904 WAKD J. 



mission (1917) have emphasized the fact that pellagra originates where 

 insanitary surface privies are used and much less frequently where sani- 

 tary water-carriage systems of sewage disposal are properly employed. 

 This relationship has been confirmed by the independent work of Jobling 

 and Peterson (a). 



Experimental Inoculation. Attempts to produce pellagra by experi- 

 mental inoculation have, so far, failed in every instance to yield a 

 conclusive positive result. 



Pathological Manifestations and Course 



Clinical Course. Pellagra may prove fatal in three to five weeks 

 after onset or it may persist and recur for forty years. For a discussion 

 of the clinical features of the attack and the subsequent course of the 

 disease the reader is referred to the Third Report of the Thompson Pel- 

 lagra Commission and to the paper of MacNeal (1921). 



Pathological Anatomy. The gross appearance of the cutaneous lesions 

 has been best described by Merk. Histological studies have been made by 

 several authors but there is still lacking a systematic histological study 

 of the various stages in the evolution of the pellagrous eruption. In 

 general the changes in the skin would appear to result from the action of a 

 toxic irritant carried by the blood or lymph, to which the epidermis of 

 the backs of the hands is particularly sensitive. 



The nervous lesions have been somewhat more thoroughly studied. 

 In a rapidly fatal case, Singer found the most pronounced changes in the 

 Bete motor ganglion cells of the cerebrum and in the cells of Clarke's 

 column in the cord, coupled with fiber degeneration diffusely scattered 

 throughout the white matter and not particularly abundant in any tract. 

 Perivascular infiltration was lacking, in striking contrast to the pictures 

 seen in syphilis of the central nervous system and in trypanosomiasis, 

 In more chronic cases hyperplasia of glia about the blood vessels and 

 thickening of the vessels themselves are commonly found. The nervous 

 lesions also, like the cutaneous changes, t point to the action of a diffusely 

 distributed toxic substance in solution in the. blood and lymph. 



The lesions of the alimentary tract also vary with the stage of the 

 acute attack and represent only after-effects in the interval between 

 attacks. Most of the descriptions of the pathology have failed to take 

 into account the evolution of the lesions. During life, the hyperemia of 

 the mouth, pharynx and of the rectum are often prominent features of 

 the active attack. Autopsy at this stage nearly always reveals inflamma- 

 tion throughout the intestine, patchy in distribution. The duodenum, 

 lower ileum, caput coli and rectum commonly show the most severe 

 changes. This rather diffuse enteritis tends to heal with scattered small 



