellular and humoral) in animals that it infects. Since the participation of the cholinergic system in the immune response is well documented, the aim of this study was to evaluate the relationship between N. caninum infection and activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) during the acute and chronic phase of infection. For that, tachyzoites of N. caninum (Nc-1 strain) were inoculated intraperitoneally in gerbils (Meriones unguiculatus), which were separated in two experiments, I and II, differing in infective doses of tachyzoites, aiming to reach an acute phase as well as chronic phase, respectively. Samples were collected on day 7 post infection (PI) for Experiment I and on days 15 and 30 PI for Experiment II. AChE activity was evaluated on whole blood and brain, while BChE was evaluated in plasma. On day 7 a reduction of AChE in total blood and brain was observed, along with reduction of BChE in plasma of infected animals when compared with non-infected. In Experiment II, AChE activity increased in total blood on day 30 PI; however, maintaining, during the same period, the AChE activity has a reduced in brain tissue. BChE activity was significantly increased on day 30 PI. Based on the results obtained, it was possible to observe a response of the cholinergic system, providing different grades of AChE and BChE activities, in response to the acute and chronic infection of gerbils experimentally infected with N. caninum. These results will serve as initial points to further studies of our research group about the relationship between the infection/disease and the cholinergic system.     

Trypanosoma evansi: a comparative study of four diagnostic techniques for trypanosomosis using rabbit as an experimental model

The goal of this study was to compare two parasitological diagnostic techniques, such as by Micro-Haematocrit Centrifugation Technique (MHCT) and Direct Microscopic Examination (DME) with a serological method (iELISA), and a molecular procedure PCR, in rabbits experimentally infected with Trypanosoma evansi, in order to determine their sensitivity throughout the course of disease. The parasitological methods were not able of detecting the presence of the parasite during the phases of low parasitemia, the prepatency period and the chronic phase. In contrast, PCR detected T. evansi in the prepatency and chronic phase, when increase the amount of DNA from 100 to 300 ng. 100% detection was observed with iELISA only in the chronic stage of the disease. In the acute phase, all samples were positively diagnosed using either MHCT or PCR, whereas only few samples were diagnosed by DME. Samples obtained from day 15 post infection were also detected by iELISA. The highest diagnostic register during the course of infection was achieved by the PCR technique (93.8%), followed by iELISA (71.1%), MHCT (59%) and DME (13.6%). Therefore, we recommend the use of PCR in epidemiological studies in order to implement sanitary control plans for the improvement of livestock productivity in the country.     

Trypanosoma brucei brucei: A comparison of gene expression in the liver and spleen of infected mice utilizing cDNA microarray technology

Trypanosoma brucei brucei, the infectious agent of the disease known as Nagana, is a pathogenic trypanosome occurring in Africa, where it causes significant economic loss to domesticated livestock. Although many studies on the histopathology of organs of mice infected with T. b. brucei have been reported, little work has been done regarding gene expression in these organs in infected mice. In this paper, we describe the use of cDNA microarray to determine gene expression profiles in the liver and spleen of mice infected with T. b. brucei (STIB 920) at peak parasitaemia (12 days after infection). Our results showed that a total of 123 genes in the liver and 389 genes in the spleen were expressed differentially in T. b. brucei infected mice. In contrast, however, in an acute infection in mice caused by Trypanosoma brucei evansi, a species genetically related to T. b. brucei, 336 genes in the liver and 190 genes in the spleen were expressed, differentially, indicating that the liver of mice was more affected by the acute T. b. evansi infection whilst the spleen was more affected by the subacute T. b. brucei infection. Our results provide a number of possible reasons why mice infected with T. b. evansi die sooner than those infected with T. b. brucei: (1) mice infected with T. b. evansi may need more stress response proteins to help them pass through the infection and these are probably excessively consumed; (2) proliferating cell nuclear antigen was more down-regulated in the liver of mice infected with T. b. evansi, which indicated that the inhibition of proliferation of hepatocytes in mice infected with T. b. evansi might be more severe than that in T. b. brucei infection; and (3) more hepatocyte apoptosis occurred in the mice infected with T. b. evansi and this might be probably the most important reason why mice died sooner than those infected with T. b. brucei. Studies of the changes in the gene expression profile in the liver and spleen of mice infected with T. b. brucei may be helpful in understanding the mechanisms of pathogenesis in Nagana disease at the molecular level. By comparing the gene profiles of the liver and spleen of mice infected with T. b. brucei with T. b. evansi, we have identified a number of factors that could explain the differences in pathogenesis in mice infected with these two African trypanosomes.     

Diminazene aceturate associated with sodium selenite and vitamin E in the treatment of Trypanosoma evansi infection in rats

The aim of this study was to evaluate the utilization of a standard treatment with diminazene aceturate against the infection caused by Trypanosoma evansi, associated to sodium selenite and vitamin E. In vitro tests showed trypanocidal effect related to the treatment with diminazene aceturate and sodium selenite, but vitamin E had no harmful effect on the trypanosomes. In vivo experiments utilized a total of 72 adult outbreed females rats, separated into 9 groups (A, B, C, D, E, F, G, H and I), 8 animals each. Group A was the uninfected group; groups B to I were infected with 0.2 mL of blood containing 10⁶ trypanosomes. Parasitemia was estimated daily by microscopic examination of blood smears. Group B served as positive control; group C was treated with diminazene aceturate; group D with sodium selenite; group E with vitamin E; group F received an association of diminazene aceturate and sodium selenite; group G received an association of diminazene aceturate and vitamin E; group H received an association of diminazene aceturate, sodium selenite and vitamin E, and group I received an association of sodium selenite and vitamin E. Diminazene aceturate was administrated in a single dose on the 3rd day post infection (PI). Sodium selenite and vitamin E were administered at the 3rd and 23rd day PI. In vivo tests showed increase of longevity in groups treated with diminazene aceturate associated with sodium selenite (groups F and H). No difference was found between groups C and E, thus the vitamin E did not increase the efficacy of treatment against T. evansi when associated to diminazene aceturate. The curative efficacy of treatments was 37.5, 87.7, 37.7 and 75% to the groups C, F, G and H, respectively. Other treatments showed no efficacy. The sodium selenite when combined with chemotherapy may represent an alternative in the treatment of trypanosomosis.     

Influence of Trypanosoma evansi in adenine nucleotides and nucleoside concentration in serum and cerebral cortex of infected rats

This study aimed to evaluate the adenine nucleotides and nucleoside concentration in serum and cerebral cortex of rats infected with Trypanosma evansi. Each rat was intraperitoneally infected with 1 × 10(6) trypomastigotes suspended in cryopreserved blood (Group A; n = 18). Twelve animals were used as controls (Group B). The infected animals were monitored daily by blood smears. At days 4 and 20 post-infection (PI) it was collected serum and cerebral cortex to measure the levels of ATP, ADP, AMP and adenosine by high performance liquid chromatography (HPLC). In serum there was a significant (P < 0.05) increase in the ATP, AMP and adenosine concentrations at days 4 and 20 PI in infected rats when compared to not-infected. Furthermore, in the cerebral cortex it was observed a significant (P < 0.05) increase in the concentrations of ATP, AMP and decreased adenosine levels at day 4 PI. At day 20 PI it was only observed an increase in the AMP and adenosine concentrations in cerebral cortex of infected rats when compared to not-infected. It was not observed any difference in ADP concentration in serum and brain at days 4 and 20 PI. No change was observed histologically in the cerebral cortex of infected animals. The results allow us to conclude that infection with T. evansi in rats causes an increase in the concentrations of ATP, AMP and adenosine in serum and cerebral cortex the time periods evaluated. These alterations occurred as a result of T. evansi infection which involves neurotransmission, neuromodulation and immune response impairment confirm the importance of the purinergic system in this pathology.     

Long non-coding RNA BDNF-AS modulates osteogenic differentiation of bone marrow-derived mesenchymal stem cells

Chagas disease is an acute or chronic illness that causes severe inflammatory response, and consequently, it may activate the inflammatory cholinergic pathway, which is regulated by cholinesterases, including the acetylcholinesterase. This enzyme is responsible for the regulation of acetylcholine levels, an anti-inflammatory molecule linked to the inflammatory response during parasitic diseases. Thus, the aim of this study was to investigate whether Trypanosoma cruzi infection can alter the activity of acetylcholinesterase and acetylcholine levels in mice, and whether these alterations are linked to the inflammatory cholinergic signaling pathway. Twenty-four mice were divided into two groups: uninfected (control group, n = 12) and infected by T. cruzi, Y strain (n = 12). The animals developed acute disease with a peak of parasitemia on day 7 post-infection (PI). Blood, lymphocytes, and brain were analyzed on days 6 and 12 post-infection. In the brain, acetylcholine and nitric oxide levels, myeloperoxidase activity, and histopathology were analyzed. In total blood and brain, acetylcholinesterase activity decreased at both times. On the other hand, acetylcholinesterase activity in lymphocytes increased on day 6 PI compared with the control group. Infection by T. cruzi increased acetylcholine and nitric oxide levels and histopathological damage in the brain of mice associated to increased myeloperoxidase activity. Therefore, an intense inflammatory response in mice with acute Chagas disease in the central nervous system caused an anti-inflammatory response by the activation of the cholinergic inflammatory pathway.     

Trypanosoma evansi: Hematologic changes in experimentally infected cats

This study aimed at evaluating hemogram and erythropoietic changes in cats experimentally infected with Trypanosoma evansi. Thirteen adult female non-breeding Felix catus were separated into two groups: seven animals were infected with 10⁸ trypomastigotes each, and six animals were used as negative controls. Animals were kept in air-conditioned rooms and blood smears were performed daily for 49 days. Blood samples were collected from the jugular vein at days 0, 7, 21, 35 and 49 and stored in blood-collecting tubes containing anticoagulant. Bone marrow was collected from the proximal epiphysis of the right femur at days 14 and 42 post-inoculation (PI). Total erythrocyte count, hematocrit and hemoglobin showed statistical differences among groups from the seventh day PI onwards (P < 0.05). The mean corpuscular volume and the mean corpuscular hemoglobin concentration remained normal, characterizing a normocytic-normochromic anemia. Reticulocyte count increased in the infected group from the 21st day onwards, but remained near normal values suggesting a mild regenerative anemia. Moreover, the myeloid:erythroid ratio significantly reduced at day 42 PI, evidencing a bone marrow hematopoietic response. Based on these results we conclude that cats infected with T. evansi have normocytic, normochromic, regenerative anemia.     

Oxidative Stress in the Heart of Rats Infected with Trypanosoma evansi

This study was conducted to investigate the occurrence of oxidative stress in the heart tissue of rats infected with Trypanosoma evansi. Rats were divided into 2 groups (A and B) with 12 animals each, and further subdivided into 4 subgroups (A1 and A2, 6 animals/each; and B1 and B2, 6 animals/each). Animals in the groups B1 and B2 were subcutaneously inoculated with T. evansi. Thiobarbituric acid reactive substances (TBARS), superoxide dismutase activity (SOD), glutathione S-transferase activity (GST), reduced glutathione activity (GSH), and non-protein thiols (NPSH) in the heart tissue were evaluated. At day 5 and 15 post-infection (PI), an increase in the TBARS levels and a decrease in the SOD activity (P<0.05) were observed. GSH and GST activities were decreased in infected animals at day 15 PI (P<0.05). Considering the proper functioning of the heart, it is possible that the changes in the activity of these enzymes involved in the oxidative stress may be related, at least in part, in the pathophysiology of rats infected with T. evansi.     

Energetics of heart mitochondria during acute phase of Trypanosoma cruzi infection in rats

The energetics of heart mitochondria was studied in the acute phase of Trypanosoma cruzi infection in rats. Wistar rats were infected with 2 × 10⁵ trypomastigote forms of the Y strain of T. cruzi, and heart mitochondria and submitochondrial particles isolated after 7 and 25 days of infection. Ultrastructure of mitochondria seemed to be preserved, but cytochrome c levels were significantly depressed. Respiratory control ratios (RCR) were decreased for glutamate and succinate oxidations, as a consequence of inhibition of respiration in state 3 and/or of stimulation of respiration in state 4. Stimulation of hydrolytic activity of FoF1-ATPase by energization of mitochondria was approx. 2-fold higher in relation to controls. Mitochondrial ATP concentration remained constant. In conclusion, during the acute phase of T. cruzi infection in rats there is an energy impairment at the level of heart mitochondria, but their ultrastructure and ATP concentration seem to be preserved; the maintenance of ATP may be due to an adaptative mechanism of the cell which includes inhibition of the hydrolytic activity of FoF1-ATPase.     

Trypanosoma evansi: Therapeutic efficacy of diminazine aceturate in crossbred calves, Bos taurus and B. indicus

The therapeutic efficacy of diminazine aceturate (Berenil) against Trypanosoma evansi infection (surra) in calves was determined. Seven crossbred calves, 8 to 12 months old, were inoculated subcutaneously with 5 × 10⁷ parasites of a virulent strain of T. evansi. All of the calves developed clinical infection and exhibited symptoms associated with chronic surra. Forty-one to forty-four days after inoculation, five of the calves were treated with a single dose of diminazine aceturate at 10 mg/kg body weight intramuscularly. The two remaining calves were left as infected but untreated controls. The treated calves were found free of the infection on repeated blood smear examinations and diagnostic challenge tests in mice 12 hr to 16 days later. One of the five calves, which was treated at an advanced stage of the disease, died on the fifth day after treatment. Splenectomy of the treated calves, 16 to 19 days after treatment, did not result in relapse of parasitemia, indicating that diminazine aceturate at 10 mg/kg had a rapid trypanocidal effect in surra of calves. Both of the controls died of the disease on the 45th and 47th day.     

Murine liver response to Allium sativum treatment during infection induced-trypanosomiasis

Hepatic injury induced by trypanosomiasis is one of the major health problems not only to human but also to wild and domestic animals. This study aimed to evaluate the hepatoprotective role of Allium sativum extract (ASE) against Trypanosoma evansi infection in mice. Animals were divided into 4 groups. Group I received only saline while group II received ASE (20 mg/Kg). Animals of group III and group IV were infected with T. evansi. The latter group was treated with ASE. The infrared spectroscopic analysis of A. sativum extract exhibited bands between 3700 cm⁻¹ and 599 cm⁻¹. On day 4 post T. evansi infection, ASE decreased the parasitemia by about 15 fold. Also, ASE regulated the number of erythrocytes and leucocytes and the hemoglobin content. In addition, the histopathological damage was reduced after treatment with ASE. Moreover, the oxidant and the antioxidant markers (glutathione, malondialdehyde and catalase) were regulated in the infected-treated animals. Collectively, the results proved the protective role of ASE against T. evansi infection in mice.