EFFECTS ON THE ALIMENTARY CANAL 315 



tion of glands or villi. Later ('01a) Fede stated that the athrepsia of Parrot is 

 due to defective alimentation caused by gastrointestinal intoxication, while in 

 other cases infantile atrophy with profound malnutrition is secondary to syphilis, 

 tuberculosis, etc. 



De Lange ('oo) described marked atrophic intestinal changes in two cases 

 of pedatrophy. 



Heubner ('01, '01a) opposed the doctrine of a primary intestinal atrophy 

 as the cause of infantile atrophy, ascribing the appearance to physical distension 

 of the gut, and to postmortem changes. Nothnagel ('03) found the typical 

 atrophic changes in the intestinal wall in 80 per cent of all autopsies, irrespective 

 of the causes of death, and interpreted them as due to intestinal catarrh (even 

 without clinical symptoms). 



Bloch ('03, '04, '05, '06) described the usual variably atrophic changes in 

 the intestine of atrophic infants, and agreed with the previous investigators who 

 ascribed the changes primarily to intestinal distension or inflammatory compli- 

 cations. In addition, however, he noted a decreased number of Paneth cells 

 in the intestinal glands of Lieberkuhn, and thought this might be significant. 



Tugendreich ('04), however, could not confirm Bloch's observation of a 

 deficiency in the Paneth cells. After reviewing the various theories as to the 

 cause of infantile atrophy, Tugendreich concluded that "Mit der Ablehnung 

 der Darmatrophie ist das Wesen der Sauglingsatrophie wieder in tieferes Dunkel 

 zuruckgetaucht." 



Thiercelin ('04) described the intestinal lesions at various stages of infantile 

 atrophy. The intestine is increased in length, as found by Marfan in all 

 infantile chronic dyspepsias. There are progressive but variable atrophic 

 changes in the intestinal mucosa, and also in the tunica muscularis, with 

 degenerative changes in the plexuses of Auerbach and Meissner. 



Lucien ('08) found that in athrepsia the intestinal tract shows no constant 

 changes, and does not often present gross lesions. He doubted that the athrep- 

 tic condition is due to preceding gastrointestinal disorder, and ascribed it rather 

 to lesions in the hemopoietic system, the kidney and especially the endocrine 

 glands. Herter ('08) described a form of growth retardation due to chronic 

 intestinal infection and imperfect absorption of food in the intestine. 



Helmholz ('09), like Tugendreich (versus Bloch) found no deficiency in the 

 Paneth cells in atrophic infants. He concluded that postmortem changes 

 proceed more rapidly than in normal conditions. 



Stickel ('10) described the changes in a malnourished infant and starved 

 puppies. Schelble ('10) could find no structural changes in the intestine which 

 would account for the condition of pedatrophy, and ascribed it rather to a 

 general disturbance in the intermediary metabolism. 



Lesage ('11) described an atrophy in all the elements of the alimentary canal 

 of dystrophic infants. Eosinophile cells are said to occur in considerable 

 quantities, and to show some peculiarities. The muscle fibers are much 

 diminished in diameter (Variot and Ferrand). According to Lesage and Cleret 

 ('14), in congenital spasmodic atrophy the intestines sometimes show prolifera- 

 tion of the submucous connective tissue, but a leukocytic infiltration predomi- 



