Kekkaku(Tuberculosis)
Online ISSN : 1884-2410
Print ISSN : 0022-9776
ISSN-L : 0022-9776
Volume 64, Issue 8
Displaying 1-6 of 6 articles from this issue
  • Ichiro TOIDA
    1989 Volume 64 Issue 8 Pages 487-497
    Published: August 15, 1989
    Released on J-STAGE: May 24, 2011
    JOURNAL FREE ACCESS
    Acquired immunodeficiency syndrome (AIDS) was first noticed in 1981 by Centersfor Disease Control (CDC).
    Since then, the number of patients has continued to increaseand reached 151, 790 by the end of April 1989. AIDS is caused by the infection of Human Immunodeficiency Virus (HIV), which infects CD4+ cells including helper-inducer T-cells. The infection with HIV thus induces severe impairment of the immune mechanism, especiallyof cellular immunity, of the infected host, and, as a result, various types of opportunisticinfections and special types of tumors could occur.
    Infections with mycobacteria may, of course, complicate to the AIDS patients as one of such infections.
    In this articles I tried to summarize the literatures on mycobacterial infections in AIDS patients and on the influences of AIDS on the tuberculosis programme. Such knowledge, will be indispensable for the specialists in tuberculosis and pulmonary diseases in near future.
    Download PDF (1504K)
  • Noriko MIZUKOSHI, Chiaki ISHIHARA, Ken-ichi YAMAMOTO, Kazuyuki KATO
    1989 Volume 64 Issue 8 Pages 499-509
    Published: August 15, 1989
    Released on J-STAGE: May 24, 2011
    JOURNAL FREE ACCESS
    Staphylococcal enterotoxin A (SEA), a T cell mitogen, was found to induce a high levelof interferon r (IFN-r) in mice which had been immunized with killed Bacillus Calmette Guerin (BCG) in water-in-oil-in-water (W/O/W) emulsion.
    The phenomenon wasanalysed by in vivo and in vitro experiments, and the following results were obtained.
    1. The SEA-induced IFN was inactivated by treatment with 0.2M glycine-HC1 (pH 2.0) but not by heating at 56° for 30 min. nor by treatment with anti-IFN a/18 antibodies, and the fact suggest that the IFN belonged to they type.
    2. Treatment of the BCG-sensitized mice with silica and 2-chloroadenosine (2CA), specificlethal agents for macrophages, reduced the SEA-induced IFN production.
    3. The SEA-induced IFN production occurred in mice immunized with BCG eitherintravenously or intraperitoneally, although they showed weak or no footpad reactionto purified protein derivatives (PPD).
    In contrast, mice sensitized subcutaneously with BCG showed strong foodpad reaction to PPD but not the SEA-induced IFN production.
    Thus, the mere presence of BCG-sensitized T cells does not appear to result in the SEA-indused IFN production.
    4. In vitro experiments, in which SEA-induced IFN production was determined in theculture of BCG-sensitized spleen cells, showed that principal IFN-producing cells were Lyt-1+T cells.
    5. Deprivation of macrophages from BCG-sensitized spleen cell population by passingthrough Sephadex G-10 column reduced the SEA-induced IFN production in the culture.
    Addition of 2CA to the culture medium also reduced the SEA-induced IFN productionby the BCG-sensitized spleen cells.
    6. The SEA-induced IFN production in the culture of the BCG-sensitized spleen cellswas suppressed in the presence of lipoxygenase inhibitor, i. e., caffeic acid ornordihydroguaiaretic acid.
    7. The plastic adherent spleen cells (i. e. macrophages) from mice sensitized with BCG produced leukotriene C4 (LTC4).
    The suppression of the SEA-induced IFN productionof BCG-sensitized spleen cells in the presence of the lipoxygenase in hibitor wasprevented by addition of synthetic LTC4.
    These results suggest that LTC4 released from macrophages activated by BCG causesproduction of IFN by BCG-sensitized T cells responding to SEA.
    Download PDF (1302K)
  • Michio TSUKAMURA
    1989 Volume 64 Issue 8 Pages 511-518
    Published: August 15, 1989
    Released on J-STAGE: May 24, 2011
    JOURNAL FREE ACCESS
    Comparing minimal inhibitory concentrations (MICs) determined in variousnontuberculous mycobacteria with those for Mycobacterium tuberculosis strains, whichwere isolated from patients who were untreated previously by any antituberculosis drugs, clinical efficacy of isoniazid and ethambutol in the treatment of nontuberculousmycobacteriosis was evaluated. The MICs of isoniazid for M. tuberculosis strains were0.03-0.1μg/ml, whereas the MICs for M. xenopi strains were 0.1-0.4μg/ml, those for M. szulgai 0.2-0.8, and those for M. kansasii 0.8-1.6μg/ml.
    The fact that M. xenopi strainsare susceptible to isoniazid was reported previously, and in this study, it was shown that M. szulgai and M. kansasii are also considerably susceptible to isoniazid.
    Isoniazid may beuseful in the treatment of infection due to these mycobacteria.
    The MICs of ethambutolfor M. tuberculosis strains ranged from 0.8 to 3.13μg/ml.
    The percentages of strains of various mycobacteria, which are susceptible to 3.13μg/ml ethambutol, were 100% in M. szulgai, 100% in M. nonchromogenicum, 90% in M. gordonae, 88% in M. marinum, 77% in M. kansasii, 46% in M. malmoense, and 30% in M. scrofulaceum.
    In contrast, the percentage in M. avium complex strains remained only 19%.
    It has been suggested that ethambutol iseffective in the treatment of diseases caused by M. szulgai, M. marinum and M. kansasii.
    Download PDF (834K)
  • Tatsushi ANDO, Kentaro KIMURA, Seiichi KAWABATA, Kwang-Jung KOH, Jun N ...
    1989 Volume 64 Issue 8 Pages 519-527
    Published: August 15, 1989
    Released on J-STAGE: May 24, 2011
    JOURNAL FREE ACCESS
    In seven patients with tuberculosis required ventilatory assistance, in our IRCU at the Habikino Hospital, we found worsening of the findings on chest X-ray film and clinicalstatus during initial phase of chemotherapy, although their sputum became negative foracid-fast bacilli. On admission, six of them had large infiltration with cavities and discharged a large number of bacilli with elevation of ESR and hypoalbuminemia. We could get four patents off ventirator after start of PEEP therapy and high dosecorcicosteroid therapy. But three of them died at last, because they developed severerespiratory failure again. Pulmonary histology was available in five patients. We foundinterstitial and intra-alveolar pulmonary edema, intra-alveolar organization, hyperplasiaof alveolar wall, and hyaline membrane formation. These findings were compatible withdiffuse alveolar dammage.
    Download PDF (6172K)
  • Susumu HARADA, Masahiro TAKAMOTO, Yasuko HARADA, Hideaki NINOMIYA, Mas ...
    1989 Volume 64 Issue 8 Pages 529-536
    Published: August 15, 1989
    Released on J-STAGE: May 24, 2011
    JOURNAL FREE ACCESS
    We studied tuberculin reactivity and clinical course after starting chemotherapy inpatients with active pulmonary tuberculosis divided by four age-groups less than 29, 30-49, 50-69 and 70 years and more.
    The skin test to tuberculin purified protein derivative (PPD) was examined in 178 cases of active pulmonary tuberculosis, 120 cases of lung cancer, 25 cases of atypical mycobacteriosis and 466 cases of the other respiratory diseases.
    Theaverage size of tuberculin reaction in pulmonary tuberculosis decreased with age, butsignificantly higher than that in patients with other nontuberculous pulmonary diseases ofthe same age-group.
    The size of PPD skin test in the group of 70 years and more wassignificantly lower than other age-groups in pulmonary tuberculosis.
    We compared thetime required for negative conversion of sputum by culture after primary chemotherapyamong the different age-groups in pulmonary tuberculosis.
    It revealed that the time fornegative conversion tended to be longer with age, and the time in the group 70 years andmore was significantly longer than that of the group less than 29 years of age, although nosignificant differences in the radiographic severity and conditions of chemotherapy wereobserved. Finally, the PPD-induced lymphocyte proliferation test in vitro was done innewly diagnosed patients with pulmonary tuberculosis.
    The patients were divided into twogroups by the size of PPD skin test (high responder more than 16 mm and low responderless than 15 mm of erythema induced by PPD).
    The in vitro reactivity of peripheral bloodlymphocytes to PPD in both groups was examined by analysis of lymphocyte subsets bymonoclonal antibodies and flow cytometry.
    A good correlation was shown betweenin vitro and in vivo reactivity to PPD.
    The patients in the group of low responderfrequently showed a delay of improvement of tuberculosis during chemotherapy.
    These results indicate that the elderly patients with pulmonary tuberculosis frequentlyshow a decrease of cellular immunity and a delay of improvement of disease.
    Download PDF (945K)
  • [in Japanese]
    1989 Volume 64 Issue 8 Pages 541-544
    Published: August 15, 1989
    Released on J-STAGE: May 24, 2011
    JOURNAL FREE ACCESS
    Download PDF (472K)
feedback
Top