103 i

NUTRITIONAL DISORDERS
LATHYRISM

LATHYRISM

1037

Lathyrism is a common disease in certain parts of India, especially the United Provinces, the Central Provinces and several districts of Behar. In 1868 Irving stated that nearly 7 per cent, of the population of certain districts of the former were afflicted with the disease and Acton in 1922 found that in Rewah there were 60,OK) cases chiefly affecting- men in the early prime of life. In India it has been held for a long time that lathvrisni is due to certain poisonous substances occurring in the pea Lallivnis sativa {khesari dal). Buchanan in 1904 stated that continued consumption of k iicsari dal for some months together contributed to the causation of the disease. Lathyrus is a vetch, and the peas of three species, L. sativa, L. clyincnum, L. ccera are used habitually as an article of diet in India and Algeria by the people. When consumed in moderate amount they do not produce any symptoms, but in times of famine increased consumption has given rise to epidemics of severe poisoning especially among the poorer classes who subsist on them. Besides in India outbreaks have also occurred in Italy, France and elsewhere in Rurope. Occasionally similar symptoms have been produced in cattle. In the laboratory, feeding experiments give varying results as different species of animals vary greatly in their susceptibility to the poison. F<nvls, pigeons, and partridges eat the lathvrus pea freely and with apparent immunity; ducks are readily affected. Some animals fatten on this pulse while others are immune. Horses are particularly susceptible and have often died. The outstanding symptom in animals is muscular weakness; in acute poisoning with large doses the motor nerves arc depressed but in feeding experiments with repeated doses such an effect may not be observed. In chronic poisoning the deep reflexes are increased and in monkeys and horses spasmodic attacks may occur irregularly in addition to the paretic symptoms. Death results from paralysis of the respiratory muscles. In man the symptoms are usually precipitated by exposure to cold, wet and fatigue. Sometimes there may be prodromal symptoms, such as pnin, numbness and cramps. As a rule the patient suddenly feels the legs and loins heavy ; there is dragging of the legs, increased reflexes and more or less inability to walk. Later, there may be extrem* spasticity and rigidity of the leg muscles ; the case may progress to such a condition that he can only move his hands and feet in a sitting posture. Sensory disturbances and muscular wasting are not generally evident which point only to a partial degeneration in the cord. But in many cases symptoms such as loss of control of bladder and rectum, tingling, formication, lightning pains, diminution of tactile, heat and pnin sensations and marked muscular wasting have also Ix-en recorded.

The exact nature of the lesion, occurring in man, is not known. In experimental animals no lesion of the spinal cord or nerves have been found, but well-marked degenerative changes in the ganglion cells of the grey matter of the cord, in the vagal and accessory nuclei of the medulla, in the lateral columns and motor nerve roots of the spinal cord, and in the recurrent laryngeal nerves together with thickening of the walls of the arterioles and capillaries in the spinal cord have been described in horses. Though the disease has been attributed for a long time to the consumption of the lathyrus pea in sufficient quantity over a sufficient period of time, the exact factor responsible for its production is not yet settled. Acton (1922) describing some cases in Rewah stated that Lathyrus sativa peas caused paralysis and death in ducks, but after the pulse had been steeped in water the animals lived and thrived on it. This is due to the fact that the poisonous principle is soluble in water, and can be removed by soaking the grain for 24 hours in three changes of water. It has been found however that some crops will apparently produce lathyrism while others will not and the experimental work by various workers has given discordant results as to the poisonous properties of lathyrus. Howard, Simonson and Anderson (1925) in an elaborate stndy of the subject concluded that khesari dal (Lathyrus sativa) did not contain any poisonous bases at all, and did not produce symptoms of paralysis in ducks that had been fed exclusively on this vetch, provided it had been freed from a closely allied vetch, Vicia sativa (akri or akti). When l'icia sativa was given to ducks and monkeys in the proportion of 10 to 50 per cent, in the food, it produced symptoms of nervous disease very similar to those of lathyrism, followed by death. They concluded that lathyrus is chemically free from any poisonous alkaloids and that these grains are harmless and even nourishing to these animals. Though some of the symptoms resemble those occurring in human lathyrism they are not prepared to state, in the absence of definite pathological proof, that akti is the cause of lathyrism in man. Acton and Chopra (1927) investigated the problem of the part played by Lathyrus sativa in the causation of lathyrism ; they concluded that lathyrism is due to a contaminating weed Vicia sativa in khesari dal and not to any poison in the latter. The non-germinating seeds of Lathyrus sativa freed of akti contain no alkaloid or toxic substances and similarly the seeds that have germinated for 48 hours and previously freed from akti likewise produce no toxic symptom in experimental animals. The toxic principle divicine resides in the contaminating weed. This is probably closely related to barbituric acid which forms a toxic principle in many drugs such as, veronal, luminal, etc. Divicine can be split into barbituric acid by hydrolysis when the two NH 2 groups are replaced by an H and O group and it is probably due to this hydrolysis of barbituric acid that some toxic substance is formed which acts

1038

NUTRITIONAL DISORDERS

INFANTILE BILIARY CIRRHOSIS

1039

on the centI nervous system. It lia? been found that dose; of 50 ntgtn. of this toxic base ran produce paralysis of the hind legs of guinea-pigs. The reason why lnthyrism is not prevalent throughout the year is the fact th.it in ordinary years klicsati dal is free from this contamination and hence no lathyrism occurs, but during the period of famine the diet "f poorer classes of people is wholly made up of an imported variety of lathvtus contaminated with akti, as it is the cheapest food available at the time. Moreover when a deficient diet, such as a whole diet of khesari </a/ is consumed, the general resistance of the body is lowered so that the poison can act more powerfully on the individuals. Young (1927) made a contribution of a different nature. As a result of extensive investigations he found this akti contamination to be so rare that it could have but little, if any, effect in producing symptoms of lathyrisni. In his cases lathyrism occurred when Lathyrus sativa predominated in tlie diet. In addition an analysis of the diet of those people showed that there was marked lack of fat soluble vitamin A, and he is inclined to believe that lathyrism may be to some extent, a deficiency disease. Stockman (1929) conducted a series of experiments on different species of animals and stated that lathyrus peas contain a poisonous principle and it is the cause of lathyrism, but as it is present in very small amount, its isolation in a pure state and in sufficient quantity has proved to be extraordinarily difficult. Many samples of lathyrus peas are non-poisonous or practically so unless consumed in large quantities. In human epidemics not all those wh<> consume the pens nrc affected. This is due to the fact that there is great difference in the susceptibility of different species and of individuals of the same species of animals to these poisons, and hence results ;ire- variable. Stott (1929) "ii the other hand, carried out investigation on horses by feeding them both with Lathyrus sativa, Vida sativa, and keeping one a? control. At the end of 4-] months all ponies were in the sanie excellent condition and had put on weight. It therefore appears that experimental proof of the factor responsible for the production of lathyrism is not corrol>orative, and further investigation into the problem is necessary. Prophylaxis and treatment. The prevention of the disease depends on the improvement of the economic condition of these people and abolition of the system of bondage that exists in some states of India at present. Howard suggests that khesari dal should be planted in drills and the contaminating Vicia saliva removed by weeding. This should be done not only in places where lathyrism is rife but also in those areas from where the imported grain is sent to the famine stricken areas. But in view of the divergent views on the part played by vicia in the

spread of the disease, no successful measures can yet be devised. Nourishing diet is obviously of value. There is no specific treatment. The paralysed parts should be kept warm; massage and electricity are indicated. INFANTILK BILIARY CIRRHOSIS In the tropics the liver is particularly liable to be affected in a variety of conditions. Malaria, kala-azar, amoebic dysentery, are all known to cause derangement of the functions of the liver. The frequency with which hepatitis or even abscess of the liver follows an attack of amoebic dysentery, if left untreated, is too well known. Malaria and kala-azar are known to produce cirrhosis of the liver with ascites. Various parasitic infections of the liver, such as hydatid cyst, bilharzial cirrhosis, etc., arc of common occurrence in the tropics. The treatment of these conditions naturally lies in removing the cause of the disease. Reference to these has been made in appropriate chapters. Besides the various affections of the liver enumerated, a form of cirrhosis of the liver, affecting especially children under one year of age, has been noticed. In India it is common in Bengal, Madras and Bombay Presidencies. As a rule it runs a more or less protracted course of about eight to ten months ; sometimes the disease may terminate in death in 2 or 3 weeks. The clinical picture of a case may resemble greatly the features of acute yellow atrophy or the hypertrophie cirrhosis described by Hanot. The recognition of a case of infantile biliary cirrhosis does not, as a rule, offer much difficulty. The classical signs of hypertrophie cirrhosis of the liver, such as enlargement of the liver, ascites, dilatation of the abdominal veins, jaundice, clay-coloured stools are present in the majority of cases. Some cases however are known to begin with symptoms of catarrhal jaundice followed by signs of acute necrosis and acute insufficiency of the liver. Ultimately the patient develops deep jaundice, oedema of the eyelids and lower extremities with a considerable amount of ascites, enlargement of the liver and sometimes of the spleen. The known causes of catarrhal jaundice, such as, congenital syphilis, enteric fevers, Weils disease and many chemicals including organic arsenicals, phosphorus, cinchophen, etc., may be excluded as causative agents in this condition. It has been stated that the condition is due to infection with a virus. Though definite proof of this is lacking, it is possible that the acute necrosis that occurs in these cases is due to superadded