Morphological studies were conducted on the tissues and lepra cells in the lymphnodes of tuberculoid leprosy. Tuberculoid leprosy occurs by a combination of bacilii which have decreased in proliferative activity and virulence and a host in which some resistence is already present. This stage either disappears or alters to another type. Though tuberculoid in type, it is a systemic disease so there is a proliferation of lepra bacilli and at a certain stage in the latent period or onset, lepra cells are formed. These then are converted to foam cells and then to neutral fat. The changes should be apparent histopathologically.
In the present study, 59 samples of lymphnodes were obtained from 22 cases of leprosy at death and examined for the presence of foam cells and tuberculoid lesions.
The following was observed.
1) Deposition of fat similar to that observed in the lymphnode of the lepromatous type is found in the tuberculoid type.
2) It was difficult to find tuberculoid lesions in the lymphnodes but a case was observed in which there was hyaline fine fibrosis and it is believed that this had developed from a tuberculoid lesion.
3) Deposition of fat (Mainly, fat accumulating type with numerous giant vacuoles, according to the author.) similar to the one observed in the lymphnode of lepromatous type is found in tuberculoid type. The author regards it as a lymphatic absorption process, which may perhaps stand in relation with antileprotic oil drug treatment, not as a degenerative process which might theoretically occur in proliferating bacillary foci.

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1. My. ulcerans is an acid-fast bacillus measuring 1.7-7.0μ in length and 0.2-0.5μ in width. Its morphology and staining properties resemble those of other mycobacteria.
2. My. ulcerans grows on Petrognani's culture medium, Oka-Katakura's medium, Kirchner's medium and Sauton's medium at a temperature below 37°C and above 25°C (optimum temperature 30-33°C). The colonies of My. ulcerans on the culture media have an appearance similar to those of H 37 Rv. My. ulcerans does not grow on glycerine agar or glycerine broth.
3. My. ulcerans can not easily be suspended homogenously in physiological saline.
4. My. ulcerans is strongly acid-fast, and alcohol-fast, and its "Kf (Preis)" is 2-3.
5. The catalase activity of My. ulcerans is about the same intensity as that of My. tuberculosis.
6. My. ulcerans shows resistance against the influence of temperature and disinfectants in nearly the same degree as My. tuberculosis and My. leprae murium.

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Suppressive and therapeutic studies using INAH and its derivatives were conducted in experimentally infected murine leprosy mice.
Derivatives No. 253, No. 254, No. 282 and No. 284 showed marked suppressive and therapeutic actions. The effect of these agents on the serum protein fractions was examined by paper electrophoresis and the following results obtained.
(1) In the experimentally infected non-treated mice, the albumin is reduced, β-globulin is markedly increased and γ-globulin is almost unchanged compared to the normal control.
(2) The serum protain of the mouse used in the suppressive experiment differs littlefrom that of the normal control. A reduction in albumin and rise in β and γ-globulin was observed in the mice used in the therapeutic experiment but the rise in the β-globulin was smaller compared to that of the untreated animal.
(3) The changes in the serum protein were unrelated to the kind of agent administered.
(4) There was no relationship between the changes in the serum protein of the animals in which medicament had been administered and the numberof murineleprosy bacilli found at the site of inoculation.

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This paper deals with the influences of many substrates known as nutritious elements or accelerating substances and of organ and murine leproma extracts of rats upon the respiration of the murine leprosy bacillus which had been treated with trypsin and centrifuged.
The results obtained are below:
1) Seventeen substrates, such as glycelin, succinate and vitamin B12, did not accelerate the respiration of the bacillus in single addition. When liver or testis extract inactivated 60°C30min. was combined with succinate, the respiration is accelerated.
2) Untreated murine serum prevented the respiration. Liver extract, when inactivated, produced no influence. Testis extract showed acceleration of which intensity was stronger whed untreated than when inactivated. Acceleration was observed when extracts of murine leproma in liver, testis or subcutaneous tissue were applied. In these extracts inactivation produced more intense acceleration than untreated.
Attention should be paid to the fact that extracts of various organs and murine leproma accelerate the respiration of the murine leprosy bacillus.

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Skin tests were conducted with serial dilutions of the same and different lots of lepromin preparation (the Dharmendra antigen) in guinea pigs sensitized with tubercle bacilli and in leprosy patients.
The results were as follows.
1) Serial dilutions from 150% to 66.6% of the Dharmendra antigen were administered in guinea pigs sensitized with tubercle bacilli and in leprosy patients. It was found that the animals responded with greater sensitivety and constancy and a difference in reaction size was noted compared to the leprosy patients.
2) Five lots of lepromin preparations of different manufacture, date and place were examined. The potency relation of these samples showed a similar trend.
3) Therefore, evaluation of the potency of lepromin is considered possible by using guinea pigs sensitized with tubercle bacilli.

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As a preliminary experiment, studies were conducted on the possibillity of utilizing the mouse as the experimental animal in immunological studies of murine leprosy and the best site of BCG inoculation. It was found that the greatest suppressive effect was obtained at 90 days by intra peritoneal inoculation but subcutaneous and intramuscular inoculation also showed an inhilbition compared to the control. Oral and intravenous inoculation however were ineffective. With a lapse of 120 days, the difference between the treated animals and untreated controls becomes insignificant. (See Fig. 1)
The distribution of bacilli in the lymphnodes followed the order of suppression of the leproma. (See Fig. 2)
From these results it can be seen that use of mice in immunological studies on murine leprosy is feasible and the intraperitoneal route is the most effective. In the second experiment, γ-globulin extracted from the serum of leprous rats, healthy rats, leprosy patients and healthy human subjects was injected in the mouse and the effect on the onset of murine leprosy examined. No effect was observed. It is not clear however whether this lack of effect was due to the absence of immune substances in the γ-globulin or impossibility of passive immunization in the mouse. (See Fig. 3)

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In order the clarify the role of the reticuloendothelial system in the activation of immu nization in murine leprosy, the reticuloendothelial system was blocked with India ink, BCG inoculated and the suppression of development of leproma studied. It was found that at 90 days, the leproma in the india ink injected animal was somewhat larger than that in the normal control. The inhibitory effect was less in the animal in which BCG was administered after injection of india ink than in the mouse in which BCG alone was in oculated. The leproma was larger in the mouse in which M. avium vaccine was injected after injection of india ink than in the animal in which india ink alone was injected. From these results, it can be seen that the reticuloendothelial system is related to the strength of immunity. (See Fig. 1)
Vaccine prepared from acid-fast bacilli other than BCG which have some pathogenicity in mice as the H37Rv, INAH resistant strain and avian strain have antigen activity for murine leprosy.(See Fig. 2)

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It wos previously found that isonicotinoyl-3-methoxy-4-hydroxybenzal hydrazone (No.254) markedly suppressed onset of murine leprosy and the effect was even greater than that of INAH. It was also found that the effect of isonicotinoyl-4-hydroxybenzal hydrazone, which lacks the-OCH₃ radical, was smaller than No. 254. It was therefore assumed that the-OCH3 radical may play an important role so studies were conducted with isonicotinoyl 3, 4-hydroxybenzal hydrazone (No. 282), which possesses two-OCH₃ radicals. The following was observed.
(1) The onset suppressing action of No. 282 is greater than that of INAH or No. 254.
(2) Most of the bacilli in the tissues of mice treated with No. 282 show degeneration and typical globi are rare.
(3) The ulcer of murine leprosy is cured by treatment with INAH but in most of the cases the leproma remains and acid-fast bacilli are still present. No. 254 and No. 282 however, have a moderately strong therapeutic effect on the leproma, especially No. 282.
(4) Oral administration of 5 mg daily of No. 282 results in apparent cure of the pathological changes and subcutaneous inoculation in healthy mice of an emulsion of tissue taken from the site of inoculatin does not give rise to infection.
(5) It is suggested that the-OCH₃ radical plays an important role in murine leprosy.

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Triton, Taifumin A, Minophagen AT, Chaulmoogra oil and olive oil were experimentally administered for 150 days in experimentally infected murine leprosy mice but proved ineffective.
Chaulmoogra oil was ineffective in mice but an effect was apparent in the rat. Similar results had been obtained in the rat in a series of studies conducted in 1942. From this finding, it is suggested that rats rather than mice should be used in experiments with non-chemical agents as Chaulmoogra oil.
Of the antibiotics examined, Dextromycin clearly suppressed onset but Acidomycin was without effect.

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Rat experimentally infected with murine leprosy were treated with daily subcutaneous injections of 0.2cc of frozen placental extract (containing 20mg reakdown product of placental tissue) for a total of 4.2cc-7.0cc. Histopathological examinations were then conducted and the following results obtained.
The subcutaneous tissue surrounding the leproma showed a strong inflammatory reaction and the necrosis and destruction of the leproma itself was greater than in the control.
The mechanism by which this reaction takes place must be studied.

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