A study was made on the annual changes in the positive rate for acid-fast bacilli (AFB) at the initial bacteriological examination of newly detected pulmonary tuberculosis among male NTT (Nippon Telegraph and Telephone Corporation) employees in the Tokyo area during a period of 32 years from 1960 through 1991. The influence on the changes of recent introduction of fiberoptic bronchoscopy for oftaining the specimen was also analyzed, and the following results were obtained.
1. Results obtained by the conventional bacteriological method using expectorated sputum or aspirated gastric juice as the specimens.
(1) The annual incidence of bacteriologically positive (smear and/or culture positive) cases constantly decreased and reached the lowest in 1981, then ceased to decline and remained at the level of 1981.
(2) The annual ratio of AFB positive by smear and the ratio of smear and/or culture positive cases to the newly detected cases of pulmonary tuberculosis were constant during the entire observation period.
(3) The ratio of AFB positive by smear to the newly detected cases annually increased but did not increase when the obserevation period was limited to within 1976 to 1991.
2. Results obtained by fiberoptic bronchoscopy in combination with conventional bacteriological methods.
(1) Both the annual incidence of smear and/or culture positive cases and the ratio of these cases to the newly detected cases of pulmonary tuberculosis showed a tendency to increase in both the 80's and 90's.
(2) The annual incidence of AFB positive by smear and the ratio of these cases to the newly detected cases of pulmonary tuberculosis also indicated a tendency to increase in the 80's and 90's, although not apparent when compared with the increases in the incidence of smear and/or culture positive cases and in the ratio of these cases to the newly detected cases of pulmonary tuberculosis.
In conclusion, the recent increase in number of AFB positive cases, especially those found positive by smear and/or culture at the initial bacteriological examination may be due to bronchoscopical procedures in obtaining the specimens.

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A total of 1397 patients were admitted to our hospital between 1986 and 1992. Of those patients, 68 were diagnosed as having tracheo-bronchial tuberculosis, when examined using a bronchofiberscope. We investigated the cases of 50 patients who were examined during the early stages of the diagnosed them as having pulmonary tuberculosis. The number of women in the group was larger than men, and young patients made up 30% of the group. Upon admission to the hospital, all of the patient's sputum examinations were tested positive, but their chest roentogenograms did not show a progressive stage. After treatment, patient roentogenograms showed improvement, however there was no improvement in tracheo or bronchial conditions. It was therefore believed that therapy was impeded by tracheobronchial tuberculosis, but only one patient was treated surgically. It was deemed that the delay of patients seeking treatment was not long, however, the delay for doctors in beginning therapy was very long. Many of the patients with tracheo-bronchial tuberculosis complained of coughing and sputum, therefore diagnosis and therapy should be performed as soon as possible.

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A study was performed on the therapeutic efficacy of KRM-1648 combined with LC9018 in beige mice infected with Mycobacterium intracellulare. Each mouse was intravenously infected with 3.9×10⁶CFU, and then given 0.2mg of KRM-1648 emulsified in 2.5% gum arabic-0.2% Tween 80 by gavage once a day, six times per week, beginning 24h after infection for up to eight weeks. A sc injection of 0.1mg LC9018 in saline was given once or twice per week, beginning two weeks before infection to the end of experiment. An evaluation of the therapeutic efficacy of these drugs against the infection was performed on the basis of incidence and degree of gross lung lesions and bacterial loads in the lungs and spleen. Lung lesions were not observed in all experimental groups at four weeks after infection. However, at eight weeks after infection, although lung lesions were observed in all experimental groups, the degree of lesions was much milder in those mice receiving KRM-1 648 than in the control mice. The degree of lesions in the mice receiving LC9018 was much the same as that in the control mice. Moreover, the degree of lung lesions in mice treated with a combination of KRM-1648 and LC9018 was more severe than in those mice treated with KRM-1648 alone. The CFUs of organisms in the lungs and spleen of the mice treated with KRM-1648 were considerably lower than those of the control mice (P<0.05), but the CFUs in the mice treated with KRM-1648 and LC9018 were nearly the same as those mice treated with KRM-1648.

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After complaining of right hypochondrial pain, a 36-year old man was diagnosed as having a gastric submucosal tumor at a nearby hospital and admitted to Chiba Cancer Center Hospital. On admission, a hard and immobile mass was palpable on the right upper quadrant. Laboratory findings were within normal limits.
A chest X-ray revealed bilateral pleural adhesions and streaking shadows in the bilateral lung area. These findings were assumed to be due to a prior tuberculous infection. Upper gastro-intestinal series and endoscopic examination showed a protruding lesion on the stomach body. An abdominal CT showed another lesion adjacent to the stomach antrum. A resection was carried out under the presumptive diagnosis of multiple gastric submucosal tumors.
Exploration of the abdomen revealed widespread fibrous adhesion suspected to be due to prior old tuberculous peritonitis. Two tumors were located here.
One was adjacent to the stomach body, and the other was adjacent to the liver and abdominal wall. Pathologically, both were caseated necrotizing granulomas composed of mature epitheloid cells and Langhans giant cells.
A close examination revealed that one originated from the serosa of the stomach and the other from the peritoneum. Both were believed to be relatively new lesions. Pus obtained from the tumors tested positive for acid-fast bacilli. A post-operative tuberculin skin test was given and checked highly positive. From these findings, this case was diagnosed as local reactivation of old tuberculous peritonitis. After antituberculous chemotherapy at our hospital, the patient was discharged and sent home without any symptoms.
The reason for the local reactivation was unknown.

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An autopsy case of 63-year old male of atypical mycobacteriosis with severe scoliosis was reported.
He was diagnosed as atypical mycobacteriosis in 1981 and controlled by antimycobac terial treatment. But since 1989, dyspnea and sputum have been increasing, new abnormal shadow in company with progression of curvature of the scoliosis was revealed on the chest roentgenogram.
In spite of various treatments for mycobacteriosis, he died of respiratory failure. The aggravation of this mycobacteriosis brought on advancement of malnutrition and impairment of cell mediated immunity.
Findings of autopsy showed the remarkable chest wall deformity and tuberculous change of the lung parenchyma.
In this case, chest deformity was thought as the major risk factor of onset of mycobacterial mycobacteriosis.

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Functional changes in T lymphocytes and macrophages (M0s) in host mice during the course of Mycobacterium intracellulare infection were studied. In both strains of mice, BALB/c or C57BL/6 (susceptible to M. avium complex) and CBA/JN or C3H/He (resistant to M. avium complex), the smooth, opaque and dome-shaped colonial (SmD) variants of M. intracellulare were easily eliminated from the site after week 2 of infection. In contrast, the smooth, transparent and irregularly shaped colonial (SmT) variants showed steady growth in the former strains of mice and persisted for long time even in the latter strains of mice. No difference was found between persistence of the organisms in euthymic (×/×) and athymic (nu/nu) BALB/c mice during the first 4 weeks after infection. Thereafter, more rapid growth was seen in the spleens and lungs of nu/nu mice. Thus, matured T cells may be important for the prevention of the progression of M. intracellulare infection to the terminal state.
Next, the profiles of generation and characteristics of splenic MOs which suppress the Con A mitogenic response of splenic T cells in host CBA/JN or BALB/c mice during the course of M. intracellulare infection were investigated. In M. intracellulare-infected mice, reduction in some cellular functions of host splenic T cells, such as the Con A mitogenic response and mixed leucocyte reaction, were seen around 2 weeks after infection, and this was accompanied by appearance of immunosuppressive Mc5s in spleen cells (SPCs). In this phase of the infection, M. intracellulare-induced splenic MOs showed a markedly increased ability to produce reactive oxygen radicals in response to phorbol myristate acetate. Thus, the expression of suppressor activity of M. intracellulare-induced Ms seems to be closely linked to their activated state. Indeed, Mcbs induced with various stimulants including thyoglycollate, zymosan A, OK-432, BCG, and live M. intracellulare possessed immuno suppressive activity as well as active oxygen producing ability. There was a significant correlation between them.
A large proportion of the immunosuppressive MOs exhibited suppressor activity dependent on prostaglandins, long chain fatty acids and their acyl moieties, nitric oxide, and membrane functions related to microfilaments. It was also found that the generation of IL-2-reactive T cell populations in response to Con A and the expression of IL-2 receptors on them were markedly inhibited by M. intracellulare-induced splenic Mcbs, whereas they caused no significant reduction in the IL-2-producing ability of normal SPCs. M. tuberculosis also induced similar types of immunosuppressive Mφs and their activity was considerably greater than those of M. intracellulare-induced Mφs.

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