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This study aimed to evaluate nucleoside triphosphate diphosphohydrolase (NTPDase) and adenosine deaminase (ADA) activities in lymphocytes from rats supplemented or not with curcumin 30 days prior to experimental infection with Trypanosoma evansi. Thirty-two adult male Wistar rats were divided in four groups. The pre-infection group 20 (PreI20) received orally 20 mg/kg of curcumin and pre-infection group 60 (PreI60) received orally 60 mg/kg of curcumin for 30 days prior inoculation with T. evansi. The infected e non-infected control groups received only oral vehicle for 30 days. Trypanosoma evansi infected groups were inoculated intraperitoneally with 0.2 ml of blood with 1 × 10 6 parasites. After inoculation the treatment of the groups continued until the day of euthanasia (15 days). The results showed that curcumin pre-treatment, with both doses, reduced (P < .05) NTPDase and increased (P < .05) ADA activity in lymphocytes of treated groups when compared to untreated and infected animals (control). The results of this study support the evidence that the regulation of ATP and adenosine levels by NTPDase and ADA activities appear to be important to modulate the immune response in T. evansi infection, once the treatment with curcumin maintained the NTPDase activity reduced and enhanced ADA activity in lymphocytes. It is possible to conclude that the use of curcumin prior to infection with T. evansi induces immunomodulatory effects, favoring the response against the parasite., (Copyright © 2019 Elsevier B.V. All rights reserved.)

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 60mg/kg as preventive treatment (30 and 15days 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., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

This study aimed at evaluating biochemical changes of cats (Felis catus) experimentally infected with Trypanosoma evansi. Seven animals were infected with 10(8) blood trypomastigotes per animal and six were used as controls. Blood smears were performed daily for 56 days and the hepatic, renal and muscular parameters in blood serum were evaluated at days 0, 7, 21, 35 and 49. The protozoan was found in the bloodstream 24-48 h post-inoculation (PI) and irregular peaks of parasitemia were observed throughout the experiment. Muscular enzymatic activities (aspartate aminotransferase and creatine kinase) were increased in infected cats compared to controls. Increased concentrations of total proteins and globulins and decreased levels of albumin and albumin/globulin ratio were observed in infected group versus the controls values (P<0.05). No alteration in serum activity of alanine aminotransferase, gamma-glutamyltransferase, creatinine and urea was observed in both groups., (Copyright (c) 2010 Elsevier B.V. All rights reserved.)

Five cats were experimentally inoculated with Trypanosoma evansi in order to evaluate the pathological changes induced by this protozoan infection. Clinical signs observed included vomiting, diarrhoea, hyperthermia, weight loss, facial oedema, corneal opacity, lymphadenopathy and hindlimb instability. Reduction in hematocrit was observed from 7 days post-infection (dpi) (P<0.05). One cat died at 40 dpi and the other four cats were humanely destroyed. Necropsy examination was performed in two cats at 56 dpi and two cats at 120 dpi. Gross findings in all cats included generalized muscle atrophy, pale mucosae, icterus of the subcutaneous and serosal tissue and the intima of arteries, lymphadenopathy and splenomegaly. Other findings included corneal opacity, subcutaneous oedema (mainly of the head) and hydropericardium. Trypomastigotes of T. evansi were observed in impression smears prepared from the aqueous humor. Microscopically, there was lymphoid hyperplasia of the spleen and lymph nodes. The animals with corneal opacity had mild corneal oedema and accumulation of fibrin and inflammatory cells (neutrophils and plasma cells) in the anterior chamber. Similar inflammatory cells infiltrated the iris, ciliary body, corneoscleral limbus and conjunctiva., (Copyright 2009 Elsevier Ltd. All rights reserved.)

The aim of this study was to investigate the efficacy of diminazene aceturate in the control of the infection by Trypanosoma evansi in cats. Fourteen animals were infected with 10(8) trypomastigote forms each and six were used as negative control (group A). Seven of the infected cats were used as positive control (group B) and seven were treated with diminazene aceturate (3.5 mg kg(-1)) for 5 consecutive days (group C). Biochemical and hematological parameters were evaluated during the experiment. Blood with anticoagulant was collected at day 49 post-inoculation and preserved in ethanol for DNA extraction. Samples were analyzed using PCR T. evansi-specific to assess the effectiveness of treatment. The treatment with diminazene aceturate had an efficacy of 85.7%. Alanine aminotransferase, gamma-glutamyltransferase, urea, and creatinine values remained within the normal physiological range in the treated cats. Hemogram was normalized in all the cured animals. Therefore, the therapy used is effective in controlling T. evansi in cats.

This study aimed to assess the plasma lipid peroxidation and the susceptibility of erythrocytes to in vitro peroxidation as indicators of oxidative damage in erythrocytes and their roles in the pathogenesis of anemia during the early acute phase of Trypanosoma evansi infection in rats. Fifty male Wistar rats were randomly distributed into seven groups: three trypanosome-infected groups (T(2), T(4) and T(6); n=10 animals per group) and four uninfected controls (C(0), C(2), C(4) and C(6); n=5 animals per group). Animals from trypanosome-infected groups were inoculated intraperitoneally with 10(6) trypanosomes. Blood samples were collected by cardiac puncture before infection (day 0; group C(0)) or on the 2nd (C(2) and T(2)), 4th (C(4) and T(4)) and 6th (C(6) and T(6)) day post-infection (dpi). Samples were analyzed for red blood cell (RBC) count, hemoglobin (Hb) concentration, packed cell volume (PCV), plasma malondialdehyde (MDA) and in vitro peroxidation of erythrocytes. The mean values of the hematological indices gradually decreased in the infected rats compared with the control. MDA was significantly increased (P<0.001) on the 6th dpi in infected versus control animals and was negatively correlated with PCV (P<0.001; R(2)=0.372). The values for erythrocyte in vitro peroxidation were higher for groups T(4) and T(6) than for the control rats (P<0.01). A positive correlation between erythrocyte peroxidation and MDA (P<0.001; R(2)=0.414) was observed. The results of this study indicate that T. evansi infection in rats is associated with oxidative stress, indicated by lipid peroxidation and oxidative damage in erythrocyte membranes, as demonstrated by in vitro peroxidation. This may be one of the causes of anemia in acute trypanosomosis.