Interstitial pneumonia

Pathogenesis and general morphology

The development of the disease begins with the pathogen primarily affecting the elements of the alveolar wall: type I and II pneumocytes, as well as capillary endothelium. Acute inflammation erupts in this zone, rapidly joined by immunopathological mechanisms—hypersensitivity reactions of both immediate and delayed types.

The morphological picture in interstitial pneumonias is stereotyped and includes the following features:

• Damage to the alveolar epithelium with subsequent regeneration.
• Pronounced hyperemia of alveolar capillaries.
• Inflammatory infiltration of the interstitial tissue.
• Accumulation of proteinaceous fluid in the alveolar lumens.
• Formation of hyaline membranes (very common).
• Presence of macrophages and polymorphonuclear leukocytes, sometimes with characteristic cellular inclusions.

In most cases, the disease ends in complete recovery. However, the inflammation frequently progresses to interstitial fibrosis, and in severe progressive courses, a fatal outcome is possible due to cor pulmonale / cardiopulmonary failure.

Viral and mycoplasmal lesions

Viral pneumonias are most commonly caused by influenza viruses (strain H1N1 poses a particular danger), parainfluenza, adenoviruses, and childhood infection agents. The process often acquires a viral-bacterial character. A lympho-histiocytic infiltrate in the interstitium is typical for viral etiology, reflecting a cellular immune response. Specific markers include intracellular inclusions (in cytomegalovirus and adenoviral infections) and the formation of multinucleated giant cells (in measles). The diagnosis is confirmed by immunofluorescence.

Mycoplasmal pneumonia is caused by Mycoplasma pneumoniae. It accounts for up to 15–25% of all community-acquired pneumonias in cities, especially among children, adolescents, and individuals over 45 years of age. The process is usually unilateral and localized. Microscopy reveals a picture of acute interstitial pneumonia combined with bronchiolitis and a characteristic mononuclear infiltrate. An indirect sign is the detection of PAS-positive inclusions in macrophages (using Romanovsky-Giemsa staining and the PAS reaction). A reliable diagnosis is made using immunohistochemistry (IHC).

Pneumocystis pneumonia and Legionnaires' disease

Pneumocystis pneumonia (pathogen: Pneumocystis carinii) is a marker disease for immunosuppressed individuals. In patients with HIV infection, it occurs in ~75% of cases. Clinically, it manifests as severe respiratory failure against the background of diffuse bilateral involvement. Microscopy shows diffuse interalveolar septum infiltration. Foamy eosinophilic masses (cysts) giving a positive PAS reaction accumulate in the alveolar lumens. Basophilic sporozoites can be found inside the cysts. The gold standard for diagnosis is specific Grocott's staining (Grocott).

Legionnaires' disease is caused by the bacterium L. pneumophila. It was first described in 1976 following an epidemic in Philadelphia (182 cases, 29 deaths). The disease manifests with headache, myalgia, and a dry cough. A feature of the pathogen is that it does not stain with Gram and is capable of endocytobiosis—surviving inside phagocytes. In this case, antibodies do not destroy the bacterium, but only enhance its uptake by macrophages.

Class and exam questions

What else to study on this topic

• Immediate and delayed-type hypersensitivity mechanisms in pneumonia
• Pathogenesis of hyaline membrane formation in the alveoli
• Outcomes of interstitial fibrosis and the development of cardiopulmonary failure
• Cytopathic effect of viruses: intracellular inclusions and multinucleated cells
• Methods of morphological verification: immunofluorescence, IHC, and Grocott's staining

Other topics in the "Lung Diseases" section

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