Catarrhal Pancreatitis. 539 



microbes as in the infective catarrhal icterus. The blocking of 

 the common gall and pancreatic duct, by gall stones or biliary 

 products, will entail arrest of the discharge of pancreatic juice, 

 and a consequent pancreatitis, just as blocking with pancreatic 

 products will cause hepatitis and icterus. 



Lesions. The mucosa of the pancreatic ducts is reddened, 

 congested and thickened and their lumen blocked by a white, 

 granular matter, containing pus globules, fibrine filaments, and 

 granular, ciUated epithelium. The blocked ducts become di- 

 lated, and their walls thickened, the epithelium is desquamated 

 to a greater or less extent, and the raw exposed surface maj' pre- 

 sent ulcers or granulations. The pancreatic cells undergo fatt}' 

 degeneration and the connective tissue becomes steadily indurated 

 (sclerosis). These lesions were especially noted by Megnin and 

 Nocard in a case of pancreatitis in the hor.se. 



In the horse, sheep and goat, which have a common outlet for 

 the bile and pancreatic juice, the blocking of the latter and the 

 arrest of the bile almost of necessity causes hepatitis, and infec- 

 tion in the one gland is directly transferred to the other .so that 

 pancreatitis and hepatitis are mutually causative of each other. 

 In the ox, pig, dog and cat, in which the bile and pancreatic 

 juice are poured into the duodenum through separate ducts and 

 orifices, this mutual pathogenic action is not so certain. 



When the liver is implicated, there is catarrh and dilatation of 

 the bile ducts, fatty degeneration commencing in the centre of 

 the acini, pigmentation appearing at their periphery, and .sclerosis 

 of the organ follows. 



Symptoms. In Nocard's equine case there was progressive 

 loss of spirit, energy, and endurance; appetite was poor and 

 eating listless; after two weeks jaundice set in, the visible 

 mucosas and skin showing a yellow tinge, and the scanty urine 

 becoming brownish yellow ; the bowels became costive the faeces 

 being formed of small hard di.scolored balls, but no excess of 

 fatty matter is recorded. Emaciation advanced rapidly, the most 

 marked wasting being in the muscles of the back, loins and croup. 

 Death ensued at the end of two months from the commencement 

 of the illness. In man sudden, violent colic, with nausea, 

 tympany and collapse are prominent symptoms. 



Diagnosis is more satisfactory when with digestive disorder, 



