Host Oxidative Responses to Piroplasmosis: Current Perspectives in Domestic Animals
Priya Jagota
Department of Animal Nutrition, School of Veterinary Sciences, Abhilashi University, Mandi, Himachal Pradesh, India.
Pratistha Shrivastava *
Department of Veterinary Parasitology, Institute of Veterinary Science and Animal Husbandry, Siksha ‘O’ Anusandhan, Bhubaneswar, Odisha, India.
Nitin Kumar Mishra
Department of Veterinary and Animal Husbandry Extension Education, Institute of Veterinary Science and Animal Husbandry, Siksha ‘O’ Anusandhan, Bhubaneswar, Odisha, India.
*Author to whom correspondence should be addressed.
Abstract
Piroplasmosis encompasses infections in which oxidative responses may restrict parasites, damage host tissues or sustain the survival of infected cells. These competing functions complicate the interpretation of antioxidant measurements and the development of redox-directed treatments. This critical narrative review evaluates evidence in dogs, cattle, buffaloes, sheep, goats and equids, with feline infections considered where they clarify the limits of cross-species extrapolation. Literature published through 1 August 2026 was identified through web-mediated scholarly searching, authoritative bibliographic records and citation tracking. Clinical observations were distinguished from cellular experiments, biochemical characterisation and therapeutic pilot studies. The most consistent clinical finding is an association between infection and altered lipid oxidation or antioxidant status, but the direction of individual enzyme responses varies with parasite species, disease severity, sampling compartment and analytical method. Experimental canine studies support oxidative injury and enhanced removal of both infected and uninfected erythrocytes. In contrast, transforming bovine theilerial infections demonstrate a signalling role for oxidants within infected leukocytes, making indiscriminate antioxidant suppression biologically questionable. Recent equine studies and canine acetylcysteine trials extend the evidence base but do not establish validated prognostic thresholds, prevention of organ failure or improved survival. Inconsistent case definitions, small comparison groups, non-specific assays, incomplete control of haemolysis and reliance on single-time-point sampling limit causal interpretation. A compartment-, stage- and time-resolved framework is therefore proposed to separate antimicrobial defence, collateral injury, adaptive compensation and parasite-supported cellular survival. Immediate priorities are harmonised sample handling, species-resolved longitudinal cohorts, orthogonal measurements of oxidative damage and adequately controlled adjunct-treatment trials with parasite clearance and clinically meaningful outcomes. Oxidative responses are relevant to piroplasmosis pathobiology, but their clinical value depends on identifying which process is being measured rather than assuming that a higher oxidant signal invariably warrants antioxidant treatment.
Keywords: Babesia, theileria, erythrocyte injury, redox signalling, lipid peroxidation, antioxidant biomarkers, adjunctive therapy