Objective: Elucidate the metabolic reprogramming effects of Echinococcus multilocularis infection on host energy metabolism and its associated immunoregulatory mechanisms. Methods: The levels of 57 central carbon metabolites in the serum of infected mice were detected using targeted metabolomics technology. The energy metabolic functions of peripheral blood mononuclear cells (PBMCs) and splenic CD4+ T cells were evaluated via mitochondrial stress tests and glycolytic stress tests using the Seahorse XF24 energy metabolism analyzer system. Results: The serum levels of L-arginine, succinate, isocitrate, dihydroxyacetone phosphate, and malate were significantly decreased (P < 0.05) in the infected group. KEGG analysis revealed significant alterations in five pathways, including central carbon metabolism in cancer. Both mitochondrial respiratory function and glycolytic capacity were suppressed in PBMCs of the infected group (P < 0.05). Although no significant mitochondrial dysfunction was observed in splenic CD4+ T cells, their glycolytic activity was markedly reduced (P < 0.05). Conclusion: E. multilocularis infection induces disruptions in central carbon metabolism in murine serum and significantly suppresses glycolytic function in both PBMCs and CD4+ T cells. These findings suggest that energy metabolic reprogramming may play a critical role in parasite immune evasion.