Abstract
BACKGROUND: Theileria annulata is a protozoan parasite transmitted by ticks that primarily affects cattle and causes tropical theileriosis. This disease is widespread in tropical and subtropical regions and leads to significant economic losses due to fever, anemia, weight loss, and high mortality, especially in susceptible breeds. Infecting rabbits with T. annulata was done to study their immunological and pathological responses in rabbits experimentally infected with T. annulata. METHODS: The study included 24 male rabbits divided into two groups (12 rabbits per group). The first group was injected with sterile distilled water and considered the control group. The second group was injected intraperitoneally with a single dose of 0.5 ml of blood from infected cattle containing approximately 3 × 10(6) T. annulata-infected erythrocytes. Rabbits were selected as an experimental model due to their practicality, distinct immune responses, and suitability for controlled studies of T. annulata pathogenesis. After 14 and 21 days of infection, samples were collected from the rabbits for histopathological and immunological analysis. RESULTS: Theileria annulata piroplasms were observed under a microscope as commas, spots, and rods. The progression of infection was associated with increased body temperature, which is closely related to theileriosis. The infection caused a considerable temperature increase of 39.7°C on the seventh day and 41°C on the thirteenth day. In the infected group, Interferon-gamma (IFN-γ) levels were significantly elevated, whereas IL-10 levels were markedly reduced. Transforming growth factor-beta 1 (TGF-β1) levels displayed a dynamic temporal pattern. The markers of oxidative stress showed a significant increase in malondialdehyde (MDA) levels and a notable decrease in total antioxidant capacity (TAC) levels. Furthermore, infection induces a substantial rise in Immunoglobulin G (IgG) concentrations. Rabbits infected with T. annulata had severe histological abnormalities in their lungs, liver, spleen, kidneys, and mesenteric lymph nodes. CONCLUSION: The infection altered the red blood cell structure of the host, as well as increased body temperature and mortality. Increased levels of proinflammatory markers (e.g., IFN-γ), decreased levels of antiinflammatory cytokines (IL-10 and TGF-β1), higher oxidative stress (e.g., MDA, reduced TAC), and persistent IgG responses indicate systemic immunological activation. Histopathological changes revealed increased lung, liver, spleen, kidney, and lymph node damage.