JULY, 1939] 421

Indian Medical Gazette

JULY

LATHYRISMIT is an everyday experience to encounter

victims of lathyrism in the streets of Calcutta.These people usually come from North Bihar orthe United Provinces and are beggars by occupa-tion. Most of them have been cultivators orlabourers, and the usual account they give ofthe onset of their disability is that during someyears of scarcity they had to live mainly onchick pea? and that the disease then began, in-sidiously in some cases, suddenly in others. Thedisability gradually increased until they couldwalk only with the help of sticks, their legsstiff, weak and trembling and their gait spasticand scissors-like. In advanced cases progres-sion is effected by crawling on the balls of thefeet and on the hands.

Lathyrism was first recognised in Europe overtwo hundred and fifty years ago, and it isobvious that even in those early and unscientifictimes it was ascribed to the ingestion of theseeds of various species of the genus Lathyrus,because as early as 1671 the Duke of Wurtum-berg issued an edict forbidding the use of theseseeds. Later, it was observed in Italy, France,Algeria and certain eastern countries. It is nowrarely seen in Europe and the chief interest inthis disease at present centres in India where itis shown to have been prevalent for at least aslong as written records of Indian history existand where it is still one of the most importantcauses of paralysis and deformity among thepoorer sections of the population in certain partsof the country. During the last hundred yearsit has been frequently reported upon by writerson medical matters of local interest and import-ance, and a great deal of the most recentresearch" on the still-disputed aetiology of lathy-rism has emanated from workers in India.

The disease is regarded as a form of foo'dpoisoning by most authorities and, as the nameimplies, substances in the seeds of the genusLathyrm have usually been considered to be itscause. In India, the species held responsible isLathyrus sativus. Stockman and Dilling bothlent support to this theory because they inde-pendently isolated from the seeds of this plantalkaloidal substances which when inoculatedinto animals produced symptoms suggestive oflathyrism. Acton and Chopra also held theopinion that the seeds of L. sativus contained atoxic substance, but the toxin they isolated, andwhich caused lathyrism-like signs in monkeysand ducks, was a water-soluble amine. So that,although these workers are all in agreement asto the seeds being the cause, they are at variance

as to the actual offending substance. Furtherevidence adduced by still other workers, as aresult of animal experiments, are also conflicting,probably because samples of seeds of L. sativusare very frequently contaminated by seeds ofvarious unidentified weeds, which most likelyplay some part in the production of these vary-ing results recorded. Howard, Simonsen andAnderson showed that botanically pure lathyrusseeds could not produce any toxic effect, but acontaminant of the lathyrus seed, Vicia sativa{akta), contained bases having alkaloidal prop-erties, which produced definite signs of poison-ing with involvement of the central nervoussystem in laboratory animals such as guinea-pigs. McCombie Young was of the opinion thatdeficiency of vitamins, particularly vitamin A,was a factor in the production of the disease.Stockman later reported that watery extract oflathyrus contained a salt of phytic acid whichwas toxic to the brain and spinal cord. Stottcould not reproduce the symptoms in horse? byfeeding them on L. sativus or V. sativa.

The above brief outline shows that there aretwo main views regarding the causation of thedisease, viz, (a) that it is due to food intoxica-tion, either by Lathyrus sativus or by Viciasativa and (b) that it may be to some extent adeficiency disease.

In this issue of the journal there is a papersetting forth the details of an outbreak of lathy-rism in a Punjab village, this village is in anarea where there have never been cases oflathyrism before. The paper brings out severalfeatures of interest. The disease affected theSikh agriculturists mainly, and three males toevery two females suffered. The pea Lathyrussativus was definitely not the cause of the disease,as this was not cultivated in the locality, nordid it occur as a contaminant of other cereals.It was finally found to be caused by ingestion offlour made from wheat that contained seeds ofVicia sativa. This vetch seems to have occurredas a weed in the wheat fields and was harvestedalong with the wheat. Inspection of the wheatshowed the presence of these seeds and theidentification of them as V. sativa was definitelyestablished, as plants grown from the seeds werefound to be the same specimens as of V. sativaplants supplied by a botanist.

The symptoms "of the disease became aggra-vated whenever the people took bread made fromthe old stock of wheat that was contaminatedwith vicia seeds; wheat from other sources hadno such effect. These findings have lent supportto the V. sativa {akta) contamination theoryof Howard, Simonsen and Anderson and ha:ruled out the possibility of L. sativus being th*noxious agent. Avitaminosis cannot be dismmissed completely as a possibility in view of th*poverty of the people, but avitaminosis, i Çpresent, must have been there for years whiKthe epidemic of lathyrism followed the harvesting of the wheat crop contaminated witLV. sativa seeds.

422 THE INDIAN MEDICAL GAZETTE [JULY, 193S

The disease ua a rule runs a very chroniccourse and there is little possibility of cure inthe sense of restoration of function of the limbs;therefore prevention should be aimed at.

From the above discussion it seems clear thatlathyrism might be greatly reduced, if notaltogether stamped out, in India, by education

of the agricultural population so that they migappreciate the danger of akta seeds mixed wcereals. They might also be given instructichow to recognize the plant V. sativa in its youstages before seeds are formed so that it coibe removed from among wheat cropsweeding.

Special Article

SNAKE BITES AND THEIR TREATMENTIN INDIA

PART II

THE MANAGEMENT OF SEQUELAE AND COMPLICA-TIONS

By R. X. CHOPRA, d.E., M.V, MJJ, SC.D. (Cantab.).F.R.C.P. (Lond.)

BREVET-COLONEL, I .M.S.

Honorary Physician to the King

andJ. S. CHOWHAN, CAPTAIN, M.B., 3.S., A.I.R.O.

(School of Tropical Medicine and Hygiene, Calcutta)

IntroductionTHERE are about 15,000 species of snakes in

the world and about 110 varieties exist in India.Out of these only 69 species are poisonous (40land and 29 sea snakes). Excluding thepoisonous sea snakes it is apparent that one isexposed, taking India as a whole, to the bitesof 81 species out of which only 40 (50 per cent)are poisonous. The commonest poisonous snakesare the cobra, krait, dáboia, echis and pitvipers.

Of the persons bitten by poisonous snakes,about half may not receive a fatal dose; thebite may have been through thick clothes, thefangs may have simply grazed the skin, or theattack has been unsuccessful and the venomhas only been spilled on the surface of the intactskin and so does not find its way into the tissuesand get absorbed. The fangs may have hit abony portion of the limb or the bite may be onfingers or toes from which absorption into thegeneral circulation takes place slowly. Underthese circumstances the usual procedure ofincision, ligature, suction, cauterization, etc.,may be effective. Therefore even of the 50 percent of cases bitten by poisonous snakes, onlyhalf the number (20 to 25 per cent) are inreality in a serious condition and need immediateattention and prompt treatment in order to savetheir lives. Clark (1928) reported on 46 casesof snake bite. In half the cases the snakes werenot indentified or caught and 10 per cent werefatal and these were from the bite of L. atrox.and L. mutans (Bushmaster). The bitesrecorded there were on hands and fingers in 20cases, wrist and forearm in 6, shoulder in 1,foot or toes in 10, leg in 1 and thigh in 1. Basu

(1938) reported on 27 cases of snake bite amitted into the Medical College HospitaCalcutta, for treatment. Out of these 74 \cent were vipérine and 26 per cent colubribites. The death rate was 60 per cent. Inthe cases local infiltration with gold chloride aintravenous injections of Kasauli mixed anvenene were administered. He is of opinithat the present treatment of both the scorpiand snake bites is unsatisfactory and a bet-form of treatment should be worked out.

The above figures show that hardly 25 rcent of all persons bitten are in real dangerlosing their lives and if adequate and proirmeasures are taken we may be able to savegood number of these lives also. Our effortthis paper is to outline the present situatiregarding snake bite poisoning and to point cwhat treatments should be carried out in diffient stages of poisoning and for the diffèresequelae. Keeping in view the fact that speciantivenene and expert medical aid is not readavailable in the places where snake bites usuaoccur, the following measures may be fouuseful :—

In persons who are badly bitten, where ivenom has found a direct passage into a laivessel, and if more than half an hour has elapsbetween the bite and the availability of pro]medical aid, so much harm has probably bedone that there is not much chance of savilife. Frequently such cases occur in out-of-tlway places and jungles where medical aid aantivenene are not available.

Acton and Knowles (1914),Bannerman (19Jand Chopra and Chowhan (1935a) have reporthat almost all the poisonous snakes, wl:giving a good and satisfactory bite, inject a d<ranging from two to fifteen times the minim'lethal dose for man. Fitzsimons (19Íobserved that two drops of venom usually coprise a fatal dose for a strong healthy adman. An adult cobra or mamba is capabledischarging as much as 8 to 10 drops of venat a bite. On an average, an adult cobrajects about five to six drops of venom insingle bite. It is obvious therefore that this little hope of recovery for a person whobitten by an adult cobra when the lattergiven a successful bite. In such cases the ^tims rarely survive over six hours, unless spectreatment is given immediately. This being