[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.

Pathological investigation of armadillos infected with Mycobacterium leprae.

An infection experiment with M. leprae was carried out using 20 nine-banded armadillos. As a result, the development of leprous lesions and a marked multiplication of AFB were confirmed in a high rate of 13 out of 15 cases (86.8%) in the inoculated groups. These changes were found to be progressing at post mortem of one case even with the shortest life period for 7.5 months and were very serious in one case with the longest life period for 33 months, suggesting the continuation of symptoms, though it is an expression neglecting the individual difference in susceptibility to leprosy. Among infected viscera with AFB, the most conspicuous lesions were found in the liver and spleen. The developed lesions were found in the lung, stomach and kidney which had been never seen in HD in human cases, and so, which may characterize armadillos' leprosy. The change in the peripheral nerve was not so severe when compared with that in HD in human cases. This difference will remain as a future pathological problem to be solved.

On the beta-glucuronidase binding protein (BGBP) of microorganisms. Its purification, the antiserum preparation against that and its localization in leproma and the other infectious lesions shown by immunohistologic method.

Our previous studies suggested that M. leprae (ML) grow in peripheral nerves and lepra cells because ML metabolize hyaluronic acid (HA), and use its component for their growth by the aid of host enzyme combined to the bacilli derived beta-glucuronidase binding protein (BGBP). In this study, therefore, we examined the method to purify BGBP from a mycobacterium HI-75 originally separated from a leproma and cultured by modified Ogawa's medium containing split products of HA (glucuronic acid and N-acetylglucosamine). The distribution of BGBP in leproma and the other lesions consisting of hepatitis B virus infected liver and M. avium-intracellulare infected lung tissue were also immunohistologically examined. As the result, the best method to get BGBP was preparatory electrophoresis in the final step of the purification and not the molecular sieving. The BGBP was actually proven in leproma and the other infected tissues as described, indicating the abilities of these microorganisms to utilize the metabolic machinery of the host with the similar ways to that of ML.

Immunoepidemiological studies on subclinical infection among leprosy household contacts in Thailand.

Three-thousand-fourteen leprosy house-hold contacts in Thailand were surveyed by their personal history, physical examination, and immunological tests. The results were compared with those obtained from villagers in leprosy-endemic and nonendemic areas. The percentages of young people, students, children and grandchildren of the patient, the contacts of multibacillary leprosy cases, long duration of contact, BCG vaccination, FLA-ABS and Dharmendra's lepromin-positive responders were significantly higher in the household contacts than those in the villagers. The percentages of neural and dermal symptoms were not significantly different between the household contacts and the villagers in the endemic area, but the percentages were higher than those of the villagers in the nonendemic area. A PPD skin test was more frequently negative in the former two groups than in the latter. Both FLA-ABS and lepromin tests showed a significant correlation with the age of the contacts, their occupations, blood relation to the patient, the duration of contact, BCG vaccination, dermal signs such as an ill-defined plaque or macule with or without sensory loss, but did not correlate with sex, type of leprosy in the patient, or other skin diseases. The FLA-ABS test in the house-hold contacts and the villagers in an endemic area showed a significant correlation with the neural signs, such as enlargement of the peripheral nerve without sensory loss. These suspicious dermal and neural signs and symptoms were therefore considered signs of Mycobacterium leprae infection. The FLA-ABS test was sufficiently sensitive for detecting this infection and did not correlate with the lepromin or PPD skin tests. FLA-ABS-positive but lepromin-negative responders were found in 33.5% of the house-hold contacts. They were considered to be a high-risk group who may develop clinical leprosy. Nearly half of them were treated with dapsone or BCG according to the results of the PPD skin test. Follow up of these contacts, together with the remaining contacts without treatment, is in progress.