Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026918 (Mycobacterium)
 52,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inbred rats were immunized with Freund's Adjuvant containing proteins of Mycogacterium tuberculosis, Mycobacterium butyrium, or dinitrochlorobenzene (DNCB). Native arterial blood was then passed over glass beads coated with those antigens. The platelet retention on the glass beads was measured. Rats immunized with Complete Freund's Adjuvant developed accelerated platelet retention on beads coated with protein derivatives of tuberculosis (PPD) after just 18 seconds of blood flow. Rats immunized twice maintained selective retention longer than those immunized once. The test animals developed no cutaneous hypersensitivity nor precipitin lines on Ouchterlong gels against PPD. Rats sensitized to DNCB had accelerated platelet retention on DNCB-coated beads. Results were temperature and complement dependent, and antigen-specific. Heparin caused a dose-dependent inhibition of the accelerated retention. PPD potentiated the ADP-induced aggregation of plateletrich plasma (PRP) from immunized rats. These experiments suggest that platelets react selectively to antigens in the intravascular spaces in immune reactions.
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PMID:Selective platelet immune retention. 9 7

Seven hundred and fifty Brisbane school children were tuberculin tested, in paired groups, with purified protein derivatives of Mycobacterium tuberculosis, bovis, BCG and avium. Reaction to avian PPD were stronger than to any of the others used. This finding may be of some importance in interpreting the variation in protection afforded by BCG vaccination.
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PMID:Tuberculin hypersensitivity following BCG vaccination in Brisbane school children. 11 44

Aerogenic infection of adult thymectomized, lethally irradiated, bone marrow-reconstituted (THXB) C57B1 times C3H F1 hybrid mice with 1 to 3,000 viable BCG Montreal was followed by an extended period of logarithmic growth to a maximum population of 5 times 10-6 bacilli by day 35. The infection spread to the liver, spleen, and bone marrow with extensive multiplication in all test organs before the growth curves abruptly entered a stationary phase. Up to 30% of the THXB mice eventually died as a result of the ongoing BCG infection. There was no sign of an antimicrobial immune response in the THXB mice analogous to that seen in the control animals beginning about day 30. The THXB mice developed considerable immediate but no delayed hypersensitivity to PPD. Intravenous challenge of the BCG-vaccinated THXB mice with 105 virulent Mycobacterium tuberculosis Erdman indicated that they were as susceptible to the tuberculous challenge as a group of unvaccinated controls. Visible surface lesions developed on the lung 90 days postinfection in the T-cell-depleted host with a sharp rise in counts to 175 per lobe on day 120 followed by a plateau for the remainder of the study. Control mice developed visible lesions about day 50, with 225 lesions per lobe by day 70 and a sharp decline to undetectable levels by day 90. The histopathology of these changes was examined carefully, together with the rate of cellular proliferation (tritiated thymidine uptake) by lung and spleen cells as the BCG infection progressed in the THXB mice. Peak uptake by both organs was depressed during the early stages of the BCG infection in the T-cell-depleted mice, but later the incorporation rates were significantly elevated above control values as the infection progressed.
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PMID:Immunogenicity of an aerogenic BCG vaccine in T-cell-depleted and normal mice. 12 19

Delayed hypersensitivity that can be demonstrated with either a strong dose of tuberculin or a conventional dose of a sensitin prepared from certain nonmammalian mycobacteria (mycobacteria of Runyon Groups II and III, e.g., Mycobacterium avium), is known to be highly prevalent in most tropical and many subtropical areas and rare in many temperate zones. Whether such sensitivity interacts significantly with tuberculosis or with leprosy is not known.A study of reactions to tuberculin (PPD-S) and to a sensitin prepared from M. intracellulare (PPD-B) was carried out in villages close to an area in which a clinical trial of the preventive effect of BCG against leprosy was being conducted. The population had not been vaccinated with BCG. Some of the villages were in river valleys that become flooded every year for a long period during the rainy season; others were on slopes above the area subject to floods. The findings showed that sensitivity to the nonmammalian sensitin was prevalent in the area, and thus confirmed previous findings of low-grade tuberculin sensitivity in Burma and neighbouring countries. No difference in this prevalence was found between flooded and nonflooded villages.
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PMID:Sensitivity to tuberculin and to a nonmammalian sensitin in Mandalay District, Burma. 12 3

Four hundred and seventy tuberculosis patients were each skin tested with four of a range of 17 mycobacterial reagents in four countries in all of which tuberculosis and leprosy were endemic. Sixteen of the reagents were new tuberculins prepared from extracts of living mycobacteria disrupted by ultrasonic disintegration and the last was PPD, RT23.The effect that tuberculosis exerted on the delayed-type skin test response to these antigens was assessed by comparing results for tuberculosis patients with those for Tuberculin positive and Tuberculin negative control populations. Tuberculosis patients on Rifampicin therapy showed no difference in their skin test responses to any of the antigens from those patients on other forms of antituberculosis treatment.Amongst the normal population it was found that possession of Tuberculin positivity was associated with an enhanced response to all the other mycobacterial antigens with the exception of A(*)-in which demonstrated a reciprocal relationship with Tuberculin in Burma. It was also noted, in Burma particularly, that sensitization to mycobacterial species other than Mycobacterium tuberculosis, especially to the slow growers, plays a role in determining responses to different mycobacterial species.In tuberculosis patients enhanced skin test responses were also seen but only in those countries, e.g. Libya, where the prevalence of mycobacterial species was low. Where mycobacteria were common, as in Burma, the converse was true and tuberculosis was associated with a diminished skin test response to each antigen. The high prevalence of A(*)-in positivity in Burma, its reciprocal relationship with Tuberculin there and the results for all the antigens in the tuberculosis patients indicate that the cell mediated skin test response may have a threshold. If this is exceeded the skin test becomes negative so that non-reactors then include those who have been excessively sensitized as well as those who have not been sensitized. Despite this, a greater percentage of tuberculosis patients in each country responded to the specific reagent Tuberculin than did the control populations and their mean positive induration sizes were consistently larger. Nevertheless, amongst the tuberculosis patients in Burma 13% were complete non-reactors to Tuberculin and this apparent anergy also applied to the other reagents with which these individuals were tested.This differs from lepromatous leprosy where the anergic state pertains exclusively to M. leprae and a few seemingly closely related species. The breadth of anergy in M. ulcerans infection has not been measured but it is known to effect both Burulin and the PPD, RT23.Just as in leprosy and M. ulcerans infection, tuberculosis can be shown to have a disease spectrum here detected by multiple skin testing. The significance of this spectrum and its similarities with and differences from that of the other mycobacterioses is discussed.
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PMID:Multiple skin testing of tuberculosis patients with a range of new tuberculins, and a comparison with leprosy and Mycobacterium ulcerans infection. 26 38

Hypersensitivity to the fungal antigens of Aspergillus fumigatus may result in a spectrum of immune injury collectively known as allergic bronchopulmonary aspergillosis (ABPA). This report describes a 14-yr-old boy who presented clinical findings consistent with ABPA,including a history of asthma, blood eosinophilia, serum precipitins, and IgE antibodies to Aspergillus fumigatus. Sputum Aspergillus, pulmonary infiltrates, and dual types I and III skin reactions to Aspergillus fumigatus were observed also. Pathology of the resected right upper lobe revealed severe bronchial destruction with the findings of bronchocentric granulomatosis. Noninvasive septate fungal hyphae compatible with Aspergillus were identified. Cultures from sputum and surgical specimens grew Aspergillus and Mycobacterium intracellulare avium. The PPD-B (purified protein derivative-Batty) intradermal skin test produced a 6 mm induration (PPD-S was negative). The patient's condition has been well controlled with prednisone and several antituberculous drugs. In addition, inflammatory and immunologic parameters have begun to return to normal. The relationship between ABa and the atypical mycobacterial infection is not clear. The association of ABPA with the severe bronchial destruction seen in bronchocentric granulomatosis is emphasized to alert physicans to this serious sequelae of ABa seen in the asthmatic.
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PMID:Bronchocentric granulomatosis: a complication of allergic bronchopulmonary aspergillosis. 31 38

The responsiveness to macrophage migration inhibitory factor (MIF) of peritoneal exudate cells (PEC) from the LPS unresponsive C3H/HeJ and C57BL/10ScCR mice was assessed by the indirect agarose microdroplet macrophage migration inhibition assay. No migration inhibition with PEC from C3H/HeJ nor C57BL/10ScCR mice was detected, whereas PEC from both C3H/HeN and C57BL/10Sn mice were significantly inhibited by even a 1/32 dilution of MIF-containing supernatants. Responsiveness to MIF of C3H/HeJ PEC could, however, be induced. In vivo inoculations of Mycobacterium bovis, strain BCG, 7 days before in vitro assay rendered C3H/HeJ PEC responsive to MIF. The lack of responsiveness to MIF by C3H/HeJ PEC appeared related to some form of suppression, since a mixture of PEC from C3H/HeN mice with 10 to 15% PEC from C3H/HeJ mice resulted in undetectable migration inhibition at any MIF dilution. In contrast to the usual lack of responsiveness of their macrophage to MIF, C3H/HeJ mice were able to produce MIK in response to PPD as well as their counterpart C3H/HeN mice after BCG sensitization. These results demonstrate that macrophages from C3H/HeJ and C57BL/10ScCR mice are unable to be inhibited in their in vitro migration of MIF (possibly being directly or indirectly influenced by a suppressor cell), whereas lymphoid cells from at least one of these strains, the C3H/HeJ mice, can produce MIF in response to antigenic stimulation.
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PMID:Refractoriness to migration inhibitory factor of macrophages of LPS nonresponder mouse strains. 35 4

In 50 non-tuberculous adult patients hospitalized in the Pahlavi University Medical Center skin testing with 5 tuberculin units of purified protein derivative of mammalian Mycobacterium tuberculosis (PPD-M) and equivalent amounts of antigen from Mycobacterium kansasii (PPD-Y) and Mycobacterium Gause (PPD-G), as well as 0.1 ml mumps antigen was carried out. Thirty four per cent, 26 per cent and 12 per cent of the patients had induration greater than 10 mm in diameter to PPD-M, PPD-Y and PPD-G respectively. However, only 28 per cent, 8 per cent and 2 per cent had induration to the above antigens which was greater than 10 mm in diameter and in which the induration was greater than that produced by the other mycobacterial antigens tested. Thirty per cent of the patients had positive reactions to mumps antigen. The results indicate that subclinical infection with Mycobacterium tuberculosis is relatively common, that infection with atypical mycobacteria may occur and that the incidence of mumps skin reactivity is low in this part of the world.
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PMID:Subclinical infection with mycobacteria in southern Iran. 41 63

Cultures of the Mycobacterium avium-intracellulare-scrofulaceum (MAIS) complex, isolated from patients who lived throughout the state of Georgia, were studied using the serotyping scheme of Schaefer. One hundred four (77 per cent) of the 135 isolates tested could be classified into 16 serotypes. The rest were not typable. Fifty-eight per cent of all the typable strains were serotypes 1, 14, 16, and 42. Results of the serotyping were recorded, mapped, and analyzed by county of residence. Most frequent isolations of these mycobacteria were from patients who resided in the coastal plain of Georgia. This finding correlates with the mycobacterial skin test studies of Edwards and associates, who found that the largest percentage of reactors to PPD-Battey resided in the costal plain. The disparate distributions of certain serotypes suggest the possible importance of regional factors that may affect the serotypes of mycobacteria indigenous to an area. The data do not suggest that chicken or swine reservoirs are highly significant sources of human mycobacteria.
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PMID:Distribution of serotypes of the Mycobacterium avium-intracellulare-scrofulaceum complex in Georgia. 57 93

Delayed hypersensitivity reactions to skin test antigens prepared from rapidly growing mycobacteria were measured in patients with postoperative wound infections due to Mycobacterium chelonei and M. fortuitum. Sixteen of 19 patients with M. chelonei infection had more than 10 mm of induration to the M. chelonei purified protein derivative antigen (PPD-CG) and were significantly more likely to react to PPD-CG than patients or hospital personnel who had no evidence of infection. All but one patient had more induration with PPD-CG than with the antigen prepared from M. fortuitum (PPD-F). Three of 4 patients with M. fortuitum infection had greater than or equal to 9mm of induration with PPD-F and were significantly more likely than noninfected patients to react to PPD-F. Three of the 4 patients also had at least as much induration with PPD-F as with PPD-CG. In an outbreak of infections due to M. chelonei, testing with PPD-CG may be useful epidemiologically. Although the data are less clearly defined for PPD-F, testing with this antigen may be of value in an outbreak caused by M. fortuitum.
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PMID:Delayed hypersensitivity reactions in patients with Mycobacterium chelonei and Mycobacterium fortuitum infections. 62 86


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