BERI-BERI, a tropical disease of the greatest antiquity, and known to the Chinese from an extremely remote period. It gradually dropped out of sight of European practice, until an epidemic in Brazil in 1863, and the opening up of Japan, where it prevailed extensively, and the investigations into the disease in Borneo, brought it again into notice. The researches of Scheube and Bälz in Japan, and of Pekelharing and Winkler in the Dutch Indies, led to its description as a form of peripheral neuritis (see also Neuropathology). The geographical distribution of beri-beri is between 45° N. and 35° S. It occurs in Japan, Korea and on the Chinese coast south of Shanghai; in Manila, Tongking, Cochin China, Burma, Singapore, Malacca, Java and the neighbouring islands; also in Ceylon, Mauritius, Madagascar and the east coast of Africa. In the Western hemisphere it is found in Cuba, Panama, Venezuela and South America. It has been carried in ships to Australia and to England. Sir P. Manson has “known it originate in the port of London in the crews of ships which had been in harbour for several months,” and he suggests that when peripheral neuritis occurs in epidemic form it is probably beri-beric.
The cause is believed by many authorities to be an infective agent of a parasitic nature, but attempts to identify it have not been entirely successful. It is “not obviously communicable from person to person” (Manson), but may be carried from place to place. It clings to particular localities, buildings and ships, in which it has a great tendency to occur; for instance, it is apt to break out again and again on certain vessels trading to the East. It haunts low-lying districts along the coast, and the banks of rivers. Moisture and high temperature are required to develop its activity, which is further favoured by bad ventilation, overcrowding and underfeeding. Another strongly supported hypothesis is that it is caused by unwholesome diet. The experience of the Japanese navy points strongly in this direction. Beri-beri was constantly prevalent among the sailors until 1884, when the dietary was changed. A striking and progressive diminution at once set in, and continued until the disease wholly disappeared. Major Ronald Ross suggested that beri-beri was really arsenical poisoning. A natural surmise is that it is due to some fungoid growth affecting grain, such as rice, maize or some other food stuff commonly used in the localities where beri-beri is prevalent, and among sailors. The conditions under which their food is kept on board certain ships might explain the tendency of the disease to haunt particular vessels. Dr Charles Hose is the principal advocate of this theory. Having had much experience of beri-beri in Sarawak, he associates it with the eating of mouldy rice, a germ in the fungus constituting the poison. But Dr Hose’s views as to rice have been strongly opposed by Dr Hamilton Wright and others.
The most susceptible age is from 15 to 40. Children under 15 and persons over 50 or 60 are rarely attacked. Men are more liable than women. Race has no influence. Previous attacks powerfully predispose.
The symptoms are mainly those of peripheral neuritis with special implication of the phrenic and the pneumogastric nerves. There is usually a premonitory stage, in which the patient is languid, easily tired, depressed, and complains of numbness, stiffness and cramps in the legs; the ankles are oedematous and the face is puffy. After this, pronounced symptoms set in rapidly, the patient suddenly loses power in the legs and is hardly able to walk or stand; this paresis is accompanied by partial anaesthesia, and by burning or tingling sensations in the feet, legs and arms; the finger-tips are numb, the calf muscles tender. These symptoms increase, the oedema becomes general, the paralysis more marked; breathlessness and palpitation come on in paroxysms; the urine is greatly diminished. There is no fever, unless it is of an incidental character, and no brain symptoms arise. The patient may remain in this condition for several days or weeks, when the symptoms begin to subside. On the disappearance of the oedema the muscles of the leg are found to be atrophied. Recovery is very slow, but appears to be certain when once begun. When death occurs it is usually from syncope through over-distension of the heart. The mortality varies greatly, from 2 to 50% of the cases. The disease is said to be extremely fatal among the Malays. After death there is found to be serious infiltration into all the tissues, and often haemorrhages into the muscles and nerves, but the most important lesion is degeneration of the peripheral nerves. The cerebrospinal centres are not affected, and the degeneration of the nerve-fibres is more marked the farther they are from the point of origin. The implication of the phrenic and pneumogastric nerves, and of the cardiac plexus, accounts for the breathlessness, palpitation and heart failure; that of the vaso-motor system for the oedema and diminution of urine, and that of the spinal nerves for the loss of power, the impairment and perversion of sensation. According as these nerves are variously affected the symptoms will be modified, some being more prominent in one case and some in another.
Authorities.—See Sir Patrick Manson, Tropical Diseases (new ed., 1907), for a critical discussion of the subject, see The Times of 28th October 1905; a full bibliography is given by Manson in Allbutt and Rolleston’s System of Medicine (1907).