Beige mouse which has partially defective natural killer (NK) function, is known as a model of Chediak-Higashi syndrome in man.
Six-week-old beige mice, C57BL/6J-bg/bg and W/W^νbg/bg, were provided from Okamura and used in the experiment. CBA and C3H mice or nude mice (BALB/c-nu/nu) were added as controls.
Bacillary suspensions of M. leprae were prepared from 3 materials. Kurume-naha strain, 6th and 7th generation, was obtained from nude mouse developed experimental leprosy (obtained from a previously untreated patient and was passaged in nude mice). Suruga-YM and Amami-KM strains were prepared from a leproma taken from a relapse case of a lepromatous patient and from a newly untreated patient, respectively. The mice were inoculated with 5.0×10³, 1.1×10⁵, 5.0×10⁵, 5.0×10⁶, 2.0×10⁷ and 7.0×10⁷ M. leprae per 0.05 ml into their right hind foot pads.
No significant differences were observed in the growth of M. leprae between the beige and normal mice even though the proliferation was remarkable in nude mouse. When a small number of M. leprae, 5.0×10³, 1.1×10⁵ and 5.0×10⁵ was inoculated in beige mice, Bacillary proliferation reached up to 10⁶ in the foot pad the same as normal control group. On the other hand, no any proliferation found in the mice inoculated with a large number of the bacilli.
The results indicate that the susceptibility of beige mouse to infection of M, leprae was not over than that of normal mice.

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The segregation policy on leprosy control in Okinawa has been enforced in 1938, when the policy delayed for 30 years after proclaim of leprosy prevention law. After then, in 1944, two leprosaria have been destroyed during the 2nd World War.
So leprosy segreation policy has been performed only for 6 years in Okinawa. The number of leprosy patients in the field was 547 and the leprosy prevalence rate (per population 10, 000) was 11.6 in 1900 and these numbers in 1944, were 1, 583 and 26.9, respectively.
The patients in the field incresed very much, because the ratio of segregation of the patients was not continually kept in high level (see Tab. 3).
According to the proclaim of new leprosy prevention law by the Ryukyu Government after the War in 1961, the out-patient treatment policy on leprosy control has put in operation in 1963.
After then, many out-patients have received treatment and the high ratio of treated patient (over 70%) has been covered continually for 20 years. (see Tab. 5).
So the prevalence rate has come down until 12.7 in 1983. Also active leprosy control programs have been performed by new law as follows:
1. School Survey : Some patients in school children have been detected from 1967 to 1970, but after then, no patient has been detected. School survey was not effective in the areas where Leprosy Incidence Rate was under 0.2%.
2. Mass Survey conbined Tb Survey: In 1978 and 1979, some patients could be detected, but since 1980 no patient was detected.
3. Contact Tracing Examination: The examination was most effective among other leprosy case-finding programs. (see Tab. 8, 9).
Leprosy Prevention Program: The following programs have been carried out.
1. BCG Vaccination for contact house-hold children was not so effective (see Tab. 11).
2. Chemo-prophylaxy program for contact house-hold children has been tried. One hundred and twenty-five children have been treated by DDS and 37 children by rifampicin (RFP) puls DDS.
The Incidence Rate of chemo-prophylaxy group was 0.7%, on the contrary, that of control group was 2.1%.

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Many leprologists have reported that incidence rate on house-hold contacts of leprosy patients is higher than that on non-contact children. To prevent the incidence on the children, BCG Vaccination has been tried in several areas and chemo-prophylaxis trial also has been carried out by Dharmendra and so on. The author has tried chemo-prophylaxis for 162 leprosy house-hold children since 1970 in Okinawa. One hundred and twenty-five children were administered with DDS (2mg/kg) every day for 2 years and 37 children were administered with the same drug in combination with RFP (10mg/kg) once a month for 6 months.
Thirty-five contact children (DDS group) were examined immunologically by FLA-ABS test and Mitsuda test before and after chemo-prophylaxis. Fourty-nine percent of contacts were immunologically unchanged by FLA-ABS test and sixty-nine percent were increased by Mitsuda test.
The incidence rate on leprosy among chemo-prophylaxis group was 0.71%, on the contrary the rate on non-prophylaxis group was 2.1%. The chemo-prophylaxis trial for leprosy house-hold contact children in Okinawa is fairly effective.

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Five hundred and ninety paucibacillary patients were administered multidrugtherapy since 1981. Except for 22, all patients were regular for treatement. Thirty-two pateints developed complications during therapy. All patients responded well to treatement. In the smear positive group, the regression of the lesions was relatively slow and the lesions persisted for longer. Patients were followed up for 28 months. At 18 months of post-MDT follow up, 13% of smear positive patients and 9 % of smear negative patients relapsed. An overall relapse rate was 10%.

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Erythema nodosum leprosum would be due to a fall in the amount of alive Hansen bacilli and not to the presence of dead bacillary bodies or to the action of detritus produced by thedead bacilli.
The alive Hansen bacilli consume fatty peroxides and in that way, take these metabolites out of the leprous' organism. By suppressing this flow of roxides, such toxic-inflammatory elements-the triggers of the erythema nodosum-are eliminated. Peroxides, usually formed in the leprous, are not used when Hansen bacilli die by a bactericidal chemotherapy. So, they will circulate freely, bringing about the erythema nodosum.
The above mentioned ideas can be summed up into the following premises:
a) Erythema nodosum of the leprous is produced by the absence of alive Hansen bacilli and not by the presence of dead bacilli and/or their derivatives.
b) Hansen bacillus is useful for the leprous-considering the formation of the rythema nod-osum-because it helps to neutralize this toxic-inflammatory effect produced by the fatty pero-xides.
c) The leprosy reaction in the patient uffering from leprosy-one of its symptoms is the erythema nodosum-would be produced by the increase of fatty peroxides in the tissues, by means of the two following mechanisms: first, lack of fatty peroxide consumption due to the death of Hansen bacilli (produced by bactericidal drugs) and in second turn, increase of peroxides, for instance, after iodide administration.

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