Histopathological and functional evidence of intestinal mucosal disruption in emaciated olive flounder (Paralichthys olivaceus) infected with Enteromyxum leei.

Emaciation disease associated with Enteromyxum leei infection is a major health concern in olive flounder (Paralichthys olivaceus) aquaculture, but the structure-function basis underlying this condition remains incompletely understood. In this study, we investigated whether emaciation in E. leei-infected olive flounder is linked to intestinal mucosal disruption and impaired digestive and absorptive function. Fish were classified based on external appearance, relative condition factor, and polymerase chain reaction-based detection of E. leei. Infected fish exhibited markedly lower relative condition factor, hepatosomatic index, and viscerosomatic index, accompanied by increased gastrointestinal tract length. Histopathological profiling revealed region-specific parasite distribution from the pyloric caeca to the distal intestine, accompanied by mucosal fold shortening, epithelial disruption, goblet/mucous cell depletion, altered Alcian blue-periodic acid-Schiff staining characteristics, and reduced cholecystokinin-positive enteroendocrine cell density. In the anterior intestine, alkaline phosphatase, amylase, and trypsin levels were significantly lower in infected fish, whereas chymotrypsin and lipoprotein lipase did not differ between groups. At the transcriptional level, FABP2 and ApoA-IV were downregulated in infected fish, whereas HSL, LPL, SREBF1, and TRP2 were upregulated. Correlation analysis showed positive association between FABP2 expression and both amylase and trypsin levels, whereas the marked upregulation of TRP2 was not associated with a corresponding increase in trypsin levels. These findings indicate that E. leei-associated emaciation is characterized by intestinal mucosal failure, disruption of the digestion-absorption axis, and incomplete transcriptional compensation, supporting its interpretation as a maldigestion-malabsorption syndrome.