Right lung miliary tuberculosis

Clinical HistoryA 55-year-old woman presented with severe dyspnoea, productive cough and oral candidiasis. She was immunosuppressed due to steroid and cyclophosphamide treatment for rheumatoid arthritis. Her sputum grew Staphylococcus aureus. Despite starting appropriate therapy, she died shortly after admission.PathologyThe bisected right lung shows multiple abscess cavities, the largest measuring 4 × 3 cm in the lower lobe apex. Another cavity (3 × 2 cm) is seen in the upper lobe, surrounded by consolidation. Additional small abscesses and patchy middle lobe consolidation are present. Many bronchi are filled with pus. Cultures confirmed Staph. aureus infection.Further InformationStaphylococcus aureus is a gram-positive coccus commonly found on the skin and in the upper airways. Though usually harmless, it can cause opportunistic infections, including pneumonia and endocarditis. Hospital-acquired pneumonia, particularly post-intubation, and secondary bacterial pneumonia after viral infections (e.g. influenza) are common.MRSA (Methicillin-Resistant Staph. aureus) is increasingly found in hospitals. IV drug users are at high risk of metastatic infections like Staph pneumonia or endocarditis. Staph pneumonia is often severe and associated with cavitating abscesses and empyema.It should be suspected in high-risk groups or in patients with rapidly worsening pneumonia, haemoptysis, early multilobar involvement, cavitation, or coagulopathy. First-line treatment is usually flucloxacillin, though resistance is common. MRSA is treated with vancomycin or linezolid.

Clinical History A 45-year-old man presented with a growing lump in the left supraclavicular area, diagnosed as Hodgkin lymphoma (HL) via biopsy. Ten months later, he was readmitted with shoulder pain and arm swelling. Examination showed widespread lymphadenopathy. Despite radiotherapy and Thiotepa chemotherapy, his condition worsened. A barium meal revealed duodenal obstruction from lymph node compression. He died two weeks later.PathologyThe 3D print displays the tracheal bifurcation with enlarged, matted paratracheal and peribronchial lymph nodes. Necrotic areas are visible within the lymph nodes and surrounding tissues. The aorta is shown in cross-section, with a visible void space and branch points. Atheroma is present but not easily seen.Further InformationHodgkin lymphoma is a malignancy marked by Reed-Sternberg cells and abnormal activation of NF-?B. There are five subtypes based on morphology and genetics. Risk factors include EBV infection, immunosuppression, and family history. Symptoms often include painless lymphadenopathy, weight loss, fever, and night sweats. Diagnosis is made through imaging and biopsy. Prognosis is generally good, with early-stage survival approaching 90% thanks to modern therapies.

Clinical HistoryA 47-year-old woman was admitted with advanced carcinomatosis. Clinical examination revealed a hard liver and a pelvic mass on the right side. She had experienced general symptoms for several months before seeking medical help. She was admitted for palliative care and passed away shortly after.PathologyThe left lung shows multiple pale tumour nodules of varying sizes, scattered throughout the lung. Near the hilum, several nodules are confluent, and the hilar lymph nodes also contain tumour tissue. Tumour deposits (2 mm to 2 cm) are seen beneath the thickened pleura on various lung surfaces. Histology confirmed metastatic adenocarcinoma. Post-mortem examination revealed a primary ovarian adenocarcinoma with metastases in the lungs, liver, heart, and pericardium.Further InformationPulmonary metastases are more frequent than primary lung cancers. Because of the lungs’ rich blood supply and lymphatic drainage, many malignant tumours from other parts of the body spread there. While sarcomas usually spread via the bloodstream, carcinomas may metastasize through the blood, lymphatics, or both.

Clinical History There is no clinical history available for this specimen.PathologyThe specimen is a parasagittal section of the right lung. The boundary between the upper and lower lobes is clearly defined. The entire upper lobe is congested and pale grey, showing significant pathological change.Further InformationThis specimen represents a stage of lobar pneumonia characterized by grey hepatisation, a form of late consolidation. This stage occurs approximately 2 to 3 days after red hepatisation and typically lasts 4 to 8 days.The lung appears grey and firm, resembling liver tissue. This consistency is caused by a fibrinopurulent exudate, breakdown of red blood cells, and accumulation of haemosiderin. Macrophages become prominent in the interstitial tissue and work to clear cellular debris and resolve inflammation. When they consume red blood cells, they may contain iron and are then called siderophages.By the eighth day, the resolution process begins. Enzymatic activity starts centrally, liquefies the solid content, and gradually restores normal lung aeration.Common causative organisms of lobar pneumonia include Streptococcus pneumoniae (pneumococcus), Haemophilus influenzae, and Moraxella catarrhalis. Other possible pathogens are Legionella pneumophila, Klebsiella pneumoniae, and Mycobacterium tuberculosis, particularly in untreated cases of tuberculosis.On radiographs, an entire lobe appears radiopaque, which is a typical sign of lobar pneumonia.

Clinical HistoryA 6-year-old girl was admitted with productive cough, dyspnoea and fever. She rapidly deteriorated and died shortly after admission. She had a history of recurrent pneumonia and meconium ileus. A diagnosis of cystic fibrosis (CF) was made. Her sister had died from the same condition at age 3.PathologyThe lungs show severe, predominantly bronchial changes. Many bronchi are dilated (bronchiectasis) and filled with thick, yellow pus. The upper lobe shows a honeycomb-like area, while the lower lobe contains multiple abscesses, fibrosis and consolidation. Only minimal normal lung tissue remains. These findings are characteristic of CF.Further InformationCystic fibrosis is an inherited disease caused by mutations in the CFTR gene on chromosome 7, leading to defective chloride channels. This results in dehydrated secretions in the lungs, pancreas and other organs, causing obstruction, infection and tissue damage.In the lungs, mucus becomes thick and sticky, impairing clearance and causing chronic infection and bronchiectasis. Common pathogens include Staphylococcus aureus, Haemophilus influenzae and Pseudomonas. Lung complications are the main cause of death in CF. The average life expectancy is 40–50 years in developed countries.CF affects about 1 in 3000 live births and follows an autosomal recessive inheritance. It is most common in light-skinned populations, with 1 in 20 people being carriers. Diagnosis is usually made via newborn screening and confirmed with a sweat chloride test (> 60 mmol/L).