再発と化学療法,その実験結核モデル

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Seventy-five mice were infected intravenously with 0.02 mg of a streptomycin-dependent strain of tubercle bacilli, and streptomycin of 10 mg per day was administered intraperitoneally for the first 2 weeks to support bacillary multiplication. At the time of 10 week infection, the mice were divided into 2 groups of equal half; one group to be readministered with streptomycin and the other to be treated by combined administration of streptomycin and isoniazid (0.2 mg per day) for 4 weeks. During the whole experimental period of 20 weeks, th e timecourse examination of viable counts of the lung and spleen were made with 2 week intervals. For this purpose, mice were sacrificed sampling 4 at random from each group and a serial 10fold dilutions of homogerate of the weighed amount of tissue were inoculated onto glycerolegg media containing streptomycin in 100 mcg per ml. The results are summarized in Fig.2. In both the lung and spleen, the infecting bacilli multiplied in response to streptomycinadministration for the first few weeks and then declined in viable counts gradually. when the drug was given again at the time of 10 week infection, the bacilli in the lung were stimulated to resume multiplication. The viable counts reached the level higher than the previous peak. Many typical tubercles appeared on the surface of the lungs. In the spleen, however, the bacilli did not multiply at all despite of the streptomycin administration. This organ difference is explained by an uneven distribution of acquired immunity, being much stronger in the spleen. The acquired immunity was considered to have been produced by the bacillary multiplication during the first two weeks. Interesting was the different eff e cts of isoniazid on the fate of infecting bacilli in these organs. The drug was highly active in decreasing viable counts of the lung, but was almost inactive in the case of the spleen. This observation supported our previous assertion that isoniazid is effective only against multiplying bacilli but not against resting bacilli. On the other hand, when streptomycin was not given just after infection (Fig.1), the infecting bacilli did not multiply unlike the case of Fig.2. It is considered that, under this situation, acquired immunity was not established in these mice. Therefore, bacillary multiplication did occur even in the spleen in response to streptomycin administration at the time of 10 week infection and isoniazid was effective against these bacilli. The experimental system as described above w i l l be a model for "relapse and chemotherapy in tuberculosis in association with acquired immunity".
一般社団法人日本結核病学会の論文

再発と化学療法,その実験結核モデル

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