Objective To elucidate the metabolic reprogramming effects of Echinococcus multilocularis infection on host energy metabolism and its associated immunoregulatory mechanisms. Methods Serum levels of 57 central carbon metabolites in infected mice were detected using targeted metabolomics technology. The energy metabolic functions of peripheral blood mononuclear cell ( PBMC) and splenic CD4 ⁺T cells were evaluated via mitochondrial and glycolytic stress tests using the Seahorse XF24 energy metabolism analyzer system. Results Serum levels of L-arginine, succinate, isocitrate, dihydroxyacetone phosphate, and malate were significantly decreased (P<0. 05) in the infected group. Kyoto encyclopedia of genes and genomes analysis revealed significant alterations in five pathways, including central carbon metabolism in cancer. Both mitochondrial respiratory function and glycolytic capacity were suppressed in PBMCs in the infected group (P<0. 05). No significant mitochondrial dysfunction was observed in splenic CD4⁺ T cells, but their glycolytic activity was markedly reduced (P<0. 05). Conclusions E.multilocularis infection disrupts central carbon metabolism in mouse 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.