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CHAPTER VIII.. Treatment.

Leprosy · G. Armauer Hansen — chapter 8 of 8 · ~9,725 words · public domain

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TREATMENT.

Since many cases of Leprosy terminate in cure by the disintegration and elimination of the bacilli, one might imagine that it would be a tolerably easy task to find a suitable treatment for the disease. But this is far from being the case. Treatment of Leprosy has been carried out from time immemorial. In the Bible there is little concerning any treatment which was regularly applied in Leprosy; the disease being apparently regarded as beyond human power. Later, all possible and, we may say, impossible remedies, such as the teeth of elephants, the flesh of crocodiles and serpents, the fat of panthers, lions and bears, and so on, were applied. In mediæval times, the same class of remedies was used along with religious incantations.

In the eighteenth century, Schilling tells us he treated leprosy with success. For the first three months he ordered a rather sparing diet, consisting of bread, vegetables and soup. The real treatment began with purgatives, “not mineral ones, because these are dangerous for lepers, and often produce dangerous diarrhœa,” and was followed by warm baths, “with circumspection, when the disease is far advanced, because they produce palpitation of the heart, convulsions and fainting fits.” In addition to advising frequent exercise in the open air, Schilling regarded it as important to dilute the diseased humours by large quantities of purifying fluids, of which he used first emollient decoctions, and later, powerful sudorific ones. As mild ones he used barley water, infusions of herbs, Agrimony, Hedera terrestris, Fumaria, Veronica, etc., to which were sometimes added other softening and purgative remedies, such as Malva, Parietaria, Senna and Rhubarb.

Of these the patients took, for six weeks, 3 to 4 litres daily. He then gave powerful resolvents and sudorifics, as Saponaria, Zedoaria, Sassafras, Juniper, Fol. Scolopendrii, herb. Cardui benedicti, Pareira brava, etc. The more the patient could take, the more rapid and complete, according to Schilling, was the cure. Rich food and good wine might be given. During the treatment the patient had to guard himself from cold air. After three months the patient was bled, as much blood being taken as his strength would allow. The external remedies which were used when there were putrid ulcerations, and when fingers and toes commenced to fall off, were tincture of aloes, myrrh, and succini, which were dropped on lint and applied twice a day. Both the pharmaceutical and the dietetic remedies were to be persevered with until definite signs of cure were manifest, and the treatment was to be continued for many months after apparent recovery. Many years ago this method of treatment was carried out at the Lungegaard’s hospital, but without success.

We shall next mention all the specific remedies which have been recommended and have acquired any reputation as effective.

Madar (Mudar) is one of the oldest. It is got from the Indian plant, Caloptris gigantea (Asclepias gigantea). Only the powdered bark of the root was used. Some of it was sent from India to the Lungegaard’s hospital, and was given in large doses to many lepers. The effect was absolutely nil; one might just as well have given them flour.

Dr. George Watt enumerates the following plants of which the oils have been used in India in leprosy:--(1) Albizzea Libbek, (2) Anacardium occidentale, (3) Gynometra ramiflora, (4) Dipterocarpus turbinatus, (5) Gynocardia odorata, (6) Hydnocarpus Wightoni, (7) Hydnocarpus venenata, (8) Pongania glabra, (9) Psoralea corylifolia, (10) Sunocarpus anacardium, (11) Arachis hypogæa. Of these, only a few merit more particular mention; the others have been mostly merely popular remedies.

Cashew-nut Oil, from Anacardium occidentale, Linn., Cassuvium pomiferum, Lamk, a large tree very common in the West Indies. The oil is found in the pericarp, and is extracted by ether, which, after being evaporated in open vessels, leaves a thick, brownish black oil--the Cashew-nut oil. This is the oil with which the French physician, Dr. Beauperthuy, in Cumana, Venezuela, claimed to have cured leprosy. An English physician, Dr. Bakewell, who had investigated the treatment of Dr. Beauperthuy, sent a report to both houses of parliament on the beneficial effects of the treatment, and it thus attracted much notice. Dr. Beauperthuy’s method of treatment was the following: good nourishing diet, good hygienic surroundings, frequent warm baths followed by the inunction of olive oil, and internally 1/15 to 1/20 of a grain of bichloride of mercury twice daily, or, when this was contra-indicated, 10 to 20 grs. of carbonate of soda. As external remedies, which Beauperthuy regarded as the most important, he applied different liniments, such as tincture of iodine, to which were added potash lye, olive oil, and balsam of copaiba mixed with yolk of eggs. These liniments he principally applied where herpetic or other eruptions complicated the leprosy, and to the specific eruptions he applied solutions of nitrate of silver or sulphate of copper, but especially Cashew-nut oil. In all this there is nothing new except the oil; all the other remedies have been long, and still are occasionally, used. In the Lungegaard’s hospital, the oil was tried on five patients exactly according to the directions of Dr. Beauperthuy, and after a trial of several months, the results were anything but good. The oil induced irritation, redness, swelling and vesiculation; the leprous tubers and patches remained unaltered, and in one case a leprous eruption developed, probably produced by the irritation of the oil. In Trinidad, too, the same results of the application of the oil were seen, and Dr. Beauperthuy’s treatment has been given up.

Even before Dr. Beauperthuy’s remedy had lost its reputation, a new specific remedy appeared in the East Indies, viz., Gurjun oil, introduced by Surgeon-Major Dougall, of the Andaman Islands. The oil is procured from several species of Dipterocarpus, principally D. lævis, D. tuberatus, and D. trinervus. Dr. Dougall’s method of treatment was the following: good nourishment, fresh air, and a mixture of gurjun oil and lime water internally and externally. For internal use he gave a mixture of equal parts of oil and lime water, which forms a tolerably thick emulsion, 15 grains morning and evening. Externally, he used an ointment of oil 1 part, and lime water 3 parts. With this the patients rubbed the whole body for two hours both forenoon and afternoon. The body was thus covered with a sticky layer, to which dust and dirt adhered. To remove this, the patients rubbed themselves every morning with dry earth, and afterwards took a bath in running water, before again applying the oil. The prolonged rubbing he considered not only beneficial to the skin, but useful as a gymnastic exercise. Of twenty-four lepers whom he treated in this way for six months, all, without exception, improved; all ulcerations healed without again breaking down; and, what is most remarkable, the anæsthesia almost or completely disappeared.

According to his description of the patients, some of them evidently had syphilis, some chronic eczema, and some psoriasis. Their ulcerations had been so neglected that flies laid eggs in them, and it is little wonder that they healed under the cleanliness which Dr. Dougall induced. That old anæsthesia should disappear within six months, is, to any one who knows leprosy, absolutely incredible.

In the summer of 1887 the Lungegaard’s hospital got a sample of the oil, and nine male lepers underwent Dr. Dougall’s treatment, the only difference being that they took a warm bath instead of a bath in running water, which Dr. Dougall probably ordered because he had no bath-rooms at his disposal. Every morning and evening the patients took 15 grains of the mixture of equal parts of oil and lime water. In the forenoon, from 9 till 11, and in the evening from 5 till 7, they rubbed each other in a room at a temperature of 26 to 28° R., with oil 1 part and lime water 3 parts. In the morning they rubbed themselves with dry earth, and took a warm bath before re-applying the oil. The treatment led to no results. In some of the patients the disease advanced very little, but, nevertheless, the gurjun oil had no effect. As leprosy, so far as we know, is the same disease in the East Indies as in Norway, it was surprising that the gurjun oil should cure it in the one place and not in the other. Later trials of the treatment in India have had the same negative results as in Norway.

Chaulmoogra, which the medical department of Madras has used with success, is the oil pressed from the seeds of Gynocardia odorata, Lindl. Hydrocarpus odoratus, Lindl. The oil is given internally (2 grs. in an ounce of milk) twice daily, and externally, there is rubbed in a mixture of oil 1 part, and olive oil 16 parts, followed some hours after by a bath. We are told that the progress of the disease is stopped by a persevering use of the oil. The skin becomes smoother and more elastic, the patient becomes more energetic, the discolorations disappear, and so too does the anæsthesia, either partly or completely. Ulcerations heal, but promptly break down again. Besides the treatment, a generous diet is given, especially vegetables, milk and meat; spices and spirits are not allowed. Dr. Arjoon says that the tuberous form heals more easily than the mixed leprosy, and that anæsthetic leprosy is the most obstinate. When the disease is inherited there is no hope of a cure, and it is only in early cases that a cure can be expected. Further, he thinks that the permanence of the cure is doubtful.

In the Lungegaard’s hospital three tuberous and two anæsthetic patients were treated with chaulmoogra oil. The treatment was continued from eight months to a year, but the results were, as with the other remedies, nil.

Father Etienne sent to the Lungegaard’s Hospital from Port of Spain, Trinidad, a quantity of pills containing a vegetable, Hoang-nan, which he had received from some missionaries in Ting-King. He had used the pills for three years in leprosy with surprisingly good results. In several patients all the external symptoms of the disease disappeared, and he had good hopes of their complete cure. His report seeming to guarantee the remedy, it was given a trial in the Lungegaard’s Hospital. After prolonged use it proved to be absolutely useless, and, since no more has been heard from him, Father Etienne has probably been disappointed with his later results.

Father Damien also received from Ting-King a supply of pills for the cure of leprosy, which were, no doubt, of the same nature. He found them to consist of alum. sulph., pts. 1.5, Realgar 2.5, and Hoang-nan 2.5.

Hoang-nan belongs to the Euphorbiaceæ; the cortex contains a powerful poison which is the active remedy. At first Father Damien believed the remedy to be of some benefit “to us poor lepers”--he was then a leper--but further experience showed him that the remedy was, like so many others, unsatisfactory.

The last remedy to be mentioned is one which once attracted much notice, and on which the French academy allowed Dr. Gibert to write a report. The remedy is Assacou or Ussacou, Brazilian names of the tree Hura Braziliensis, Martin, of the family Euphorbiaceæ. It is considered very poisonous.

Several physicians in the West Indies have tried it, and amongst them Dr. Maldur, who treated four lepers in Santa-Caza da Misericordia, with, he believed, great benefit; other trials, however, failed, and the remedy has been laid aside.

The foregoing reports of the results of the treatment of leprosy with different specific remedies, are taken from the experience of the late Dr. Danielssen, who spent half a century trying to cure leprosy, and we shall now give some of the various methods of treatment he used.

Early in the development of bacteriological research, Dr. Danielssen already suspected the bacterial nature of the disease, and began to use germicides.

Carbolic acid was given in solution, 8 grains to 8 ounces, 1 tablespoonful four times daily, and he went so far as to give 20 grains to 8 ounces in the same way. Externally, he applied carbolic acid as an ointment or a lotion. It was used by fifty-three lepers from three to eighteen months, but had no effect on the disease.

Creasote was used in 1838 by the late Dr. Hjort, and later by Danielssen, without any good effect. Prof. Langerhans of Madeira, told Dr. Danielssen that he had seen several lepers on Teneriffe, whom Dr. Perez, at his suggestion, treated with creasote in increasing doses, with good effect, and he therefore asked Dr. Danielssen to try it once more. Consequently, creasote in pills (0.025 gr. in each pill) was administered to five tuberous lepers, in an early stage of the disease. They took the pills for six months without any effect on their leprosy. Two of them took the pills for fifteen months, and as many as 20 pills a day. The pills did neither good nor harm; their influence on leprosy was nil.

In the early years of the Lungegaard’s hospital (1849-50) glacial phosphoric acid was largely used without benefit.

Phosphorus was given in doses of 2 to 3 milligrammes daily. After some months it was given up because it caused indisposition and destroyed the appetite, while the leprosy remained unaltered.

Arsenic has been used by many physicians in the treatment of leprosy. Dr. Danielssen tried it in the form of Fowler’s solution, and the so-called Asiatic pills, in gradually increasing doses, but the prolonged use of arsenic, instead of doing good, made the patients worse, causing gastro-enteritis and emaciation. The emaciation caused diminution in the size of the tubers, which has been regarded by many physicians as an improvement; but this is a fallacy, for, when the patient regains his former good condition, the nodules regain their former size.

Ichthyol was tried internally in the form of pills, 10 centigrammes thrice daily, increased up to 2 grammes daily; but no benefit was observed, although it was continued for almost a year.

From Dr. Englemann, in Kreuznach, Dr. Danielssen got a sample of Kreuznach salt, and directions how to use it. The bath was prepared thus: 3 lbs. of common salt, 4 lbs. of Kreuznach salt, 264 litres of water. Temperature 35°C. After the lapse of a week the Kreuznach salt was increased to 6 lbs., after a fortnight to 12 lbs., and after three weeks to 16 lbs. The patient remained from one-and-a-half to two hours in the bath, and no other medicine was taken. Forty-six baths were used by five lepers, four tuberous, and one anæsthetic. At the same time, a young man with a recent eruption of leprosy was sent to Kreuznach to take the baths under Dr. Englemann’s directions. After a year Dr. Danielssen saw him again, when no improvement was to be observed, and the same was the result in the cases treated here.

Mercury in its different combinations has been tried internally and externally, but instead of producing any good effect it has rather made the condition of the patient worse.

Iodine has been used as iodide of potassium, and externally as tincture of iodine and iodine ointment. At the beginning of his studies in leprosy Dr. Danielssen had great confidence in iodine, but he soon learned what a very dangerous remedy it was in this disease. Even small doses of iodine produce new eruptions of leprous tubers or patches, and Dr. Danielssen therefore ultimately used it as a test in cases of apparent cure. When a patient was considered cured, he gave him iodide of potassium, and if no new eruption developed, the cure was considered complete.

Some years ago Dr. Unna, of Hamburg, claimed to have cured three lepers, and Dr. Danielssen, using Unna’s method, cured one. The treatment is the following: Internally, pills of ichthyol in increasing doses; externally, the rubbing of arms and legs morning and evening with an ointment of 10 per cent. pyrogallic acid in lanolin, and the breast, back, neck, and cheeks, with 10 per cent. chrysarobin in lanolin; the covering of the forehead and chin with a plaster consisting of chrysarobin, salicylic acid, and creasote, which is changed every second or third day. This treatment was continued from December 16th, till January 11th; then followed a few days of plain baths, and then the same treatment again. In the Lungegaard’s hospital Dr. Unna’s treatment was tried by thirteen lepers, five nodular, four anæsthetic, and four mixed. The results of the treatment were not so satisfactory as in Dr. Unnas hands, and there was certainly no question of a cure.

Koch’s tuberculin was administered to five anæsthetic, three tuberous, and three mixed cases, as a rule, daily, from January 8th to May 8th. The dose at the commencement was 1 milligramme, and in several cases as much as 320 milligrammes were finally injected. The injections were made, sometimes daily, sometimes at intervals of a few days, according to the degree of reaction which followed the injections. In some cases the injections had to be stopped very soon, because they produced fresh leprous eruptions; and in one case bacilli were found in the blood. It seemed as if the tuberculin had set the bacilli afloat. We came to the following general conclusions:--(1) Tuberculin administered to lepers produces a general and local reaction, usually forty-six hours after the injection, seldom after twelve hours, and very seldom after two to three days. The local reaction becomes evident later. (2) These reactions do not beneficially influence the leprosy, they rather aggravate the disease by causing fresh eruptions just as iodide does. (3) Tuberculin does not kill the lepra bacillus. (4) Immunity against tuberculin can be attained, but this immunity does not influence the progress of leprosy.

Dr. Carreau, in Guadaloupe, treated a leper with chlorate of potassium, he believed with great benefit; he gave the remedy in enormous doses. Dr. Hjort had, already, in 1838-39 tried this remedy without effect. Dr. Beaven-Rake has also tried the remedy according to Dr. Carreau’s directions, but also without result. Dr. Danielssen, too, tried it, but without any benefit.

During the last few years the following remedies have been tried in the Lungegaard’s hospital: Hydroxylamin, Europhen, Naphthol, Salol, Methylene blue, Aristol.

Hydroxylamin forms colourless crystals, easily soluble in alcohol and glycerine. It is decidedly poisonous, and is, according to some authors, a more powerful reducing agent than chrysarobin or pyrogallic acid; 2 to 5 hydroxylamin to 20 glycerine and 80 alcohol, was painted on the patches of four maculo-anæsthetic lepers. In two of them there developed, after the painting, an erythema, during the persistence of which the painting was discontinued. The painting was continued for two months, and then a 2 per cent. hydroxylamin ointment was applied, but as no amelioration could be noted after four or five months, the remedy was laid aside. In four tuberous patients the painting could only be continued for two or three days, because the spots re-acted severely, grew red and painful, and vesicles formed. The tubers somewhat diminished, but otherwise the condition remained unaltered.

Europhen has some resemblance to iodoform, but gives up its iodine less readily. It is a fine yellow powder, insoluble in water, but soluble in alcohol, ether, chloroform, and oil. A solution in oil was used for hypodermic injections: at first 0.015 europhen was injected, and after a month 0.025. At the end of another month an eruption developed in one of the patients; in the others no effects were evident, and thereupon 0.030 was injected. After three weeks an iodine eczema developed in three of the patients, and a leprous eruption in another, and consequently no further trials were made. Dr. Julius Goldschmidt of Madeira, has also used this remedy, and considers one of his patients as almost cured, while four others remain unchanged.

Aristol was tried by three patients, partly internally, dissolved in ether, and partly externally, in the form of ointment; the effect was the same as after the use of iodide of potassium, and it was stopped after three weeks’ trial.

Naphthol and Salol were tried for a long time, but the effect was almost nil. Salol has also been used by Dr. Lütz in the Sandwich Islands, and by Surgeon Major Cook in Madras, but though some amelioration in the condition of the patients has been noted, no case has been cured.

Methylene Blue was given to one tuberous patient, both internally and hypodermically. The skin, especially the tubers, became deeply blue, but a microscopical examination showed the bacilli unaltered. The treatment was continued from May 20, 1891 till January 30, 1892. Some tubers diminished a little, but most of them became larger, so that the disease as a whole grew worse.

Nerve stretching was first tried by Dr. Gerald Bamfert, who stated that he had done the operation with success on an anæsthetic patient, in whom both hands were atrophic and sensibility much diminished. The ulnar nerve was stretched and incised longitudinally. The sensibility in the right hand re-appeared immediately after the operation; and after some days the muscular power was almost completely restored. In three anæsthetic patients in the Lungegaard’s hospital the operation was performed; the ulnar nerve was stretched and incised along a length of three to four inches. All went well, only the anæsthesia remained unchanged; neither sensibility nor muscular power was restored. Dr. Beaven-Rake, who has done numerous nerve-stretchings in Trinidad, says, “on the whole the results of nerve-stretching for anæsthesia cannot be considered satisfactory.”

Dr. Beaven-Rake has also done the operation for pains in the limbs, for which hypodermic injections of morphine have been successfully used in the Lungegaard’s hospital.

Electricity, both faradic and galvanic, has been used for anæsthetic leprosy, and electric baths, but no good effect has been attained.

Surgical measures are often needed. Section of the cornea, as introduced by Dr. Boeckmann, in the case of tubers growing into it, has already been mentioned, as has the operation of tarsoraphia interna in ectropion of the lower eyelid. Iridectomy has often to be performed, when the pupil has been obliterated by adhesions of the iris or by exudation.

Tracheotomy is necessary when the larynx is occluded by leprous-growths or by cicatrices.

Necrotomies should always be performed when there is necrosis of the bones of the hands and feet. It is astonishing how well the wounds heal in the anæsthetic parts, and patients are spared from long-standing suppuration by the removal of the necrosed bones.

The best remedy for leprosy Dr. Danielssen found in his experience to be Salicylate of soda. If the patients were badly nourished, he first administered quinine, iron, cod-liver oil, and nutritious food, and when the patient’s condition was satisfactory he gave 1.0 gramme salicylate of soda four times daily, and for six months or a year the dose was gradually increased. Its good effects were seen in both forms of the disease. In the maculo-anæsthetic form the patches and the less extensive anæsthesias slowly disappeared. In the tuberous form, when not of too long duration and severity, the rapidity of progress was diminished, and fresh eruptions were prevented. A complete cure has, however, not been attained, unless, at the same time, there have been applied regularly “cucurbita cruenta,” steam baths, alternating with warm water and sea-water baths, exercise in the fresh air, good hygienic surroundings, and good diet. From time to time irritants were applied, such as, carbolic and salicylic acids, in the form of fomentations and ointments. It is only in cases in the first six to twenty-four months that a favourable issue can be hoped for. The results of the treatment in the Lungegaard’s hospital are nothing to boast of, but they show, according to Dr. Danielssen, that leprosy at its commencement can be cured. In our opinion this is true, but with the reservation that the cure is not due to the treatment, but is the natural development of the disease. We have seen cases of leprosy, in the country, both tuberous and maculo-anæsthetic, completely recover without any treatment whatever. So far as we know, in most of the patients discharged cured from the Lungegaard’s hospital the anæsthesia has increased, which is in conformity with the general progress of the disease, the nerve fibres continuing to undergo atrophy from the pressure of the contracting inflammatory tissue in the nerve trunks, as described above.

Treatment ought theoretically to be directed to the destruction of the bacilli, and this is what Dr. Unna sought to attain by his reducing remedies, pyrogallic acid, chrysarobin, etc.; but while Dr. Unna and Dr. Deichmann succeeded in Hamburg, Dr. Danielssen had no success when using the same remedies. Dr. Danielssen believed that the bacilli were destroyed by salicylate of soda; but we fear that others will not succeed with this same remedy.

As we are then, in our opinion, unable to destroy the bacilli with remedies, either internal or external, it only remains to us to prevent infection, and that can only be attained by isolation of those affected. For this isolation no very costly measures are required. From what we saw in North America in 1888, all that is wanted is cleanliness, both personal, and in the household. But amongst the people where leprosy prevails, it is almost impossible to get sufficient cleanliness thoroughly enforced. We think, therefore, that the best measures are those which have been taken in Norway, where the lepers are isolated at their own request, and where the communities can get rid of the disease, if they will, since the sanitary authorities have the power to order the leper to live sufficiently isolated from his family, and, if he cannot or will not assent to this, can compel him to enter an asylum. At the same time, the doctrine of cleanliness and isolation and the necessity of their observance in order to prevent the spread of the disease, is constantly preached.

Since the state pays all the expenses of the lepers in the asylums, their families are generally relieved by getting rid of the lepers, who are almost invariably bad workers and unable to earn their living.

These measures are quite adequate in a democratic country like Norway, where the communities have governed themselves since 1836, and the results are most satisfactory, seeing that we had in 1856, 2833 lepers, and at the end of 1890 only about 950, which number, when corrected, will probably amount to about 1100.

Whether the same measures would be adequate in other countries where leprosy prevails, we cannot of course say; it must depend on the social condition of the community. But we are firmly convinced that isolation must be carried out in some appropriate fashion.

TABLES.

TABLE I.

KEY:

Column heading D - Duration of disease in years

Body of table A - Amyloid F - Fatty degeneration L - Leprous N - Normal NpA - Acute nephritis NpI - Interstitial nephritis NpP - Parenchymatous nephritis P - Pneumonia Tr - Tubercular Ts - Tuberculosis U - Ulceration

---------------------------------------------------------------------- SHOWING THE FREQUENT COMPLICATION OF NODULAR LEPROSY WITH TUBERCULOSIS. ---+----+---------------+----------+----------+----------+------------ | | LUNGS AND | | | | INTESTINAL NO.| D. | PLEURA. | LIVER. | SPLEEN. | KIDNEYS. | CANAL. ---+----+---------------+----------+----------+----------+------------ 1 | 11 | Normal. | A and L. | A and L. | F. | Amyloid. 2 | 6 | | Leprous. | Tr. | F. | Normal. 3 | 10 | Hydro-thorax. | A and L. | Leprous. | ? | Normal. 4 | 5 | | Leprous. | Amyloid. | Amyloid. | A and Tr U. 5 | 12 | Normal. | Amyloid. | Amyloid. | Amyloid. | Normal. 6 | 8 | Lobular P in | Leprous. | Leprous. | F. | Normal. | | the right | | | | | | lung. | | | | 7 | 13 | Lungs | Leprous. | Leprous. | F. | Normal. | | œdematous. | | | | 8 | 7 | | Leprous. | Leprous. | Normal. | Normal. 9 | 5 | | A and L. | Leprous. | A and F. | Amyloid. 10 | 6 | Œdema. | Leprous. | Leprous. | F. | Normal. 11 | 5 | | A and L. | A and L. | Amyloid. | Amyloid. 12 | 11 | Normal. | Leprous. | Leprous. | NpI. | Normal. 13 | 9 | | A & L. | L (?). | A and | A and Tr, | | | (?) | | Tr. | Tr peri- | | | | | | tonitis. 14 | 10 | Normal. | A and L. | Leprous. | Amyloid. | A U in the | | | | | | ileum. 15 | 14 | Tr peri- | Tr. | Tr. | A and | A and Ts | | bronchitis | | | Tr. | of omentum | | and | | | | and | | pleurisy. | | | | mesentery. 16 | 4 | Tr peri- | Tr, A, | Tr and A | Tr and | A, Tr U, | | bronchitis | and L. | and L. | A. | mesenteric | | and | | | | Ts. | | pleurisy. | | | | 17 | 7 | Normal. | L and A. | L and A. | Amyloid. | Amyloid. 18 | 10 | Numerous | L and A. | L and A. | F. | | | cavities and | | | | | | gelatinous | | | | | | pneumonia. | | | | 19 | 6 | Numerous | Leprous. | Leprous. | NpI. | Ulcerating | | cavities and | | | | plaques | | gelatinous | | | | and | | pneumonia. | | | | solitary | | | | | | glands. 20 | 15 | Normal. | F. | Amyloid. | Amyloid. | Amyloid. 21 | 2 | Normal. | Leprous. | Leprous. | Normal. | Normal. 22 | 14 | A small P | Leprous. | Leprous. | A and F. | Amyloid. | | in R. | | | | 23 | 7 | | Leprous. | L and A. | A and F. | Tr U. 24 | 13 | Bronchi- | Leprous. | Leprous. | A and F. | Normal. | | ectasis and | | | | | | lobular P. | | | | 25 | 8 | Bronchi- | Leprous. | Leprous. | Slight | Normal. | | ectasis and | | | F. | | | lobular P. | | | | 26 | 5 | Normal. | Leprous. | Leprous. | Slight | Normal. | | | | | F. | 27 | ? | Small cavi- | L and A. | L and A. | Amyloid. | Normal. | | ties and | | | | | | lobular P. | | | | 28 | 3 | Small cavi- | L and | L and | F and A. | A ulcerated | | ties and | Tr. | Tr. | | follicles | | lobular P. | | | | and | | | | | | plaques. 29 | 1½ | Ts of lungs | L and | L and | NpA, Ts | Normal. | | and pleura. | Tr. | Tr. | in R. | | | | | | kidney. | 30 | 4 | Caseous areas | Leprous. | Leprous. | | Normal. | | in both | | | | | | lungs. | | | | 31 | 6 | Œdema, | Amyloid. | Amyloid. | Amyloid. | Amyloid. | | bronchitis. | | | | 32 | 24 | Lobular P. | Amyloid. | Amyloid. | A and F. | Amyloid. 33 | 6 | Cavities and | L and A. | L and A. | Normal. | Amyloid. | | lobular P. | | | | 34 | 5 | Normal. | Leprous. | L and A. | A & NpI. | Amyloid. 35 | 4 | Pleuritic | Leprous. | Leprous. | Normal. | Peritonitis, | | adhesions. | | | | U of the | | | | | | vermiform | | | | | | process. 36 | 14 | Œdema. | Amyloid. | Normal. | A and F. | Amyloid. 37 | 4 | Left Tr pleu- | Amyloid. | A and | Tr. | A, Tr peri- | | risy; R. Tr | | Tr. | | tonitis. | | peri- | | | | | | bronchitis. | | | | 38 | 6 | | Leprous. | Leprous. | Normal. | 39 | 6 | | L and A. | L and A. | Tr & A. | Amyloid. 40 | 7 | Normal. | L and A. | L and A. | Amyloid. | Normal. 41 | 8 | Lobular P. | Leprous. | L and A. | Amyloid. | Normal. 42 | 2 | Tubercular. | L & Tr. | L & Tr. | Normal. | Tr U. 43 | 12 | Lobular P. | Leprous. | Leprous. | A and F. | Normal. 44 | 8 | Lobular P, | L and A. | L and A. | NpA. | Normal. | | pleurisy. | | | | 45 | 4? | Cavities and | L and A. | L and A. | Normal. | Amyloid | | lobular | | | | ulcer- | | caseous P. | | | | ations. 46 | 4 | Ts, double P. | Leprous. | Leprous. | Normal. | Normal. 47 | 10 | Œdema. | Amyloid. | Amyloid. | Amyloid. | Amyloid. 48 | 4 | Tuberculosis. | Tr and | Amyloid. | Tr and | A, Tr | | | A. | | A. | ulcer- | | | | | | ations. 49 | ? | Normal. | L and A. | L and A. | Amyloid. | Amyloid. 50 | 4 | | Leprous. | Leprous. | Normal. | Tr U. 51 | 7 | Bronchi- | Leprous. | Leprous. | Normal. | Normal. | | ectasis, | | | | | | lobular P. | | | | 52 | ? | R. lobular P. | Leprous. | Leprous. | Normal. | Normal. 53 | ? | Pleuritic | Amyloid. | Amyloid. | Amyloid. | Amyloid. | | adhesions, | | | | | | lungs N. | | | | 54 | 5 | Ts of lungs | L, Tr, | L and | Amyloid. | A, Tr U. | | and pleura. | and A. | Tr. | | 55 | 12 | | L. (?) | | Nephr- | Amyloid. | | | | | itis. | 56 | 3 | Tuberculosis. | Cirrh- | L (?) | Normal. | Normal. | | | osis. | | | 57 | 13 | Normal. | Normal. | Normal. | Amyloid. | Normal. 58 | 7 | Apical Ts. | Leprous. | Leprous. | NpI. | Normal. 59 | 21 | Œdema. | L (?). | L (?). | NpP. | Normal. 60 | 2 | Ts, cavities. | Amyloid. | Amyloid. | A and | Tubercular. | | | | | Ts. | 61 | 10 | Normal. | Fatty. | Normal. | NpP. | Tr (?) 62 | 9 | Croupous P. | Amyloid. | Amyloid. | Amyloid. | Normal. 63 | 7 | Œdema. | Leprous. | Leprous. | Normal. | Hyperæmia. 64 | 7 | Lobular P. | Normal. | Leprous. | Normal. | Normal. 65 | 9 | Normal. | Leprous. | Leprous. | NpP. | Normal. 66 | 3 | Tuberculosis. | Leprous. | Leprous. | | Normal. 67 | ? | | Fatty. | Tr. | ? | Normal. 68 | ? | | Leprous. | Leprous. | Normal. | Normal. 69 | ? | Tuberculosis. | Normal. | Normal. | NpI. | Normal. 70 | ? | Normal. | L and A. | L and A. | NpP. | Normal. 71 | ? | Normal. | Leprous. | Leprous. | NpI. | Normal. 72 | 17 | Normal. | Cancer- | Leprous. | Normal. | Normal. | | | ous. | | | 73 | 7 | Tuberculosis. | L and A. | L and A. | Amyloid. | Normal. 74 | ? | Ts of lungs | Tr. | Tr. | Tr. | Tubercular. | | and pleura. | | | | 75 | ? | Œdema. | Amyloid. | Amyloid. | Amyloid. | Amyloid. 76 | 2- | Tuberculosis. | Tr & A. | L and A. | Amyloid. | Tr., Tr. | 3 | | | | | peri- | | | | | | tonitis. 77 | ? | Tuberculosis. | Leprous. | L & Tr. | Normal. | Tubercular. 78 | 10 | Tuberculosis. | L and A. | Leprous. | Amyloid. | Amyloid. 79 | 7 | Cavities. | L and A. | Amyloid. | NpP. | Normal. 80 | ? | Cavities. | L & Tr. | L & Tr. | Normal. | Tr. 81 | 7 | Normal. | L and A. | L and A. | Amyloid. | Amyloid. 82 | ? | Double P. | Amyloid. | Amyloid. | NpP & A. | Amyloid. 83 | ? | Normal. | Leprous. | Leprous. | Normal. | Amyloid. 84 | ? | Œdema. | L & can- | Leprous. | NpI. | Normal. | | | cerous. | | | 85 | ? | Œdema. | L and A. | L and A. | NpI & A. | Normal. 86 | ? | Tuberculosis. | Leprous. | L & Tr. | Normal. | Tr. 87 | 1½ | Tuberculosis. | L & Tr. | L & Tr. | Normal. | Tr. 88 | ? | Normal. | L and A. | Leprous. | NpP. | ? 89 | ? | Tuberculosis. | L and A. | Leprous. | NpI & A. | Normal.

Footnotes ---------

1 Left-sided Tr pleurisy; in lower lobes, lobular pneumonia.

2 Cavities in both apices; Tr peri-bronchitis in the upper lobes.

3 In both lower lobes pneumonia, with commencing cavity formation.

4 In the left lung, cavities in the apex, and widespread lobular pneumonia. The same without cavity formation in the R.

5 In upper lobes, cavities, and lobular pneumonia.

6 Cavities, tubercular peri-bronchitis, pleural tuberculosis.

7 Peyer’s patches and solitary glands tubercular with commencing ulceration.

8 Cavities, tubercular peri-bronchitis, and lobular pneumonia in left lung.

9 R. tubercular, L. hydronephrosis, tubercular cystitis.

10 Tubercular peri-bronchitis and lobular pneumonia; tubercular pleurisy in left lung.

11 Amyloid, localised tubercular peritonitis around the spleen.

12 Tubercular peri-bronchitis, lobular pneumonia and small cavities.

13 Tuberculosis, numerous large cavities, tubercular pleurisy.

14 Pleuro-pneumonia on right side, hydro-thorax sinistra, hydro- pericardium, ascites.

15 Leprous (?) commencing amyloid degeneration.

16 Congested, otherwise normal.

17 Double pleurisy, caseous node of the size of a walnut in the left lung.

18 Marked stenosis of larynx. Both apices infiltrated.

TABLE II.

THE PROPORTION OF TUBERCULOSIS IN MACULO-ANÆSTHETIC LEPROSY.

---+-----------+----------+----------+----------+--------+----------+--------- NO.|BRAIN. |SPINAL |LUNGS. |LIVER. |SPLEEN. |KIDNEYS. |NERVES. | |CORD. | | | | | ---+-----------+----------+----------+----------+--------+----------+--------- | | | | | | | 1 |Nothing. |Nothing. |Tuberc- |Enlarge- |Nothing.|Hyperæmia.|Ulnar | | |ular. |ment and | | |nerve | | | |hyperæmia.| | |thickened | | | | | | |in the | | | | | | |under | | | | | | |third of | | | | | | |the upper | | | | | | |arm. | | | | | | | 2 |Nothing. |Nothing. |Tuberc- |Nothing. |Nothing.|Enlarge- | | | |ular. | | |ment and | | | | | | |fatty | | | | | | |degener- | | | | | | |ation. | | | | | | | | 3 |Hydroceph. |Nothing. |Tuberc- |Fatty. |Nothing.|Nothing. |Ulnar |internus. | |ular. | | | |nerve |Thickening | | | | | |thickened |of the pia | | | | | |through- |mater. | | | | | |out a |Gelatinous | | | | | |length |exudation | | | | | |of about |between | | | | | |10-15 cm. |pia and | | | | | |about the |arachnoid. | | | | | |elbows. | | | | | | |Median | | | | | | |nerve | | | | | | |thickened | | | | | | |at the | | | | | | |wrist. | | | | | | | 4 |Nothing. |Not |Tuberc- |Fatty. |Normal. |Fatty | | |examined. |ular. | | |degener- | | | | | | |ation. | | | | | | | | 5 |Nothing. |Not |Normal. |Fatty. |Normal. |Fatty | | |examined. | | | |degener- | | | | | | |ation. | | | | | | | | 6 |Nothing. |Not |Normal. |Normal. |Normal. |Granular, | | |examined. | | | |atrophic. | | | | | | |Fatty | | | | | | |degener- | | | | | | |ation. | | | | | | | | 7 |Solitary | | | | |Tubercu- | |tubercle | | | | |losis of | |in the | | | | |the left | |cerebellum.| | | | |kidney. | |Hydroceph. | | | | | | |internus. | | | | | | | | | | | | | 8 | |Not |Normal. |Fatty. | |Fatty |Ulnar | |examined. | | | |degener- |nerve | | | | | |ation. |as thick | | | | | | |as a | | | | | | |little | | | | | | |finger. | | | | | | | 9 | |Not |Tuberc- |Tubercu- |Amyloid.|Hyperæmia.|Ulnar | |examined. |ular. |losis of | |Fatty |nerve | | | |periton- | |degener- |contrac- | | | |eum. Liver| |ation. |ted. | | | |amyloid. | | | | | | | | | | 10 |Hydroceph. |Not |Tuberc- |Tuberc- |Normal. |Normal. | |internus. |examined. |ular. |ular. | | | | | | | | | | 11 |Normal. |Not | |Amyloid. |Amyloid.|Amyloid. | | |examined. | | | | | | | | | | | | 12 |Normal. |Not |Tuberc- |Hyper- |Abscess.|Abscess. | | |examined. |ular. |trophic. | | | | | | | | | | 13 |Tubercular |Not |Miliary |Miliary |Miliary | | |meningitis.|examined. |tubercu- |tubercu- |tubercu-| | | | |losis. |losis. |losis. | | | | | | | | | 14 | |Degener- | |Fatty and |Amyloid.|Fatty |Ulnar | |ation of | |amyloid. | |degener- |nerve | |the pos- | | | |ation and |scler- | |terior | | | |amyloid. |otic. | |columns. | | | | | | | | | | | | 15 | | | |Fatty and |Amyloid.|Fatty |Ulnar | | | |amyloid. | |degener- |nerve | | | | | |ation and |scler- | | | | | |amyloid. |otic. | | | | | | | 16 |Hydroceph. |Normal. |Normal. |Hyper- | | | |internus. | | |trophy | | | | | | |(?). | | | | | | | | | | 17 |Normal. |Lumbar |Normal. |Normal. |Normal. |Normal. | | |cord | | | | | | |thickened,| | | | | | |the mem- | | | | | | |branes | | | | | | |thickened | | | | | | |and | | | | | | |hyperæmic.| | | | | | | | | | | | 18 |Normal. |Thin, |Normal. |Large. |Normal. |Normal. |Axillary | |atrophic | | | | |plexus | |(?). | | | | |atrophic. | | | | | | |Ulnar and | | | | | | |radial | | | | | | |nerves | | | | | | |thick- | | | | | | |ened. | | | | | | | 19 | | | |Amyloid. |Amyloid.|Inter- | | | | |Intestine | |stitial | | | | |also | |nephritis.| | | | |amyloid. | | | | | | | | | | 20 | | | | |Amyloid.|Amyloid. | | | | | | | | 21 | | | | | |Inter- |Ulnar | | | | | |stitial |nerve | | | | | |nephritis.|scler- | | | | | | |osed. | | | | | | | 22 | | |Tuberc- |Amyloid. | | | | | | ular. | | | | | | | | | | | 23 |Normal. |Normal. | | | | | | | | | | | | 24 |Normal. |Normal. |Double | | | | | | |pleurisy. | | | | | | | | | | | 25 |Sero- |Normal. | |Fatty | | | |purulent | | |degenera- | | | |meningitis.| | |tion | | | | | | | | | | | | | | | | | 26 |Normal. |Normal. | | | | | | | | | | | | 27 |Normal. |Normal. | | | | | | | | | | | | 28 | | |Tuberc- |Fatty |Tuberc- | | | | |ular. |degenera- |ular. | | | | | |tion. | | | | | | |(Intes- | | | | | | |tine also | | | | | | |tuberc- | | | | | | |ular.) | | | | | | | | | | 29 |Normal. |Normal. | |Amyloid. |Amyloid.|Fatty | | | | | | |degener- | | | | | | |ation. | | | | | | | | 30 |Normal. |Normal. | |Amyloid. |Amyloid.|Amyloid. |Ulnar | | | | | | |nerve | | | | | | |contr- | | | | | | |acted. | | | | | | | 31 | | |Tuberc- |Normal. |Normal. | | | | |ular. |(Intes- | | | | | | |tine also | | | | | | |tuberc- | | | | | | |ular.) | | | | | | | | | | 32 | | |Tuberc- |Amyloid. |Amyloid.|Nephritis | | | |ular. | | |parenchym-| | | | | | |atous. | | | | | | | | 33 | | | |Fatty. |Normal. |Tubercu- | | | | |(Intes- | |losis of | | | | |tine also | |the left | | | | |tuberc- | |kidney. | | | | |ular.) | | | | | | | | | | 34 | | |Croupous | | |Cirrhotic | | | |pneumonia.| | |kidney. | | | | | | | | 35 | | |Tuberc- |Tuberc- |Tuberc- |Fatty | | | |ular. |ulous. |ulous. |degener- | | | | | | |ation. | | | | | | |Amyloid. | | | | | | | | 36 | |Degener- | | | | | | |ation of | | | | | | |the | | | | | | |posterior | | | | | | |columns. | | | | | | |Atrophy | | | | | | |of the | | | | | | |posterior | | | | | | |roots | | | | | | |Sclerosis | | | | | | |of the | | | | | | |spinal | | | | | | |ganglia. | | | | | | | | | | | |

TABLE III.--THE PROPORTIONS OF THE TWO FORMS OF LEPROSY.

+------------------+-------------------------------------------------+ | | OF EVERY HUNDRED LEPERS FROM 1856 TO 1890 THERE | | | BELONGED TO THE | | | NODULAR FORM: |MACULO-ANÆSTHETIC FORM: | + +--------+------+--------+--------+------+--------+ | |Altoget-|Males.|Females.|Altoget-|Males.|Females.| | | her. | | | her. | | | +------------------+--------+------+--------+--------+------+--------+ | In the Eastern | | | | | | | | part of Norway | 47.7 | 26.6 | 21.1 | 52.3 | 27.5 | 24.8 | | Littoral | | | | | | | | Districts. | | | | | | | | { Lister | | | | | | | | { and Mandal | 58.8 | 41.2 | 17.6 | 41.1 | 29.4 | 11.7 | | { Stavanger | 60.6 | 34.7 | 25.9 | 39.3 | 21.0 | 18.3 | | { Söndre | | | | | | | | { Bergenhus | 68.0 | 34.2 | 33.8 | 31.9 | 15.3 | 16.6 | | { Nordre | | | | | | | | { Bergenhus | 66.8 | 34.9 | 31.9 | 33.0 | 17.2 | 15.8 | | { Romsdal | 73.3 | 44.4 | 28.9 | 27.2 | 15.8 | 11.4 | | { Söndre | | | | | | | | { Trondhjem | 74.3 | 48.5 | 25.8 | 25.7 | 16.4 | 9.3 | | { Nordre | | | | | | | | { Trondhjem | 70.6 | 46.8 | 23.8 | 29.5 | 17.4 | 12.1 | | { Nordland | 71.5 | 44.1 | 27.4 | 28.5 | 17.1 | 11.4 | | { Tromsö | 79.1 | 52.9 | 26.2 | 20.9 | 13.1 | 7.8 | | { Finmarken | 82.5 | 65.0 | 17.5 | 17.5 | 12.5 | 5.0 | | Sogn | 56.6 | 31.8 | 24.8 | 43.4 | 23.0 | 20.4 | | Söndfjord | 72.6 | 37.4 | 35.2 | 27.4 | 14.3 | 13.1 | | Nordfjord | 68.5 | 33.9 | 34.6 | 31.3 | 16.9 | 14.4 | + -----------------+--------+------+--------+--------+------+--------+

TABLE IV.

------------------------------------------------------------------------ THE RESULTS OF ISOLATION IN NORWAY -----+----------+-------+-----------------------+----------------+------ | | | | Number at end | | Total at | | Result. | of Year. | Total | commence-| +------+-------+--------+----------------+at end | ment | New | | | Emi- | At | In | of Year.| of Year. | Cases.| Died.| Cured.| grated.| Home.| Asylums.| Year. -----+----------+-------+------+-------+--------+------+---------+------ 1856 | -- | 238 | ? | ? | ? | 2598 | 235 | 2833 1857 | 2833 | 242 | 293 | 3 | 15 | 2339 | 427 | 2766 1858 | 2766 | 210 | 224 | 3 | 3 | 2294 | 475 | 2769 1859 | 2769 | 239 | 213 | 8 | 7 | 2267 | 523 | 2790 1860 | 2790 | 219 | 251 | 1 | 6 | 2218 | 539 | 2757 1861 | 2757 | 219 | 239 | 6 | 14 | 2028 | 711 | 2739 1862 | 2739 | 211 | 215 | 5 | 11 | 2009 | 698 | 2707 1863 | 2707 | 196 | 192 | 5 | 4 | 1947 | 749 | 2696 1864 | 2696 | 201 | 202 | -- | 8 | 1914 | 781 | 2695 1865 | 2695 | 201 | 205 | 5 | 8 | 1910 | 772 | 2682 1866 | 5682 | 203 | 214 | 3 | 10 | 1879 | 795 | 2674 1867 | 2674 | 200 | 191 | 8 | 4 | 1876 | 787 | 2663 1868 | 2663 | 206 | 210 | 6 | 7 | 1865 | 788 | 2653 1869 | 2653 | 183 | 199 | 10 | 13 | 1820 | 787 | 2607 1870 | 2607 | 187 | 203 | 4 | 13 | 1762 | 764 | 2526 1871 | 2526 | 170 | 238 | 2 | 16 | 1681 | 747 | 2428 1872 | 2428 | 131 | 205 | 5 | 10 | 1627 | 708 | 2335 1873 | 2335 | 129 | 177 | 9 | 17 | 1592 | 672 | 2264 1874 | 2264 | 137 | 183 | 6 | 9 | 1566 | 643 | 2209 1875 | 2209 | 134 | 203 | 5 | 14 | 1499 | 623 | 2122 1876 | 2122 | 115 | 187 | 3 | 6 | 1440 | 613 | 2053 1877 | 2053 | 110 | 163 | 3 | 7 | 1372 | 629 | 2001 1878 | 2001 | 105 | 149 | 10 | 8 | 1341 | 618 | 1959 1879 | 1959 | 88 | 162 | 5 | 10 | 1277 | 602 | 1879 1880 | 1879 | 72 | 150 | 7 | 7 | 1178 | 617 | 1795 1881 | 1795 | 60 | 164 | 5 | 8 | 1092 | 608 | 1692 1882 | 1692 | 66 | 137 | 11 | 7 | 1061 | 553 | 1614 1883 | 1614 | 87 | 127 | 9 | 5 | 1022 | 535 | 1557 1884 | 1557 | 55 | 140 | 10 | 2 | 944 | 519 | 1463 1885 | 1463 | 71 | 146 | 9 | 12 | 855 | 522 | 1377 1886 | 1377 | 48 | 135 | 16 | 9 | 748 | 522 | 1270 1887 | 1270 | 47 | 111 | 2 | 3 | 704 | 514 | 1218 1888 | 1218 | 27 | 99 | 8 | 1 | 631 | 524 | 1156 1889 | 1156 | 27 | 86 | 9 | 12 | 551 | 530 | 1081 1890 | 1081 | 10 | 122 | 6 | 2 | 447 | 507 | 954

PLATE VI.

PLATE VI.

Fig. 1.--Two cells from a fresh nodule in 1 per cent. osmic acid (Gundlach, No. viii).

Fig. 2.--Part of a section of a cutaneous leproma. Round cells with clear stellate cells between them (Hartnack, No. ix).

Fig. 3.--From a corneal leproma. Round cells with corneal corpuscles between them (Hartnack, No. ix).

Fig. 4.--From the border of a corneal leproma. Capillary surrounded by round cells. Müller’s Fluid (Hartnack, No. ix).

Fig. 5.--From the inside of a corneal leproma. A capillary surrounded by round cells in among globi and corneal corpuscles unchanged or filled with brown granules. Müller’s Fluid (Hartnack, No. ix).

Fig. 6.--The brushed-out network of a cutaneous leproma (Hartnack, No. ix).

Fig. 7.--From a corneal leproma. Capillary surrounded by round cells free from bacilli, and outside these, cells filled with bacilli. Seibert homogen. immersion 1/16.

Fig. 8.--Cells from a cutaneous leproma. Eosin, Bismarck brown, and Gentian-violet. Hardening in Fleming’s Solution. Seibert homogen. immersion 1/16.

PLATE VII.

PLATE VII.

Fig. 1.--Cells and globi from cutaneous lepromata. Müller’s Fluid (Hartnack, No. ix).

Fig. 2.--Globi from a leprous spleen.

Fig. 3.--Two globi from the retina.

PLATE VIII.

PLATE VIII.

Fig. 1.--Corneal corpuscles filled with brown granules (Hartnack, No. ix).

Fig. 2.--From a leproma of the iris. Round cells with stellate cells (Hartnack, No. ix).

Fig. 3.--Corneal space with round cells near the corneal corpuscles (Hartnack, No. ix).

Fig. 4.--Cells with two nuclei full of bacilli from a cutaneous leproma. Seibert homog. immersion 1/16.

Fig. 5.--Two cells with bacilli from a leprous spleen. Fuchsin, methyl blue. Seibert homog. immersion 1/16.

Fig. 6.--From a leprous liver. White blood corpuscles with bacilli in a capillary. Seibert homog. immersion 1/16.

PLATE IX.

PLATE IX.

Fig. 1.--From a leprous liver. Bacilli in an endothelial cell of a capillary. Seibert homog. immersion 1/16.

Fig. 2.--Piece of a very leprous liver. Capsule below, cut surface above.

Fig. 3.--Cut surface of a very leprous spleen.

Figs. 4 and 5 and Plate X, Fig. 1.--Cross section of the seminal canals with bacilli around the nuclei of the walls and in the epithelium; in Plate X, Fig. 1, is shown an epithelial cell filled with bacilli.

PLATE X.

PLATE X.

Fig. 1.--Epithelial cell from a seminal canal, filled with bacilli.

Fig. 2.--A globus with a vacuole in which are fragments stained with Bismarck brown, probably the remains of nuclei.

Fig. 3.--A globus lying in a cell; the nucleus and a part of the cell-protoplasm preserved.

Fig. 4.--An epithelial cell from a seminal canal, filled with bacilli broken down into granules.

Fig. 5.--Cross section of a blood-vessel with bacilli in the endothelium and a white blood corpuscle filled with bacilli.

Fig. 6.--Longitudinal section of a blood-vessel showing bacilli in the endothelium, and a fibrinous coagulum enclosing two white blood corpuscles, one of them filled with bacilli.

Fig. 7.--Bacilli free between the red blood corpuscles.

Fig. 8.--A connective tissue space from the tunica albuginea filled with bacilli.

Fig. 9.--Cross section of a blood-vessel with bacilli around the nuclei of the surrounding connective tissue.

All the preparations from the testicle were hardened in Fleming’s or Müller’s solutions, and the drawings made with a Seibert homog. immersion lens 1/16. Plate IX, Fig. 5 with Seibert 1/8.

PLATE XI.

PLATE XI.

Fig. 1.--Bundle of nerve fibres from a ciliary nerve, the cells of Schwann’s sheath filled with brown granules.

Fig. 2.--The myelin sheath pressed in by a cell filled with granules.

Fig. 3.--Section from an old leprous macule.

Fig. 4.--Section from a recent leprous macule.

Both sections stained with Fuchsin and Methyl-green. Seibert homogen. immersion 1/16.

PLATE XII.

PLATE XII.

Fig. 1.--Cross section of a leprous ulnar nerve. The darkly hatched cells represent those filled with brown granules. It will be noted that the axial cylinder is wanting in many of the nerve fibres (Hartnack, No. ix).

Fig. 2.--A piece of neurilemma with flat connective tissue cells lying on it, containing brown granules darkened by osmic acid (Gundlach, No. viii).

PLATE XIII.

PLATE XIII.

Fig. 1.--Cross section of an atrophic muscle, growth of nuclei in the perimysium. Low power.

Fig. 2.--Cross section of an atrophic muscle with great development of connective tissue. Low power.

Fig. 3.--Proliferation of the nuclei of the perimysium. High power.

TRANSCRIBER’S NOTE-

1. Enclosed italics font in underscores.

2. Hyphenation has been standardized.

2. TABLE I.: Abbreviations have been used as shown in the Key. Longer entries have been replaced by indexes to Footnotes, which are listed at the foot of the Table.

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