In 1898 Hirota first noted the existence of a condition in infants nourished by beriberi mothers which has more recently been carefully studied by McLaughlin and Andrews and to which the name infantile beriberi is now generally given. In the Philippines it is called “taon.” Clinically there is restlessness, vomiting, altered voice, increased heart action, oedema and cyanosis. After death there is found a marked hypertrophy and dilatation of the right side of the heart with no change of the left side. The peripheral nerves also show the lesions of beriberi of adults but of less intensity. The disease most often shows itself in an acute form, the child rather suddenly being seized with great pain, crying constantly and soon becoming cyanosed. Death, which may occur in a few minutes or hours, is often thought to be due to meningitis, although there is no fever or true convulsions. There is only rigidity of the body. Less frequently the disease appears in a chronic form in which vomiting and constipation are most marked. There is often a history of the loss by the mother, who herself may have only a rudimentary beriberi, of several children from this disease. The infants improve rapidly when other infant feeding is substituted for the mother’s milk. An extract of rice polishings gives striking results in these cases. _Asylum Beriberi._—The beriberi outbreaks which have frequently been reported from European and American camps, prisons and asylums do not differ from the cases one may see in the classical distribution of the disease among the rice-eating populations of the Orient. The cause is the same, a deficiency in beriberi-preventing vitamines, and the symptoms are similar. These vitamines may be deficient in the rice or other cereal or proteid food supplied. Again they may have originally been present in sufficient quantity but later destroyed by too great heat or otherwise. =Types of Beriberi.=—The ordinary clinical division of beriberi is into (1) _wet or dropsical beriberi_ and (2) _dry or atrophic beriberi_. At the same time, in a typical case, we find such a combination of the vasomotor disturbances which lead to the oedematous or dropsical manifestations of wet beriberi, and likewise of those of peripheral nerve involvement causing more or less development of muscular palsies or atrophies, as seen more strikingly in dry or atrophic beriberi, that it does not seem advisable to employ such a division. In fact typical cases of wet or dropsical beriberi after a profuse diuresis may change in a short time, as Manson has so aptly stated, from a bloated carcass to little more than skin and bones and assume all the appearance of a case of dry or atrophic beriberi.