Murlin12 found that the quantity of hippuric acid excreted by pellagrins, especially those kept on a corn-vegetable diet, was from two to three times the quantity excreted by normal men on a normal diet, and suggests that this may be a factor of some importance in connection with the disease.

Voegtlin and Harries12a made chemical analyses of the breast milk from five cases of uncomplicated pellagra and found no striking deviations in composition from normal human milk. Lactose, fat, total N, and total solids were within normal limits but below the average. Casein and lactalbumin showed but a very moderate diminution. Total ash and P205 content were normal. CI and Na were present in larger amounts than normal. The percentage of Ca, Mg and K was slightly below normal. Tests were not made for the vitamin content of the milk, and it may possibly have been lacking in these compounds. The total volume of the milk was frequently greatly diminished. Both total N and non-protein N in the milk were apparently increased by a change from a low-protein to a high-protein diet.

Gastric digestion is frequently below normal, due to hypoacidity13 and to reduced pepsin content14 in the gastric juice. Preti and Pol-lini15 report that several enzymatic processes are either entirely suppressed or proceed irregularly. In many cases neither rennin nor rennin zymogen could be detected and failure of the proteolytic and amylolytic power of the feces was also observed. Some cases are characterized by profuse diarrhoea, others by persistent constipation.

12 Murlin, Hyg. Lab. Bull. 116, p. 45, 1920.

12a Voegtlin and Harries, U. S. Public Health Ser. Hyg. Lab. Bull. 116, 73, 1920.

13 See Meyers and Pine, Am. J. Med. Sci. 145, 705, 1913.

14 Hunter, Givens, and Lewis, Hyg. Lab. Bull. 102.

15 Preti and Pollini, Rif. Med. 1911, No. 27; Zentr. Bioch. Biophys. 13, 54.

A great variety of theories have been advanced as to the cause of pellagra. From the frequency of its occurrence among maize-eating people it was at one time believejl that this grain or some constituent of it was responsible,16 but this hypothesis, so far at least as it supposes a toxic substance in or formed from maize, has been discredited.17

Voegtlin18 concluded from the clinical and pathological aspects of the disease that it represents a chronic intoxication from some unknown substance in the vegetable food, but notes that deficiency of either vitamins or amino acids might also be accountable.

Raubitschek 19 regarded the symptoms as due to a photodynamic action of sunlight in the presence of some constituent of corn. This view is supported to some extent by Suarez,20 but disputed by Ruhl21 and Rondoni.22 Allcsandrini and Scola 23 suggest that pellagra is silica poisoning, due to the presence of colloidal silica in the drinking water. Aulde 24 has advanced the theory that calcium depreciation is responsible. Blosscr25 ascribes it to excess of sugar cane products in the diet, since exclusion of partially refined sugars and sirups from the diet was followed by a cure in 121 of his cases and improvement in eight, while four died. Yarborough26 regards it as an autointoxication (acidosis) due to a diet rich in carbohydrates. Certain authors have endeavored to trace a connection between the intestinal bacteria and pellagra.27 Others28 have regarded it as an infection, probably of a protozoal nature, carried by sand flies. All attempts to transmit the disease from one person or one animal to another have failed, however.29

16 See Horbacxevaki, Gas. Lek. Cee., 1020, No. 37; Zentr. Bioch. Biophys. 10, 032; Carbone and Caxaamalli, Giora. r. soc. ital. d' igiene, 1914, 5, 51, 00, 151; Zentr. Bioch. Biophys. 17, 635, 1015; Volpio, Pathologica, 5, 174; Zentr. Bioch. Biophys. 16,370; Volpino and Bordoni, Pathologica, 5, 602; Zentr. Bioch. Biophys. 18, 450, 1015; Rondoni, Sperimentale, 60, 723, 1015; Trop. Dia. Bull. 7, 63, 1016.

17 Sainton, Brit. Med. J. 1013, ii, 1, 0, 207.

18 Voegtlin, J. Am. Med. Aas. 63, 1004, 1014.

19 Raubitachek, Centr. Bakt. 1, Abt. Orgi. 57, 103; Wiener Klin. Wochena., 1010, 063.

20 Snares, Bioch. Z. 77, 17, 1016.

21 Ruhl, Dermatol. Woch. 60,113,151,176, 1015; Trop. Dis. Bull. 7, 65, 1016.

22 Rondoni, Lo speriment, 65, 307; Zentr. Bioch. Biophys. 12, 716.

23 Alleeandrini and Scola, Z. Chemother. Orig. 2, 156.

24 Aulde, J. Med. Rec. 00, 181, 1016.

25 Blower, South Med. J. 8, No. 1; J. Am. Med. Ass. 64, 573, 1015.

26 Yarborongh, Med. Rec. Sept. 1016.

27 Neuaaer, Wien. Med. Presee, 1887, iv, 146. De. Giaxa, Annali dTgien. Soer. Roma, 1802, 1003; McNeal, Am. J. Med. Sci. 145, 801, 1013.

28 Sambon, J. Trop. Med 13, 271, 287, 305, 310,1010; Roberts, J. Am. Med. Abb. 56, 1713, 1011.

The Thompson Pellagra Commission30 has compiled a mass of evidence which they believe indicates that the disease is communicable and has its origin in defective sanitary conditions. They state that new cases usually occur during or within six months of residence in close proximity to a pellagrin in the active stage of the disease, and that the installation of a water-carriage system of sewage disposal at Spartan Mills, without any change in the habits or mode of life of the inhabitants, transformed the community from a pellagra focus to one in which pellagra no longer spreads. Although old cases still suffer recurrence, even these have decreased in number.

29 Lavinder, Francis, Grim, and Lorenz, J. Am. Med. Ass. 62, 1003, 1014; Goldbergcr, Publ. Health Repts. 31, 3150, 1016.

30 Siler, Garrison and McNeal, 2nd and 3rd Repts. Thompson Pellagra Commission.