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MEDICAL SOCIETY OF LONDON

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340 owing to the danger of aggravating the disease ; in the third stage the drug could be pushed. Dr..T. H. SEQUEIRA referred to the case of a patient with advanced maculo-anaesthetic leprosy, a Kuropean, aged 44, who was given an injection of 100 c.cm. of a sterile s iline solution. Within half an hour of the injection he had rigors and the temperature rose to 100" F. A few days later he was given a similar injec- tion, and it was again followed by a rigor and the temperature was 101°. After this second injection the leprous eruption began to fade. A third similar injection resulted in a rigor and a temperature of 100.4°. Thereafter the lesions had disappeared and during the following 16 years had not recurred. , Dr. G. PERNET said that he had found that the best treatment of leprosy in the nodular form was chaulmoogra oil, but it must not be looked upon as in any sense a specific. Those who undertook treat- ment of this disease must remember how remarkably the bacilli were generalised throughout the body. He emphasised the importance of hygiene, good food, and fresh air, and suggested the use of thyroid extract because it increased general metabolism. Dr. G. C. Low agreed there was not yet available any specific cure for leprosy, but urged that the work being done on the subject, apparently with a con- siderable measure of success. should be persisted in. Mr. T. A. HENRY, D.Sc. (Wellcome Chemical Research Laboratories said that it was thought by chemists that the beneficial action of chaulmoogra and hydnocarpus oils in leprosy was due to chaul- moogrxc acid and hydnocarpic acid, which were now being administered in the form of sodium salts, ethyl esters, or carefully refined natural oils. Sir Leonard Rogers had pointed out that in order to be useful the acids must be employed in the liquid state, or nearly so, at the body temperature. A mixture of the two acids gave the best results, and American workers had been so impressed with this fact that they were importing the seeds of the various trees for cultivation fn their own country. Research had shown that mercury, gold, and copper compounds appeared occasionally to exert a favourable influence on buth tuberculosis and leprosy. Most hope seemed to centre round the mercury derivatives. Dr. ROBERT COCHRANE spoke of his experiences in connexion with the Mission to Lepers. He remarked that hydnocarpus oil with 4 per cent. creosote was now the cheapest of the remedies. Dr. E. A. O. TRAVERS gave an account of his work as physician at the Qualalumpore establishment in the Federated Malay States. There the main treat- ment was by the powdered whole nut of the hydno- carpus. Of his cases 81 per cent. were improved and 11.5 per cent. became negative under the treat- ment, while the improvement in the general health of most of the patients was remarkable. The remedy was taken by the mouth twice daily, and was popular. Injections were given in addition when a case did not seem to respond well. Dr. JAMES I-IA8S0N said he had found chaulmoogra disappointing, but most of his cases had the disease in an advanced form. He did not agree that the results of treatment by vaccines were due to protein shock ; he thought that the action of vaccines was specific. Dr. F. HALL spoke of his work of ten years at Fiji Leper Asylum. The tendency of leprosy, he said, was towards cure if cases came under care and were given the best conditions early. Intercurrent diseases must be carefully treated in every case. Sir LEONARD ROGERS said that though a 3 per cent. solution of sodium salts of the oils caused irritation in some patients, it did not do so in all, and he had found that a small vein would stand six injections of a 1 per cent. solution without pain, and that here was no preci- pitationin the vein. The cost was five doses for a penny. Moreover, the 1 per cent. solution was as beneficial as the 3 per cent. Recent researches showed that the situation was now much more hopeful. Leprosy was largely a question of house infection and means were at hand to reduce the disease to very small dimensions in two or three decades. In South Africa early sufferers were seeking to enter the sanatoria -a welcome change in the public point of view. lie concluded by paying a warm tribute to the work being done in this matter by the Americans. MEDICAL SOCIETY OF LONDON. AT a meeting of this Society held on Feb. 7th, Sir HUMPHRY ROLLESTON, the President, in the chair, Dr. F. M. R. WALSHE opened a discussion on , POLIOMYELITIS. Ilis-paper appears in full on p. 326 of this issue. Prof. JAMES MCINTOSH gave a summary of the experimental work which had been done on the aetiology and pathology of the disease. Acute anterior poliomyelitis, he said, was now a very clearly defined disease at the stage at which the paralytic symptoms had developed. Knowledge of its pathology was comparatively recent. It had been placed on a sound basis by the monographs of Harbitz and Vickman (in connexion with the Swedish epidemics) and by Miiller, Lansteiner, Levaditi, and others. In post- mortem exarninations of acute cases of the disease evidence was found of a toxaemia; mild degeneration of internal organs was found, and general enlarge- ment of lymphatic glands, including those of the intestinal canal. Tn the central nervous system, and especially in the cord, there were minute hæmor- rhages and congestion of the grey matter. Lesions of the central nervous system were practically con- fined to the grey matter of the cord : only rarely were there marked lesions in the cortex. There was definite involvement of the pia-arachnoid, particularly of the perivascular type-i.e., in the perivascular lymphatic sheath of the blood-vessels of the cord. The pia- arachnoid was found to be densely packed with cells. In the anterior horn of the grey matter of the cord there was an intense inflammatory reaction, with minute haemorrhages and destruction of the ganglion- cells. Later these were removed by the phagocytic cells. The main cells found were lymphocytes. but there was also a small number of the larger endothelial leucocytes, and some polynuclear leucocytes, and sometimes plasma-cells. The chief lesion of the cord was a degeneration of ganglion-cells, followed later by complete disappearance of the cells-hence the anaesthesia and the complete paralysis which developed. Softening of the cord occurred only in rare cases. Ilistological findings confirmed the conclusion arrived at earlier on clinical grounds that this disease was an acute infection. In 1909 Lansteiner and Kocher, working in Vienna. had succeeded, for the first time, in transmitting the disease to monkeys ; they took the spinal cord from a fatal case of the disease, ossified it in saline, and injected it into two monkeys by the intracerebral route, following a trephine opening ; 1 c.cm. of the fluid was injected and the monkeys developed the disease 16 to 18 days respectively after the injection, and had paralysis of the lower limbs. One of them died of the disease, and the lesion found in its cord was absolutely identical with that found in human cases. Confirmation of this had since come from practically every civilised country. In 1912 and 1918 Prof. H. M. Turnbull and the speaker had successfully done the same inoculation. It was not so easy to transmit the disease to rabbits. The Incubation Period and the Virus. It was always difficult to work out incubation periods of human infections, but work on monkeys showed an incubation period varying between 4 and 17 days ; it worked out in a number of cases at 9 to 10 days. In the Swedish epidemic the period was 14 to 16 days. The monkey when given the disease showed prodromal symptoms, was out of sorts, and lost relish for food ; it had tremor of limbs and the
Transcript

340

owing to the danger of aggravating the disease ;in the third stage the drug could be pushed.

Dr..T. H. SEQUEIRA referred to the case of a patientwith advanced maculo-anaesthetic leprosy, a Kuropean,aged 44, who was given an injection of 100 c.cm. ofa sterile s iline solution. Within half an hour of theinjection he had rigors and the temperature rose to100" F. A few days later he was given a similar injec-tion, and it was again followed by a rigor and thetemperature was 101°. After this second injection theleprous eruption began to fade. A third similar injectionresulted in a rigor and a temperature of 100.4°.Thereafter the lesions had disappeared and during thefollowing 16 years had not recurred. ,

Dr. G. PERNET said that he had found that the best treatment of leprosy in the nodular form waschaulmoogra oil, but it must not be looked upon asin any sense a specific. Those who undertook treat-ment of this disease must remember how remarkablythe bacilli were generalised throughout the body.He emphasised the importance of hygiene, goodfood, and fresh air, and suggested the use of thyroidextract because it increased general metabolism.

Dr. G. C. Low agreed there was not yet availableany specific cure for leprosy, but urged that the workbeing done on the subject, apparently with a con-siderable measure of success. should be persisted in.

Mr. T. A. HENRY, D.Sc. (Wellcome ChemicalResearch Laboratories said that it was thought bychemists that the beneficial action of chaulmoograand hydnocarpus oils in leprosy was due to chaul-moogrxc acid and hydnocarpic acid, which were nowbeing administered in the form of sodium salts, ethylesters, or carefully refined natural oils. Sir LeonardRogers had pointed out that in order to be usefulthe acids must be employed in the liquid state, ornearly so, at the body temperature. A mixture ofthe two acids gave the best results, and Americanworkers had been so impressed with this fact thatthey were importing the seeds of the various treesfor cultivation fn their own country. Research hadshown that mercury, gold, and copper compoundsappeared occasionally to exert a favourable influenceon buth tuberculosis and leprosy. Most hope seemedto centre round the mercury derivatives.

Dr. ROBERT COCHRANE spoke of his experiences inconnexion with the Mission to Lepers. He remarkedthat hydnocarpus oil with 4 per cent. creosote wasnow the cheapest of the remedies.

Dr. E. A. O. TRAVERS gave an account of his workas physician at the Qualalumpore establishment inthe Federated Malay States. There the main treat-ment was by the powdered whole nut of the hydno-carpus. Of his cases 81 per cent. were improvedand 11.5 per cent. became negative under the treat-ment, while the improvement in the general healthof most of the patients was remarkable. The remedywas taken by the mouth twice daily, and was popular.Injections were given in addition when a case did notseem to respond well.

Dr. JAMES I-IA8S0N said he had found chaulmoogradisappointing, but most of his cases had the diseasein an advanced form. He did not agree that the resultsof treatment by vaccines were due to protein shock ; he thought that the action of vaccines was specific.

Dr. F. HALL spoke of his work of ten years at FijiLeper Asylum. The tendency of leprosy, he said,was towards cure if cases came under care and weregiven the best conditions early. Intercurrent diseasesmust be carefully treated in every case.

Sir LEONARD ROGERS said that though a 3 per cent.solution of sodium salts of the oils caused irritation insome patients, it did not do so in all, and he had foundthat a small vein would stand six injections of a 1 percent. solution without pain, and that here was no preci-pitationin the vein. The cost was five doses for a penny.Moreover, the 1 per cent. solution was as beneficialas the 3 per cent. Recent researches showed thatthe situation was now much more hopeful. Leprosywas largely a question of house infection and means

were at hand to reduce the disease to very smalldimensions in two or three decades. In South Africaearly sufferers were seeking to enter the sanatoria-a welcome change in the public point of view.lie concluded by paying a warm tribute to the workbeing done in this matter by the Americans.

MEDICAL SOCIETY OF LONDON.

AT a meeting of this Society held on Feb. 7th, SirHUMPHRY ROLLESTON, the President, in the chair,Dr. F. M. R. WALSHE opened a discussion on

, POLIOMYELITIS.

Ilis-paper appears in full on p. 326 of this issue.Prof. JAMES MCINTOSH gave a summary of the

experimental work which had been done on theaetiology and pathology of the disease. Acute anteriorpoliomyelitis, he said, was now a very clearly defineddisease at the stage at which the paralytic symptomshad developed. Knowledge of its pathology wascomparatively recent. It had been placed on a soundbasis by the monographs of Harbitz and Vickman(in connexion with the Swedish epidemics) and byMiiller, Lansteiner, Levaditi, and others. In post-mortem exarninations of acute cases of the diseaseevidence was found of a toxaemia; mild degenerationof internal organs was found, and general enlarge-ment of lymphatic glands, including those of theintestinal canal. Tn the central nervous system, andespecially in the cord, there were minute hæmor-rhages and congestion of the grey matter. Lesionsof the central nervous system were practically con-fined to the grey matter of the cord : only rarely werethere marked lesions in the cortex. There was definiteinvolvement of the pia-arachnoid, particularly of theperivascular type-i.e., in the perivascular lymphaticsheath of the blood-vessels of the cord. The pia-arachnoid was found to be densely packed with cells.In the anterior horn of the grey matter of the cordthere was an intense inflammatory reaction, withminute haemorrhages and destruction of the ganglion-cells. Later these were removed by the phagocyticcells. The main cells found were lymphocytes. butthere was also a small number of the larger endothelialleucocytes, and some polynuclear leucocytes, andsometimes plasma-cells. The chief lesion of the cordwas a degeneration of ganglion-cells, followed laterby complete disappearance of the cells-hence theanaesthesia and the complete paralysis which developed.Softening of the cord occurred only in rare cases.

Ilistological findings confirmed the conclusion arrivedat earlier on clinical grounds that this disease was anacute infection.

In 1909 Lansteiner and Kocher, working in Vienna.had succeeded, for the first time, in transmitting thedisease to monkeys ; they took the spinal cord froma fatal case of the disease, ossified it in saline, andinjected it into two monkeys by the intracerebralroute, following a trephine opening ; 1 c.cm. of thefluid was injected and the monkeys developed thedisease 16 to 18 days respectively after the injection,and had paralysis of the lower limbs. One of themdied of the disease, and the lesion found in its cordwas absolutely identical with that found in humancases. Confirmation of this had since come frompractically every civilised country. In 1912 and 1918Prof. H. M. Turnbull and the speaker had successfullydone the same inoculation. It was not so easy totransmit the disease to rabbits.

The Incubation Period and the Virus.It was always difficult to work out incubation

periods of human infections, but work on monkeysshowed an incubation period varying between4 and 17 days ; it worked out in a number of cases at9 to 10 days. In the Swedish epidemic the periodwas 14 to 16 days. The monkey when given the diseaseshowed prodromal symptoms, was out of sorts, andlost relish for food ; it had tremor of limbs and the

341

temperature was raised. In from 24 to 48 hours

paralyses suddenly supervened, commencing usuallyin the lower limbs and thence extending upwards.In the monkey. in most instances, the disease wasfatal. In a few it was mild and transient and recoverywas quick. Investigations on monkeys showed thatthe responsible virus was a filter-passer ; it couldeven pass through some of the coarser porcelainlilters. For that reason it had not yet been cultivated.The research revealed the curious fact that the virushad some extraordinary powers of resistance. Aninfected cord could be completely dried over causticsoda and yet would remain virulent for 24 days ;it could be kept in ice indefinitely, or frozen, withoutits virulence being thereby diminished. Even a

j0 per cent. dilution of glycerine had no lethal effecton the virus which also showed a special resistanceto antiseptics ; apparently 5 per cent. carbolic hadno effect on it. On the other hand, it was verysusceptible to a 1 in 1000 solution of potassiumpermanganate, which killed it at once. Hydrogenperoxide was in the same category. This was impor-tant as it affected prophylactic measures directed tothe nasopharynx. The question of the distributionof the virus in the body had been worked at chieflyby inoculating monkeys with the organs of monkeyswhich had the disease or with the organs of humanbeings who had died of the disease. In the monkeydisease, wherever the inoculation was made—brain,peritoneum, skin, nerve-the result and the successionof symptoms was the same, being chiefly due to acord lesion. This demonstrated an extraordinarilyselective action on the spinal cord. The blood veryrarely contained the virus, nor did the spleen, liver,or kidneys. It had been discovered only in thecentral nervous system and the lymphatic system.

Mode of Spread.Vickman had attributed one outbreak in Sweden

to contamination by milk, continued Prof. McIntosh,and many patients suffered from gastro-intestinaldisorder. It was not, however, easy to give thedisease to monkeys by infecting their food. Thecommon portal of entry of the virus seemed to bethe nasopharynx. Plugging the nasal cavity of theanimals with infected material sometimes succeeded,but it was evident that the mucous membrane thereoffered some resistance. This was generally overcomeby abrading its surface. The spread of the diseaseby excretions and secretions had also been investigated.Vickman, in 1905, had brought forward evidence ofits spread by means of carriers, also by drawings andbooks. There had not yet been any satisfactoryevidence that bites of insects played any part indisseminating the disease. It seemed to be mainly spread by direct contact-i.e., by contamination bythe saliva and by coughing. The nasopharyngealmucus had been shown by Kling to contain the virusfor many weeks after an attack of the disease. Patientswho had recovered from one attack remained immunefor the rest of their lives ; monkeys which hadrecovered from an attack, even if abortive, could notagain be inoculated with the disease, and their serumwas found to have antibacterial properties. Thishad been the basis of attempted serum therapy,and good results were claimed for such treatment inFrance and America. The quick onset of the diseasewas, however, a practical difficulty. Experimentalattempts had been made to immunise monkeys byvaccination, either by means of a killed virus or anattenuated living one, and there had been somesuccess. As regards general measures of prophylaxisevery effort should be made to keep the nasopharynxas free as possible from infection. As the virusremained in the throat for some time after the diseasehad apparently subsided, cases should be isolatedfor about three weeks. Estimates of the prophylacticvalue of serum must rest on future experirnent.In the face of a big epidemic the speaker did not see whyattempts to vaccinate with the killed virus shouldnot be made. He concluded by pointing out possiblediagnostic errors, especially in regard to progressive

muscular atrophy of the infantile type, Landry’sparalysis, and forms of toxic neuritis.

Discussion.Sir THOMAS HORDER said that Dr. Mervyn Gordon,

whom illness prevented from being present, had senthim a communication in which he said that thecharacteristic lesions in poliomyelitis were two-thecondition termed neuronolysis and that namedneuronophagia. Thus there were the perivascularinfiltrative lesions, which were not so peculiar to thisdisease, and the more purely nervous specific lesionsinvolving the cells of the grey matter.

Sir Thomas Horder then spoke of the differentialdiagnosis of poliomyelitis from other acute infectionswhich had little or no specific effect on the centralnervous system. He said that pneumonia, and especiallythe broncho-pneumonia of children, might resemblepoliomyelitis when the subarachnoid was involved,and that in any case the possibility of encephalitis andinfective polyneuritis must also be carefully bornein mind. Three times he had seen retention of urineas the first symptom in poliomyelitis, all three patientsbeing young adults. Focal pains at the onset of theillness were significant, and should arouse suspicion.Generalised and especially local or focal tendernessand sensory disturbance he placed in the same cate-gory. Hexamine in full doses at the earliest possiblemoment seemed a likely mode of treatment ; he hadalso given salicylate of soda intravenously morningand evening for three to six days. In this diseasethe virus was a filter-passer, and he suggested-therewas an affinity between groups of infecting agentsand drugs. He had also given, as early as possible,collosol iodine intravenously.

Dr. JAMES COLMEB said that the finding of thevirus in the mouth of a person 17 days after an attackdid not mean that that person was capable of infectinga fresh patient with the disease. He related a numberof facts which had strengthened his belief that this.was a disease which was disseminated by non-sufferingcarrier cases.

Dr. A. F. HURST dealt with the administration ofhexamine in the disease. He believed that the reasonit had not given uniformly good results was that thedoses given were not large enough ; 10 even 20 gr.thrice daily was not nearly enough. If 60 gr. each ofpotassium citrate and sodium bicarbonate were givenat the same time, 100 gr. of hexamine could safelybe given thrice daily without any anxiety about theurine. He had not carried out this treatment inpoliomyelitis, but he had in encephalitis, and it waseasily borne by the patients.

Dr. H. M. RAVEN spoke as a patient who hadrecovered from the disease, and gave an accountof the Broadstairs visitation of poliomyelitis. Therehad been two or three cases at each of several schools,but half the epidemic had been in separate houses.From his observations and experience he could notconsent to the idea that dust and fiies could be leftout of the agencies of spread. During the epidemiche had found constipation very rife as well as somecases of suppression of urine. He reminded membersthat macerated flies had been proved to be capable ofinfecting monkeys.

Mr. R. C. ELMSLIE said that 30 per cent. or more ofthe cases of past poliomyelitis which he saw as asurgeon had not been correctly diagnosed when theyhad the acute disease. The brief febrile conditionwas apt to be unnoticed in little children. A largenumber of cases were not part of epidemics, butisolated cases. Often the diagnosis had to be madefrom some form of arthritis of the hip-joint. Twoor three years ago he with others had interestedhimself in the matter and had got the London CountyCouncil to agree to set aside a certain number of bedsfor segregating cases of poliomyelitis, but the purposehad been largely spoiled by the decision that to thesereserved beds no case could be admitted until threemonths had elapsed since the onset of the disease.

Dr. WALSHE and Prof. MCINTOSH very brieflyreplied.


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