[Hansen's disease and nephropathy as its sequence].

Nephropathy as the sequences of Hansen's disease before and after the introduction of chemotherapy was compared referring to the report by Hayashi in 1943 and the summary of the autopsy reports from 1978 to 1981 at National Hansen's disease hospital Zenseien. Unlike the high rates of tuberculosis as the cause of death before the introduction of chemotherapy (41.3%) those thereafter decreased to be negligible. On the other hand the comparison of the rates of nephropathy with the same way as that of tuberculosis was impossible since the description about nephropathy by Hayashi was not sufficient to characterize each nephropathy since he included arteriolitis, glomerulonephritis and interstitial nephritis together in the term of nephritis. Death rate due to nephritis among Hansen's disease patients according to Hayashi at that time was 21.2% which was twice as many comparing to that in the other cases. According to the report about the cases of Zenseien those reported to have glomerulonephritis was 37.3% though those were not necessarily listed as the cause of death. Also the nephropathy including fibrinoid angitis with occasional microaneurysmal dilatation of afferent arteries, glomerulitis, sclerosis and stricture of efferent arteries likewise ischemic acute tubular necrosis possibly as the result of these angiopathy seemed to be present. These vascular changes partially resemble to that of microscopic periarteritis nodosa but seems to be common in the smaller arteries. In conclusion, unlike the case of tuberculosis the rate of nephritis including glomerulitis, arteriolitis and interstitial nephritis as Hayashi used as his criteria does not seem to have decreased. Therefore, the critical analysis of the nephropathy especially of that relating to the arteriolitis should be done to obtain the knowledge to suppress its occurrence.

A genomic study on the cultivable and nerve invading Mycobacterium HI-75 after the recovery 3 months of the inoculation to nude mice.

The sequence of the polymerase chain reaction (PCR) product of 16S ribosomal RNA (16S rRNA) of the leproma-derived and cultivable Mycobacterium HI-75 (M. HI-75) which was obtained from the infected regions of inoculated mice, was examined and compared with that of the cultured bacteria by the direct sequencing techniques. The sequence was completely consistent with the cultured bacilli in the comparable 837 bases of 16S rRNA. The mycobacterium examined in this study was originally isolated as M. leprae (ML) by Skinsnes, et al. in 1975 from leproma of a lepromatous type Hansen's disease patient and therefore named as Mycobacterium leprae HI-75 by them, and was maintained from 1984 using either Ogawa's or Sauton's media in the beginning and Ogawa's medium enriched with glucronic acid and N-acetyl-D-glucosamine recently. Sasaki and Hamit reported the nerve invasion and the growth of the inoculated bacilli either to the nude mice or the I131 treated immunocompromised Swiss mice. We previously reported that cultured HI-75 was most similar to M. scrofulaceum by the direct sequencing of the gene of 16S rRNA. The 16S rRNA obtained from the mouse tissue in the present study indicated that M. HI-75 would be a variant of M. scrofulaceum possessing an ability to invade into peripheral nerve. The results suggest that the HI-75 strain claims a nature as a pathogen to develop a leproma-like lesion.

[An experimental nerve lesion simulating leprous neuropathy produced in the nude mice by the inoculation of a leproma-derived and cultivable mycobacterium HI-75].

Among the lesions caused by mycobacteriosis, peripheral neuropathy has been regarded as the pathognomonic one peculiar to leprosy which is caused only by M. leprae (ML) which can not be cultivated. If that whole sentence is correct, no past report should be in existence concerning the peripheral neuropathy caused by the experimental inoculation of certain cultivated mycobacterium and not of ML. There was, however an exception challenging to that theory which was done by Sasaki et al. in 1985. The author, therefore, tried to reproduce this type of lesion in the nude mice modifying their method to know whether a leproma derived and cultivable mycobaceterium HI 75 (III 75) still have the ability to cause neuropathy as they observed. The mycobacterium utilized in the study was originally separated from a leproma by Skinsnes et al. as M. leprae (ML) III 75 in 1975 and was identified as M scrofulaceum (MS) by Stanford et al. in 1977. The strain was kept on cultivating in his laboratory till 1984 and in our thereafter. The groups of mice served for the present experiments consisted of two. The mice in the first group were infected intravenously and those in the latter group were by subcutaneous injections in the cheeks mixed with hyaluronic acid. The first one was unsuccessful to make remarkable neuropathy, however, the second one showed the marked invasions of the bacilli in peripheral nerves encompassed by numerous macrophages which were heavily loaded with the mycobacteria. The author believes that the present result is helpful to solve the question about the differences of the characteristics of HI-75 before and after causing neuropathy in vivo, the mutual relationship between ML, MS and III 75 and the causative organism beside ML if present.