Myxosporean disease caused by Carassius auratus gibelio in Yancheng City, Jiangsu Province, China, in recent years. The pathogen specifically parasitizes the pharyngeal tissue of C. auratus gibelio, histopathological observations at different stages of the disease, and pathophysiological analyses in the middle stage of the disease, were carried out. Histopathological results showed that, at the trophozoite stage, M. pharynae parasitized the pharyngeal submucosa of fish, resulting in slight hyperemia of the pharynx, and sporocysts were formed by fibroblast packages, but no pathological changes were found in other tissues and organs at this early stage of the disease. The pharynx was greatly enlarged in the middle stage of the disease due to the increasing number of small sporocysts and proliferation of trophozoites, which developed into mature spores that formed a large sporocyst. Serious congestion appeared within the walls of sporocysts, which were mainly composed of the connective tissue of fibrocytes, collagenous fibers and elastic fibers. The nuclei of fibrocytes underwent karyopyknosis and necrosis, and there was atrophy in the connective tissue in the walls, which gradually thinned. Pale staining was seen in epithelial cells and taste buds in the pharyngeal mucosa, which eventually became necrotic. Cell hyperplasia mainly appeared in secondary gill lamellae. Renal glomeruli expanded, hyaline degeneration appeared in renal tubular epithelial cells and necrocytosis occurred in some parts of the kidney. No pathological changes appeared in the liver, spleen, intestine or in the head of the kidney. Further necrotic tissues and cells in the walls of sporocysts, and in the pharyngeal mucosa and submucosa, resulted in holes through which mature spores and necrotic tissues passed into the blood stream during the late stage of the disease. Many necrotic cells and mature spores came from necrotic pharynx regions in the intestine. Histopathological changes in other organs and tissues were similar to those in the middle stage of the disease. Pathophysiological analysis in the middle stage of the disease showed that the number and size of red blood cells, hemoglobin, thrombocytes, total pro-tein, albumin, globin, glucose, alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase in the diseased fish were significantly lower than those in the healthy fish (<0.01). Erythrocyte osmotic brittleness, numbers of white blood cells, neutrophils and monocytes, and total bilirubin, creatinine, urea and lactate dehydrogenase were significantly higher in the diseased fish than those in the healthy fish(<0.01). There were no significant differences in lymphocytes and eosinophils between diseased fish and healthy fish (>0.05). Diseased fish eventually died because of feeding difficulty and respiratory dysfunction caused by the enlarged pharynx, which blocked the oropharyngeal cavity, leading to hyperplasia in secondary gill lamellae, kidney lesion, anemia and other changes and further necrotic pharyngeal tissues forming a bleeding hole.