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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Typical CT findings of active postprimary pulmonary tuberculosis include centrilobular nodules and branching linear structures (tree-in-bud appearance), lobular consolidation, cavitation, and bronchial wall thickening. The CT findings of inactive pulmonary tuberculosis include calcified nodules or consolidation, irregular linear opacity, parenchymal bands, and pericicatricial emphysema. The typical appearance of primary tuberculosis on CT scans is homogeneous, dense, well-defined segmental or lobar consolidation with enlargement of lymph nodes in the hilum or the mediastinum. Miliary nodules may be seen in primary and postprimary tuberculosis. On CT, tuberculomas appear as a nodule with surrounding satellite nodules and internal cavitation on CT. Atypical radiologic manifestations of tuberculosis, encountered in as many as one third of the cases of adult-onset tuberculosis, are single or multiple nodules or masses, basilar infiltrates, miliary tuberculosis with diffuse bilateral areas of ground-glass opacity, and reversible multiple cysts. Underlying histopathologic findings of typical and atypical CT findings of tuberculosis are caseating granulomas or pneumonia in the active phase and fibrosis and dystrophic calcification in the inactive phase.
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PMID:Pulmonary tuberculosis: CT and pathologic correlation. 1104 87

Tuberculosis, once thought to have been controlled, is now resurgent in many parts of the world. Many gaps exist in understanding the pathogenesis of tuberculosis, especially secondary and cavitary disease. Evidence presented here suggests that cord factor (trehalose 6,6'-dimycolate, TDM) is a key driver of these processes. It is the most abundant lipid released by virulent M. tuberculosis (MTB) and can switch between two sets of activities. On organisms, TDM is non-toxic and protects them from killing by macrophages. On lipid surfaces, it becomes antigenic and highly toxic. Caseating granulomas, the hallmark of primary tuberculosis, develop from interaction of TDM with lipid within granulomas. New evidence indicates that secondary tuberculosis begins as a lipid pneumonia that accumulates mycobacterial antigens and host lipids in alveoli before developing conditions for activation of the toxicity and antigenicity of TDM. This rapidly produces caseation necrosis that leads to cavities. Finally, virulent MTB release large amounts of TDM during growth as a pellicle within cavities. We propose that such growth results in activation of the toxicity and antigenicity of TDM at the air interface and that presence of the activated TDM perpetuates the cavity.
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PMID:Multiple roles of cord factor in the pathogenesis of primary, secondary, and cavitary tuberculosis, including a revised description of the pathology of secondary disease. 1712 24

We studied radiographic features of pulmonary tuberculosis (PTB) described in the report forms for 907 adolescents from two Brazilian cities. A descriptive analysis showed that the most common radiographic lesions were post-primary tuberculosis (53.3%), tuberculous expansile pneumonia (27%) and primary complex with adenomegaly (1.8%). Cavitary lesions occurred in 67/243 (27.6%) patients aged 0-15 years and in 116/321 (36.1%) adolescents aged 16-19 years (P = 0.031). Most of the PTB cases had forms similar to those in adults.
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PMID:Pulmonary tuberculosis in adolescents: radiographic features. 1991 79

Post primary tuberculosis occurs in immunocompetent adults, is restricted to the lungs and accounts for 80% of all clinical cases and nearly 100% of transmission of infection. The supply of human tissues with post primary tuberculosis plummeted with the introduction of antibiotics decades before the flowering of research using molecular methods in animal models. Unfortunately, the paucity of human tissues prevented validation of the models. As a result, it is a paradigm of contemporary research that caseating granulomas are the characteristic lesion of all tuberculosis and that cavities form when they erode into bronchi. This differs from descriptions of the preantibiotic era when many investigators had access to thousands of cases. They reported that post primary tuberculosis begins as an exudative reaction: a tuberculous lipid pneumonia of foamy alveolar macrophages that undergoes caseation necrosis and fragmentation to produce cavities. Granulomas in post primary disease arise only in response to old caseous pneumonia and produce fibrosis, not cavities. We confirmed and extended these observations with study of 104 cases of untreated tuberculosis. In addition, studies of the lungs of infants and immunosuppressed adults revealed a second type of tuberculous pneumonia that seldom produces cavities. Since the concept that cavities arise from caseating granulomas was supported by studies of animals infected with Mycobacterium bovis, we investigated its pathology. We found that M. bovis does not produce post primary tuberculosis in any species. It only produces an aggressive primary tuberculosis that can develop small cavities by erosion of caseating granulomas. Consequently, a key unresolved question in the pathogenesis of tuberculosis is identification of the mechanisms by which Mycobacterium tuberculosis establish a localized safe haven in alveolar macrophages in an otherwise solidly immune host where it can develop conditions for formation of cavities and transmission to new hosts.
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PMID:Pathology of post primary tuberculosis of the lung: an illustrated critical review. 2173 55

Mycobacterium tuberculosis produces two distinct types of disease: primary and post primary tuberculosis. We recently reported that post primary tuberculosis begins in immunocompetent adults as an endogenous lipid pneumonia that abruptly undergoes necrosis to produce cavities. Obstruction of bronchi by endobronchial tuberculosis is a consistent finding in developing post primary tuberculosis. This paper reports a case of obstructive pneumonia caused by cancer that underwent rapid necrosis to produce a cavity that was similar to those produce by tuberculosis. Analysis of this case with the relevant literature supports the hypothesis that bronchial obstruction is an essential contributor to the development of post primary tuberculosis and that it may help explain the localized suppression of host defense mechanisms in adult pulmonary tuberculosis.
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PMID:On the pathogenesis of post primary tuberculosis: the role of bronchial obstruction in the pathogenesis of cavities. 2208 17

M. Tuberculosis (MTB) is an obligate human parasite even though humans are more resistant than any of the animals used for study. It is a human parasite because only humans develop post primary tuberculosis (TB) in their lungs that mediates transmission of infection to new hosts. The extreme paucity of human lung tissue with post primary TB has forced scientists to study animal models and human tissues that do not have the disease. Consequently, the unique features of post primary TB remain largely unknown and misconceptions are widely accepted. This manuscript presents a revised pathogenesis of post primary TB based on studies of lung tissues of thousands of patients by multiple authors and related literature. Primary TB stimulates systemic immunity that kills organisms and heals granulomas resulting in both protection from disseminated TB and resistance to new infection. Post primary TB, in contrast, requires systemic immunity that it subverts to produce local susceptibility in the apex of the lung. It begins in the part of lung with the lowest ventilation, perfusion and movement and then proceeds to paralyze alveolar macrophages, block the exits and suppress inflammation to further isolate the area with post obstructive pneumonia. This provides a safe place for a small number of MTB to drive prolonged accumulation of host lipids and mycobacterial antigens in an otherwise immune person. After many months, the affected lung suddenly undergoes caseation necrosis with vanishingly few MTB. The necrotic tissue fragments to produce a cavity or hardens to develop fibrocaseous disease. Evidence suggests that this is triggered by a hypersensitivity reaction against cord factor and then progresses as the Koch phenomenon against many antigens. MTB grow in perfusion only in dead tissue or on a cavity wall. We anticipate that a more accurate understanding of the pathogenesis of post primary TB will facilitate focusing modern technologies to produce rapid advances in understanding and combating TB.
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PMID:Pathogenesis of post primary tuberculosis: immunity and hypersensitivity in the development of cavities. 2536 20

Primary and post-primary tuberculosis (TB) are different diseases caused by the same organism. Primary TB produces systemic immunity. Post-primary TB produces cavities to support massive proliferation of organisms for transmission of infection to new hosts from a person with sufficient immunity to prevent systemic infection. Post-primary, also known as bronchogenic, TB begins in humans as asymptomatic bronchial spread of obstructive lobular pneumonia, not as expanding granulomas. Most lesions regress spontaneously. However, some undergo caseation necrosis that is coughed out through the necrotic bronchi to form cavities. Caseous pneumonia that is not expelled through the bronchi is retained to become the focus of fibrocaseous disease. No animal reproduces this entire process. However, it appears that many mammals utilize similar mechanisms, but fail to coordinate them as do humans. Understanding this makes it possible to use human tuberculous lung sections to guide manipulation of animals to produce models of particular human lesions. For example, slowly progressive and reactivation TB in mice resemble developing human bronchogenic TB. Similarly, bronchogenic TB and cavities resembling those in humans can be induced by bronchial infection of sensitized rabbits. Granulomas in guinea pigs have characteristics of both primary and post primary TB. Mice can be induced to produce a spectrum of human like caseating granulomas. There is evidence that primates can develop bronchogenic TB. We are optimistic that such models developed by coordinated study of human and animal tissues can be used with modern technologies to finally address long-standing questions about host/parasite relationships in TB, and support development of targeted therapeutics and vaccines.
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PMID:Pathogenesis and Animal Models of Post-Primary (Bronchogenic) Tuberculosis, A Review. 2941 34

Post-primary tuberculosis (TB) disease is characterized by paucibacillary necrosis of the early lesion, tuberculous pneumonia, in the adult human lung. The mechanism is speculated to be a strong localized delayed type hypersensitive response (DTH). However, up to this date, no one has been able to identify the source of the large accumulation of MTB antigens required for the DTH response. Although it is known and accepted that the pathogen, Mycobacterium tuberculosis (MTB), significantly affects macrophage function and activity, few studies have focused on macrophages at the site of the early lesion of developing post-primary MTB in human lungs. In vitro studies have examined the effect of MTB on skewing the macrophage phenotype, specifically the dynamic of the M1 and M2 differentiation. Additionally, it is also well documented that MTB infection induces macrophages to become foamy, accumulating host, and potentially MTB, lipids in the cytoplasm. The foamy macrophage is necessary for prolonging MTB survival in the infected lung. Using autopsy derived lung samples from untreated TB diseased individuals, this report, by applying morphoproteomics, demonstrates that the alveolar macrophages present in the early lesion of TB are primarily of the M2 phenotype. The M2 foamy alveolar macrophages (FAM) are also loaded with MTB antigens by immunohistochemistry and are paucibacillary. Moreover, the M2 alveolar macrophages predominately express PD-L1, leading to suppression of PD-1+ lymphocytes and host immunosurveillance. These morphoproteomic analyses indicate that early lesion of MTB in the adult human lung leads to a skewed M2 foamy alveolar macrophage phenotype that creates a protective microenvironment that accumulates high concentrations of MTB antigens, which when released can lead to necrosis and eventual cavitation.
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PMID:Morphoproteomics Identifies the Foamy Alveolar Macrophage as an M2 Phenotype with PD-L1 Expression in the Early Lesion of Post-Primary Tuberculosis: Implications for Host Immune Surveillance and Therapy. 3282 37


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