Hepatic damage in experimental and clinical paragonimiasis.

The hepatic damage induced by Paragonimus skrjabini, and the migration route of this species and that of P. westermani, were investigated in a series of animal experiments and in 34 clinical and four autopsy cases of paragonimiasis. The major symptoms and signs of an unique case reported from Sichuan Province included hepatic tenderness, disturbance of hepatic functions, remittent fever, and cough with bloody sputum. Laparotomy revealed marked adhesions surrounding the liver, spleen and duodenum. Diagnosis was made by finding P. skrjabini in a bulla on the abdominal wall about 5 months after the onset of illness. After specific treatment with bithional, body temperature and liver functions returned to normal. Twenty-three of 33 cases independently studied from Fujian Province also showed similar hepatic function disturbance. Autopsy cases showed hepatic chronic eosinophilic abscesses with Charcot-Leyden crystals. Experimentally, P. skrjabini infection caused hepatic damage in all laboratory animals used. The main pathologic changes were initially acute eosinophilic abscesses in the liver, worms being found sometimes in the necrotic cavities of the abscesses; hepatomagaly also occurred. Some cysts containing mature worms were found in the liver of dogs 3-9 months after infection. Numerous eggs were deposited in the cyst walls. The migration route of P. skrjabini was studied in young dogs. Worms appeared in the liver initially on day 3 and reached their highest level on day 14. P. westermani also migrated into liver, but their numbers were less than those of P. skrjabini.