EJMS

Abstract

Trypanosomiasis is a large group of diseases which affect human and animals. Trypanosoma evansi is the most commonly widespread pathogenic trypanosome that infects mainly wild and domestic animals and rarely humans. During trypanosomiasis brain lesions and tissue damage develop due to the presence of the parasite in blood vessels and secretion of toxic substances. Autophagy is a self-eating process that occurs to overcome several conditions such as starvation, oxidative stress and tissue damage. However, to author knowledge, the role of autophagy during the acute infection with T. evansi has not been investigated before; therefore, this study was designed. Thirty mice were divided into three groups (n = 10); group I was the normal control; group II was infected with T. evansi and group III was infected and treated with diminazene aceturate at a dose of 7 mg/kg once intraperitoneally on the 2nd day post infection (p.i.). The experiment was terminated 15 days p.i. and each mouse was subjected to histopathological examination of brain tissues, immunohistochemical detection of the expression of iNOS and Atg5 as a marker for autophagy. Additionally, estimation of the oxidative stress in brain homogenates was done by measurement of the amounts of the end product of lipid peroxidation malondialdehyde (MAD) and superoxide dismutase (SOD) antioxidant enzyme activity. The histopathological examination revealed the development of basophilic neuronal cell necrosis, intramyelinic oedema and congestion of blood vessels in brain tissues of the infected mice. A state of oxidative stress was manifested with a significant increase in the amount of MAD and a significant decrease in SOD associated with a significant expression of iNOS and Atg5 in group II. However, treatment resulted in significant improvements in these findings. In conclusion, acute infection with T. evansi induces autophagy in the brain to overcome the infection-induced oxidative stress and tissue damage.