Se 
Fe? ae Faroue .)« 
715 
and that, whatever might be the cause of the malady, we can not deny that diet 
seems to have a potent influence on its frequency. 
Two Japanese investigators, Ternuchi and Saiki,"° have carried on some chemical 
investigations on a beriberi case which showed cdema, paralysis, hypes- 
thesia and other disturbances of motion and sensation. They found no inter- 
ference with the digestion and absortion of nitrogenous food, but demonstrated 
that the nitrogen excretion in the urine was much increased, the amount being 
in excess of the nitrogen ingested. An increase in the amount of nitrogenous 
food taken into the system was followed by a proportionate rise in the amount 
of excreted nitrogen. These results are in opposition to some statements of 
Scheube and Durham, according to whom proteid metabolism in kakke patients 
is diminished. Careful urine analyses carried on in 43 cases of beriberi failed 
to show either albumen or sugar. 
Duerck * has recently studied beriberi in Sumatra, and his histologic investiga- 
tions confirm the description of the profound changes in the peripheral nerves 
and the skeletal muscles previously recorded by other writers. He advances the 
following hypothesis as to the cause of these lesions: 
“The ubiquitous character of the degenerative lesions in the peripheral nerves 
and muscles and the absence of such changes in other organs compels one peremp- 
torily to conclude that the harmful agent, acting in so specific a manner, can 
not be a liying organism either of a vegetable or of an animal type. One can 
not, of course, exclude the possibility that the non-vital poison may enter the 
body, perhaps through the intestinal tract by the aid of a micro-parasite. How- 
ever, if this be so, the absence of an obvious primary lesion or primary reaction 
is very striking. Lesions of the peripheral nerves caused by toxic substances are, 
of course, frequent. In this connection we may mention degenerations and 
inflammatory lesions due to alcohol, lead, arsenic, carbon bisulphide, ergotin, and 
other intoxicants; and it is also well known that substances formed in the body 
itself may, by processess of autointoxication, lead to lesions of the peripheral 
nerves.” 
Yamagiwa” has recently reaffirmed his former statements regarding the 
etiology of the disease in the following words: “Kakke or beriberi is an intoxica- 
tion due to the daily use of boiled rice which has been improperly stored and 
preserved. The intoxication causes a contraction of the small arterial branches 
of the circulation. This again produces dilatation and hypertrophy of the heart, 
local anemia of the skin, mucous membranes, peripheral nerves, muscles, and 
kidneys, and finally regressive metamorphoses in the tissues named.” 
Wright, in giving a summary of the theories regarding the etiology of the 
disease, mentions the following: (1) Gelbke’s theory that beriberi is due to 
dry fish infected with a trichina; (2) that of M. Miura that it is due to the 
ingestion of certain kinds of raw fish; (3) Grimm/’s theory that it is caused by 
the ingestion of infected fish; (4) Takagi’s that it is due to a pathogenic diet 
in which nitrogen is deficient; (5) Ross’s that it is the result of arsenical poison- 
ing; (6) the belief that it is due to the ingestion of moldy rice; (7) Braddon’s 
theory that the ingestion of a specific organism which develops on growing rice 
causes beriberi; (8) Manson’s that it is due to a place germ, and (9) Glogner’s 
that it is produced by a hemic plasmodium. 
” These investigations have not been published. I am indebted to Professor 
Shiga, of the Tokyo Institute for Infectious Diseases, where they were carried 
on, for a communication concerning their result. 
™ Duerck: Ueber Beriberi, etc. Miinch. Mediz. Wochenschrift. (1905), 52, 1913. 
“Yamagiwa (and Yamanowchi): Ueber das wesen der Kakke. NSalkowski 
Festschrift, Virchow’s Archiv., 156, 451. ; 
