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== Clinical Summary == This 29During the course of a routine physical examination two months prior to admission, this 57-year-old black female had white male was noted to have a history lesion in the upper lobe of scleroderma involving the right lung. Initially, kidney, heart, and skin. Her main clinical problems centered on her restrictive lung diseasehe was treated for two weeks with ampicillin. She He was able then admitted to live at home with supplemental oxygen but recently she had developed edemaan outside hospital for further study. All studies including sputum studies for tubercle bacilli, chest pain, weakness, light-headednessbronchial washings, and a loss bronchoscopy were negative and he was discharged. Review of appetite. The patient was admitted to systems revealed the hospital with a working diagnosis presence of congestive heart failure brought mild dyspnea on exertion, accompanied by her lung diseasea slightly productive cough. Echocardiographic evaluation revealed a pericardial effusion Of interest was the fact that was tappedthe patient had been PPD positive for the past 4 to 5 years, but this had never been evaluated. Soon after On this procedure her respiratory status degenerated hospital admission, physical and she required intubationlaboratory examinations were negative. Despite aggressive supportive treatment for her cardiac and pulmonary problems, she could not be weaned from Radiographic examination of the chest revealed a 2 x 2-cm density in the ventilatorright lower lung field. Two weeks after admission she became febrile and Gram positive cocci Several small cavities were isolated from sputum culture. She was placed identified in this area on antibiotics but her condition deteriorated and she developed bradycardia followed by electromechanical dissociation (EMD)CT scan.
== Autopsy Findings == Upon opening the thorax there was 600 cc The patient underwent a thoracotomy, at which time a portion of cloudy serous fluid in each hemithorax and 100 cc of similar fluid in the pericardial sac. The heart weighed 530 grams and there was thickening upper lobe of both the left and right ventricular walls. The liver weighed 1880 grams and was congested. The spleen weighed 200 grams and was also congested. The combined lung weight was 1875 grams; the lungs were markedly fibrotic with severe emphysemaremoved. In addition, dermal thickening was evident throughout the body and the wall Examination of the esophagus was thickened and firmcut surface revealed small white nodules measuring up to 0.2 cm in diameter.
== Images ==
File:IPLab6TB6.jpg|This is a high-power (oil immersion) photomicrograph of granuloma stained with an acid-fast stain. Mycobacterium tuberculosis bacilli stain red.
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== Virtual Microscopy ==
=== Lung: TB H&E ===
<peir-vm>IPLab6TB_HE</peir-vm>
=== Lung: TB AFGT ===
<peir-vm>IPLab6TB_AFGT</peir-vm>
=== Normal Lung ===
<peir-vm>UAB-Histology-00107</peir-vm>
== Study Questions ==
* <spoiler text="What is the Ghon complex?">In primary pulmonary TB you get (1) parenchymal subpleural lesions, often just above or just below the interlobar fissure, and (2) enlarged caseous lymph nodes draining the parenchymal focus (usually the hilar lymph nodes).</spoiler>
* <spoiler text="What factors are responsible for the virulence of M. tuberculosis?">M. tuberculosis has no known exotoxins, endotoxins or histolytic factors. Its pathogenicity is due to the fact that it resists phagocytic killing and sets up a delayed hypersensitivity reaction. Virulent M. tuberculosis organisms have cord factor, sulfatides, LAM, heat shock protein and they activate complement.</spoiler>
* <spoiler text="What is the sequence of events after primary exposure to M. tuberculosis?">The initial infection with M. tuberculosis leads to a T cell-mediated immune response that controls 95% of infections. Alveolar macrophages phagocytose the organisms and then transport them to the hilar lymph nodes. Macrophages cannot kill the mycobacteria so the organisms multiply, lyse the host cell, infect other macrophages, and sometimes disseminate via the blood to other parts of the lung and elsewhere in the body.
After a few weeks, T cell-mediated immunity develops and leads to activation of macrophages so they can kill intracellular mycobacteria via reactive nitrogen intermediates. This process leads to formation of epithelioid cell granulomas and clearance of the mycobacteria. Also, CD8+ suppresser T cells kill macrophages that are infected with mycobacteria, resulting in the formation of caseating granulomas. These processes during the primary infection with M. tuberculosis result in a calcified scar in the lung parenchyma and in the hilar lymph node. This combination is called the Ghon complex.
</spoiler>
== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/230802-overview eMedicine Medical Library: Tuberculosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/mycobacteria/tuberculosis_tb.html Merck Manual: Tuberculosis (TB)]
=== Journal Articles ===
* Rodrigues DS, Medeiros EA, Weckx LY, Bonnez W, Salomão R, Kallas EG. [http://www.ncbi.nlm.nih.gov/pubmed/11982602 Immunophenotypic characterization of peripheral T lymphocytes in Mycobacterium tuberculosis infection and disease]. ''Clin Exp Immunol'' 2002 Apr;128(1):149-54.
=== Images ===
* [{{SERVER}}/library/index.php?/tags/259-tuberculosis PEIR Digital Library: Tuberculosis Images]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html#4 WebPath: Granulomatous Diseases]
== Related IPLab Cases ==
* [[IPLab:Lab 1:Tuberculosis|Lab 1: Lung: Tuberculosis (Caseous Necrosis)]]
* [[IPLab:Lab 3:Tuberculosis|Lab 3: Lung: Tuberculosis]]
{{IPLab 6}}
[[Category: IPLab:Lab 6]]
