[Clinicopathologic conference. Heerfordt syndrome in sarcoidosis with simultaneous detection of Mycobacterium tuberculosis by bacterial culture].
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Microbiological culture
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We describe the case of a 47-year-old Caucasian male patient who developed sarcoidosis 18 months after he was diagnosed with pulmonary tuberculosis for which he was treated according to guidelines. The presentation of sarcoidosis was very similar to his first presentation when he was diagnosed with tuberculosis. Mycobacterium tuberculosis as a possible aetiological agent in sarcoidosis has been point of debate since many years and has been studied thoroughly. Recent advances in immunologic and molecular techniques have strengthened the association between mycobacteria and sarcoidosis.1 Sarcoidosis is a systemic inflammatory disorder of unknown aetiology, characterised by the presence of non-caseating epitheloid cell granulomas. It is generally agreed that this is a tissue reaction to environmental agents in a genetically susceptible individual.2 Tuberculosis is an infectious disease caused by M. tuberculosis and characterised by caseating granulomas. In both clinical and histopathological features sarcoidosis is remarkably similar to tuberculosis and therefore can be difficult to distinguish. First, this case report demonstrates the need of diagnostic testing when reactivation of tuberculosis is suspected. And second the role of M. tuberculosis in the aetiology of sarcoidosis will be discussed.
Etiology
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Abstract Much is known regarding the antibiotic susceptibility of planktonic cultures of Mycobacterium tuberculosis, the bacterium responsible for the lung disease tuberculosis (TB). As planktonically-grown M. tuberculosis are unlikely to be entirely representative of the bacterium during infection, we set out to determine how effective a range of anti-mycobacterial treatments were against M. tuberculosis growing as a biofilm, a bacterial phenotype known to be more resistant to antibiotic treatment. Light levels from bioluminescently-labelled M. tuberculosis H37Rv (strain BSG001) were used as a surrogate for bacterial viability, and were monitored before and after 1 week of treatment. After treatment, biofilms were disrupted, washed and inoculated into fresh broth and plated onto solid media to rescue any surviving bacteria. We found that in this phenotypic state M. tuberculosis was resistant to the majority of the compounds tested. Minimum inhibitory concentrations (MICs) increased by 20-fold to greater than 1000-fold, underlying the potential of this phenotype to cause significant problems during treatment.
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Critical to the complete expression of the virulence of M. tuberculosis and thereby its pathogenesis in human infection, is the ability of this pathogen to interact with the host in a specific manner. To date, cytokine circuits during tuberculosis and M. tuberculosis infection have been studied most intensely. With this regard, both the whole M. tuberculosis and its protein and non-protein moieties appear to be influential on the in situ cytokine profile, and consequently, to the final outcome of infection. The interplay and final balance of macrophage activating and immuno-enhancing cytokines versus macrophage deactivating and immunosuppressive cytokines most likely determines the final expression of M. tuberculosis infection. Further, cytokine circuits also underlie the immunopathology of tuberculosis. Modulation of the in vivo cytokine milieu may allow the development of more effective vaccines to prevent M. tuberculosis infection, and adjunctive immunotherapy to improve treatment of tuberculosis.
Pathogenesis
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OBJECTIVE--To investigate the prevalence of Mycobacterium tuberculosis DNA in granulomatous tissues from patients with sarcoidosis and from controls matched for age, sex, and tissue by using the polymerase chain reaction. DESIGN--Single blind control trial. SUBJECTS--16 patients with sarcoidosis who had undergone diagnostic biopsy of lung, skin, or lymph node and 16 patients with squamous cell carcinoma or Hodgkin9s disease to act as controls. In addition, four lung specimens infected with M tuberculosis were included as positive controls. RESULTS--M tuberculosis DNA was present in sarcoid tissues containing granulomas from seven of the 16 patients and one of the 16 matched controls. Two of the four specimens known to be infected with M tuberculosis were positive in the controlled experiment. CONCLUSION--These figures suggest that M tuberculosis DNA is detected as readily in patients with sarcoidosis as in patients with frankly tuberculous tissues and imply that M tuberculosis may be linked to the cause of sarcoidosis.
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Host-pathogen interactions in tuberculosis should be studied at the disease site because Mycobacterium tuberculosis is predominately contained in local tissue lesions. Although M. tuberculosis infection involves different clinical forms of tuberculosis, such as pulmonary tuberculosis, pleural tuberculosis, and lymph node tuberculosis, most studies of human tuberculosis are performed using cells from the peripheral blood, which may not provide a proper reflection of the M. tuberculosis-specific immune responses induced at the local site of infection. A very low proportion of M. tuberculosis-specific effector T cells are found in the blood compared with the infected tissue, and thus there may be considerable differences in the cellular immune response and regulatory mechanisms induced in these diverse compartments. In this review, we discuss differences in the immune response at the local site of infection compared with the peripheral circulation. The cell types and immune reactions involved in granuloma formation and maintenance as well as the in situ technologies used to assess local tuberculosis pathogenesis are also described. We need to strengthen and improve the exploratory strategies used to dissect immunopathogenesis in human tuberculosis with the aim to accelerate the implementation of relevant research findings in clinical practice.
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Much is known regarding the antibiotic susceptibility of planktonic cultures of Mycobacterium tuberculosis , the bacterium responsible for the lung disease tuberculosis (TB). As planktonically-grown M. tuberculosis are unlikely to be entirely representative of the bacterium during infection, we set out to determine how effective a range of anti-mycobacterial treatments were against M. tuberculosis growing as a biofilm, a bacterial phenotype known to be more resistant to antibiotic treatment. Light levels from bioluminescently-labelled M. tuberculosis H37Rv (strain BSG001) were used as a surrogate for bacterial viability, and were monitored before and after one week of treatment. After treatment, biofilms were disrupted, washed and inoculated into fresh broth and plated onto solid media to rescue any surviving bacteria. We found that in this phenotypic state M. tuberculosis was resistant to the majority of the compounds tested. Minimum inhibitory concentrations (MICs) increased by 20-fold to greater than 1,000-fold, underlying the potential of this phenotype to cause significant problems during treatment.
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The clinical and pathological features of sarcoidosis and tuberculosis may mimic each other, and when the caseous necrosis is not seen in tuberculosis tissue, differentiation is not easy.This study evaluates the ability of real-time PCR quantification and sets the quantitive value to differentiate sarcoidosis from TB.Formalin-fixed and paraffin-embedded sections of biopsy samples, from 104 patients with sarcoidosis, 31 patients with tuberculosis, and 55 controls with other respiratory diseases (26 with nonspecific lymphadenitis and 29 with emphysema bullae), were collected to amplify insertion sequence IS986 of Mycobacterium tuberculosis (MTB) genome by real-time quantitative PCR. The diagnostic performance of qualitative and quantitative analysis of real-time quantitative PCR was assessed by receiver-operating characteristic (ROC) curves.MTB DNA was detected in 20 of the 104 sarcoidosis samples and 7 of the 55 control samples, but was detected in all of the 31 tuberculosis samples. The numbers of MTB genomes were 0-4.71x10(3) copies per ml in sarcoidosis samples, 1.58x10(2)-5.43x10(7) copies per ml in tuberculosis samples and 0-1.02x10(3) copies per ml in controls with quantitative analysis. Receiver-operating characteristic (ROC) curves showed that MTB genome quantification had greater diagnostic performance than MTB genome qualitation in discriminating patients with sarcoidosis from those with tuberculosis (area under the ROC curves: 0.994 vs 0.904, P<0.001). The sensitivity and specificity of qualitative analysis were 100% and 80.8% respectively. At cutoff value of 1.14x10(3) copies per ml for MTB genome quantification, the sensitivity was 96.8% and specificity was 98.1%.The real time PCR quantification is a valuable test for differentiation between sarcoidosis and tuberculosis, and the MTB genome copies number of 1.14x10(3) copies per ml should be preferred as quantitative cutoff value for the differentiation.
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Inflammation plays a crucial role in the control of Mycobacterium tuberculosis infection. In this study, we demonstrate that an inflammatory pulmonary environment at the time of infection mediated by lipopolysaccharide treatment in mice confers enhanced protection against M. tuberculosis for up to 6 months postinfection. This early and transient inflammatory environment was associated with a neutrophil and CD11b
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Globally, about 36.7 million people were living with HIV infection at the end of 2015. The most frequent infection co-occurring with HIV-1 is Mycobacterium tuberculosis—374,000 deaths per annum are attributable to HIV-tuberculosis, 75% of those occurring in Africa. HIV-1 infection increases the risk of tuberculosis by a factor of up to 26 and alters its clinical presentation, complicates diagnosis and treatment, and worsens outcome. Although HIV-1-induced depletion of CD4 + T cells underlies all these effects, more widespread immune deficits also contribute to susceptibility and pathogenesis. These defects present a challenge to understand and ameliorate, but also an opportunity to learn and optimize mechanisms that normally protect people against tuberculosis. The most effective means to prevent and ameliorate tuberculosis in HIV-1-infected people is antiretroviral therapy, but this may be complicated by pathological immune deterioration that in turn requires more effective host-directed anti-inflammatory therapies to be derived.
Pathogenesis
AIDS-Related Opportunistic Infections
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