SummaryBackgroundTheileria equi latently infected horses remain under oxidative stress which can be easily determined by evaluating the concerned biomarkers. Until now, very limited data are available regarding study of oxidative stress alongside hepatorenal biomarker alterations in carrier equids.ObjectivesThis study was aimed to investigate oxidative stress and hepato‐renal alterations in respective biomarkers in latently T. equi‐infected exotic and indigenous horses.Study designThe study involved 24 (n = 24) T. equi latently infected horses (11 exotic and 13 indigenous) while 50 horses (n = 50) served as the non‐infected group. Haematological, hepato‐renal and oxidative stress biomarkers analysis was carried out to evaluate the effect of latent T. equi infection on these parameters.ResultsIn the T. equi‐infected exotic horse group, significant decreases in Hb, PCV, TLC and eosinophils were observed in comparison with the T. equi‐infected indigenous horse group. Blood glucose and SOD levels were significantly lower while serum MDA levels were significantly increased in T. equi‐infected horses than the noninfected groups. Higher MDA levels are suggestive of biochemical changes in parasitised erythrocytes making their membrane rigid and liable to erythrolysis. Decreased SOD levels were indicative of a disturbance in anti‐oxidative mechanisms leading to accumulation of free radicals attributing to oxidative injuries to T. equi‐infected erythrocytes.Main limitationsLatently infected animals with very low parasitaemia which are unable to damage host cells may lead to false negative results. Another limitation is the difficulty in ruling out other similar disease‐causing oxidative stresses.ConclusionThese observations indicated that T. equi naturally latently infected exotic horses were more liable to develop a condition in comparison to indigenous infected horses. From the above results, we can conclude that T. equi infection exerts a marked effect on the hepato‐renal biomarkers and significantly affects the key antioxidant defence mechanisms of infected erythrocytes, leading to oxidative damage to the erythrocytes membrane and ultimately its haemolysis.