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Unlabelled: The aim of this research was to clarify epidemiological characteristics of nontuberculous mycobacteriosis deaths in Japan. We analyzed the frequency of deaths due to nontuberculous mycobacteriosis (NTM) and regional differences using the Vital Statistics of Japan, published by the Ministry of Health, Labour and Welfare. The crude death rate was calculated using the Population Census of Japan published every 5 years (Ministry of Internal Affairs and Communications). In addition, changes in the proportions of death cases due to NTM disease among total autopsies were calculated using the Annual of the Pathological Autopsy in Japan (The Japanese Society of Pathology)., Results: NTM disease deaths appeared for the first time in 1970, with a marked increase by 2007, when there were 912 certified deaths. The increase was more marked after the mid-1990s. The number of women's deaths exceeded 300 in 1999 and reached 570 in 2007, while that of men exceeded 300 in 2001 and remained at nearly the same level until 2007. The death rate increased in all eight regions of Japan. The highest single-year regional death rate was 212 in Kanto in 2005. However, correcting by population size, the crude death rate was higher in the western regions of Japan than in the eastern ones. The proportion of NTM among total autopsies also showed an increase from 0.066% in 1993 to 0.304% in 2007. Included in the report is a comparison of trends of NTM deaths with those of major respiratory diseases including tuberculosis, emphysema, bronchial asthma and airway cancers.

Accumulated information obtained in the 10 years since the clarification of the whole genome arrangement of tubercle bacilli has enabled us to presume a long history of tubercle bacilli from its first appearance on earth to the present epidemics in the world. It is presumed that tubercle bacilli appeared around 35,000 years ago through horizontal transfer mutation from a kind of environmental mycobacteria that could be tracked back 2,500,000 years, and expanded thereafter by 'bottleneck effects'. These mutated mycobacterial species adapted to humans, appearing in central Africa and then being carried to India-Oceanian and Middle East countries. The oldest human bone tuberculosis in a mummy of 9,000 years ago was found on the east coast of the Mediterranean Sea. Explosive transmission of tuberculosis was presumed to have progressed along with urbanized human life in the world-oldest Mesopotamian culture, followed by spreading to other areas, including East Asia, the Mediterranean region, Russia, and North Europe. The second epidemics, caused by a mutated Beijing family of the modern type, prevailed in central China and Southeast Asian countries, following the marked population growth in this area during the next 1,000 years. The majority of Beijing family strains isolated in Japan and Korea are, however, found to be of the ancient type, differing from the isolates from continental China, which are mainly of the modern type. The results of these studies may cast a new light on the understanding of tuberculosis epidemiology and also clinical medicine.

A 90-year old man was admitted to a hospital because of consciousness loss with hyponatremia. Although his symptom promptly improved with Na supply, his chest X-ray film showed pulmonary infiltration and direct microscopy of sputum smear was positive for acid-fast bacilli, then he was referred our hospital and was admitted. We made a clinical diagnosis of pulmonary tuberculosis with SIADH based on detailed examinations. But he should neither respiratory symptoms nor fever. He was medicated with the standard antituberculosis drugs with fluid restriction, and his tuberculosis and hyponatremia were improved gradually. We should be more careful about pulmonary tuberculosis irrespective of its severity as a cause of SIADH.

Histopathological examinations were carried out on 2 cases of Mycobacterium avium complex (MAC) disease of nodular bronchiectasis (NB) type on radiograms. The removed lung specimens revealed histological findings of granulomatous bronchiolopneumonia, consisting of epithelioid cell granulomas with lymphocytic infiltrations without exudation in the alveolar areas surrounding the respiratory bronchiole. The central bronchiolar walls were also affected by epithelioid cell granulomas with lymphocytic infiltration, occasionally showing polypoid protrusion into the bronchiolar lumen accompanying emphysema in the peripheral alveolar area. Bronchial lesions seemed to progress from peripheral to central airway with consequent atrophy and disappearance of intramural smooth muscles, resulted in bronchioloectasis. These histological findings well correspond to radiographical 'nodular bronchiectasis'. Large histiocytic granulomas without caseous necrosis developed in some area, which are not usually found in tuberculosis lesions. Epithelioid cell granulomas were occasionally found in the hilar lymph nodes as well as in the walls of lymphatic vessel in the pulmonary interlobular tissues, indicating intrapulmonary lymphatic spread of the mycobacteria.

Two different processes have been proposed for pathogenesis of Mycobacterium avium complex (MAC) disease which show the middle lobe syndrome: 1) middle lobe bronchiectasis followed by MAC infection and 2) MAC disease resulted in secondary bronchiectasis. Two surgical specimen from MAC cases showing middle lobe syndrome were studied histo-pathologically. The first case was a 60 year-old female with frequent bloody sputum, who had been diagnosed as bronchiectasis in her childhood. Pathological examination of the resected middle lobe showed prominent cylindric bronchiectasis in the indurated middle lobe, and epithelioid cell granulomas were scattered limited to the fibrous bronchial walls, without any granulomas in the lung parenchyma. These findings suggested a secondary infection of MAC to the non-specific pre-existed bronchiectasis. The second case of a 55 year-old female having repeated bloody sputum, who was diagnosed to be tuberculosis but no improvement with anti-tuberculosis drugs. Pathological examination of the middle lobe showed scattered epithelioid cell granulomas with lymphocytic infiltration in the lung parenchyma. A few epithelioid cell granulomas were also found in the mucosa of middle lobe bronchi. In this case, pulmonary MAC lesions seemed to precede the central bronchial lesion with later development of bronchiectasis. Summarizing above findings two different mode of pathogenesis ways may be considered; one is non-specific bronchiectasis followed by middle lobe MAC disease and the other is pulmonary MAC lesion in the middle lobe as a primary change.

For the purpose to know the pathogenesis of caseous necrosis in tuberculous lesion, authors compared the presence and the number of mycobacteria in the pulmonary tubercles of various histological types. Forty pulmonary tubercles obtained from 16 patients (9 males, 7 females; mean age 51) were examined. By Ziehl-Neelsen (ZN) method, acid-fast bacilli were detected in 40% of 5 proliferative, in 12.5% of 24 productive and none of 11 sclerotic granulomas. By immunohistological staining with anti-BCG antiserum, positive staining was observed in 60%, 87.5% and 91% of each type of granuloma, respectively. Types of necrosis were classified by silver-staining as necrosis after exudative reactions (EN), necrosis after productive reactions (PN) and filled materials after softening and liquification of necrotic lesions (LN). EN was observed in 24 tubercles, and mycobacteria were stained in 8% of EN by ZN method and in 75% by immunohistological method. PN was observed in 21 tubercles, and mycobacteria were detected in none and 5% of such type of necrosis by respective method. LN was observed in 28 tubercles, and mycobacteria were detected in 11% and 71% of these lesions by respective method. So, positive ratio by immunochemical method was significantly higher in EN and LN than in PN. Further, mycobacteria were stained with anti-BCG antiserum as granules and the number of such granules were much more numerous in EN and LN than in PN (p < 0.01). From these results, it was suggested that necrosis might occur by different mechanisms in exudative reactions and in productive reactions.

Forty-eight cases of tuberculous hilar lymphadenopathy were studied comparatively between the groups experienced before and after 1975. We found the following characteristics in the clinical manifestations and in the mode of onset among the recent cases as against the classical ones. (1) Age distribution of cases shifted from younger to elderly groups. (2) Roentgenologically, typical primary complex has been decreasing, while the atypical patterns such as solitary mediastinal lymphadenopathy or those associated with healed pulmonary lesions have increased. (3) Since the introduction of RFP to the treatment of tuberculosis, cases of hilar lymphadenopathy incidentally diagnosed with the early exacerbation due to RFP has been increasing. (4) Of the total of 48 cases, 10 were presumed not being originated from the primary infection, but from reactivation. (5) Relative increase of such cases may partly explain the shift of hilar lymphadenopathy to elderly group.

Pathological examination of tuberculosis sequelae was carried out to clarify the nature and pathogenesis of sequela. Twenty-one cases were chosen from autopsied cases in the past 15 years; male 20, female 1, and age ranged from 43 to 78 and mean age was 59 years. Sequela cases were divided into two subgroups; low lung function subgroup (LLFS) and non-low lung function subgroup (NLLFS). LLFS had 10 cases and mean age was 55 years. Ten cases of bilateral fibrotic cavities, 10 cases of bilateral upper lobe atelectatic indurations, 4 cases of pneumonectomy, 4 cases of thoracoplasty, and others were basic lesions of sequela. Lobar atelectatic induration was formed of organized destructive pneumonia and suspected to follow the tuberculous granulomatous pneumonia. Seven cases of localized emphysema, 11 cases of bullae were seen as the secondary change. Mean heart weight was 335 gr and left ventricle + septum: right ventricle (LV+S: RV) ratio decreased to 1.24 among LLFS and mean heart weight 273 gr and Lv+S: RV ratio was 2.35 in NLLFS. Remaining of cavities were observed in 15 cases and Aspergillus infection was seen in 11 cases (7 cases formed fungus ball, 4 cases showed semi-invasive growth and 2 out of 4 showed necrotizing pneumonia and formed direct cause of the death). Terminal infection was seen in 10 cases. According to our data, chronic lung failure with cor pulmonale, secondary fungus infection in the remained cavity, and terminal infectious pneumonia were serious consequence of tuberculosis sequela.