Abstract
This study presents the first documented case of a disease syndrome in cultured largefin longbarbel catfish (Hemibagrus macropterus). The condition is characterized by massive abdominal pseudotumor formation, severe cachexia, and functional gonadal arrest. Comprehensive pathological investigation revealed that the pseudotumor was encapsulated by fibroblasts and primarily composed of host-derived, poorly differentiated hyperplastic cells, interspersed with invasive, basophilic Type III cells. These cells and associated inflammatory-fibrotic lesions were also disseminated in the gill, kidney and spleen. Systematic diagnostic approaches, including microbiology and transmission electron microscopy, found no evidence of conventional bacterial or viral pathogens. Metagenomic analysis further supported these findings and suggested a link to infection by an as-yet-unidentified eukaryotic parasite, with Microsporidia or Ichthyosporea being the primary candidates. Functional (KEGG) profiling of the pseudotumor tissue further revealed a molecular signature consistent with active cellular proliferation and metabolism. We propose that the pseudotumor acts as a metabolically active "nutrient sink," driving the systemic catabolism that underlies the severe cachexia and reproductive arrest. This work provides the first case of a eukaryotic parasite-induced pseudotumorous syndrome in fish, which represents an emerging threat to conservation aquaculture and offering novel insights into parasite-mediated host metabolic hijacking and tumor-mimicry.