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Simple Summary: The Chinese soft-shelled turtle (Trionyx sinensis) is an important cultured reptile in East Asia. Hemorrhagic sepsis caused by Aeromonas hydrophila infection is the dominant disease in the aquaculture of Chinese soft-shelled turtles, while the molecular pathology is far from clear due to the lag of research on turtle immunology. It has been reported in mammals and fish that the dysfunction of immune responses to pathogen infections causes host tissue hemorrhagic sepsis. In this study, two groups of turtles with different susceptibility to A. hydrophila infection are found. A comparative transcriptome strategy is adopted to examine the gene expression profiles in liver and spleen for these two phenotypes of turtles post A. hydrophila infection, for the first time revealing the full picture of immune mechanisms against A. hydrophila, which provides new insight into the molecular pathology during A. hydrophila infection in T. sinensis. The findings will promote further investigations on pathogenic mechanisms of hemorrhagic sepsis caused by A. hydrophila infection in T. sinensis, and also will benefit their culture industry. Although hemorrhagic sepsis caused by Aeromonas hydrophila infection is the dominant disease in the aquaculture of Chinese soft-shelled turtle, information on its molecular pathology is seriously limited. In this study, ninety turtles intraperitoneally injected with A. hydrophila exhibited two different phenotypes based on the pathological symptoms, referred to as active and inactive turtles. Comparative transcriptomes of liver and spleen from these two groups at 6, 24, and 72 h post-injection (hpi) were further analyzed. The results showed that cytokine–cytokine receptor interaction, PRRs mediated signaling pathway, apoptosis, and phagocytosis enriched in active and inactive turtles were significantly different. Pro-inflammatory cytokines, the TLR signaling pathway, NLR signaling pathway, and RLR signaling pathway mediating cytokine expression, and apoptosis-related genes, were significantly up-regulated in inactive turtles at the early stage (6 hpi). The significant up-regulation of phagocytosis-related genes occurred at 24 hpi in inactive turtles and relatively lagged behind those in active turtles. The anti-inflammatory cytokine, IL10, was significantly up-regulated during the tested periods (6, 24, and 72 hpi) in active turtles. These findings offer valuable information for the understanding of molecular immunopathogenesis after A. hydrophila infection, and facilitate further investigations on strategies against hemorrhagic sepsis in Chinese soft-shelled turtle T. sinensis. [ABSTRACT FROM AUTHOR]