Abstract

Changes of abdominal organs in early paragonimiasis are described in dogs and cats. Experimental infection was induced by feeding 40-50 and 20-30 metacercariae of Paragonimus westermani to 15 dogs and 15 cats respectively. These animals were killed sequentially starting from 8 days to 120 days after infection. Complete autopsies were carried out in all animals and the tissues were examined microscopically with the main emphasis on changes of the liver and the diaphragm. A definite bout of acute diffuse fibrinoexudative peritonitis with ascites ranging from 5 to 20 ml was present in both dogs and cats at the time of 20 days after infection. This was also the period of the maximum liver damage and diaphragmatic injuries. The peritonitic changes became minimized after 45 days of infection. The liver changes were of two folds. The first one was characterized by numerous pin-point or linear tissue defects on the surface of the lobes, which were often covered with fibrin clots. Some of these defects were impacted by the larvae. These 'scratch' marks appeared to be of mechanical effect, and the margins were often banal without a significant inflammatory reaction. The scratch marks were no longer observed in animals examined after 45 days. The second was noted in the Kupffer cells of the liver. A large amount of hemosiderin pigment was noted in the Kupffer cells and became prominent by 20 days through 45 days. Hemosiderin-laden macrophages were found also in the spleens of these animals. Some animals in 30 days group showed the most Kupffer cells heavily loaded with hemosiderin. However, no associated degenerative changes were noted in these cells. The diaphragm was quite unique in early phase of infection in all animals examined. Numerous pinpoint perforative lesions could definitely be seen grossly, and some of these lesions included migrating larval worms inside the tunnels. These lesions were microscopically characterized by tract or tunnel formation with accompanying tissue reaction. The diaphragmatic changes were manifest by 20 days after infection. The tracts of tunnels appeared to have been made by pressure necrosis and surrounding edema, and subsequently were associated with a massive eosinophilic influx and myocytolysis. The eosinophilic abscess and multinucleated giant cells were often observed in the animals of the 30 days group. The diaphragmatic changes seemed to be repaired with or without fibrous scar formation which was occasionally seen in 45 days and later.