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Pathology · Lung Diseases

Acute interstitial pneumonia

*Pneumonia interstitialis acuta*

Acute interstitial pneumonia (Pneumonia interstitialis acuta) is a pathological process characterized by a primary acute inflammatory lesion of the interstitial tissue of the respiratory divisions and alveolar walls. The disease is accompanied by the secondary formation of exudate within the lumens of bronchioles and alveolar spaces. In scientific and medical literature, this nosology is also found under the synonymous names "acute pneumonitis" or "atypical pneumonia".

Primary lesionInterstitium of the respiratory divisions and alveolar wall
Nature of the effusionSecondary appearance of exudate in alveoli and bronchioles
Course of the pathologyProlonged persistence of the pathogen in the body
Pleural involvementFrequent development of fibrinous pleurisy
4 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Definition, terminology, and nosological status

Acute interstitial pneumonia (also known as acute pneumonitis) occupies a special place among respiratory system pathologies. This process has the following terminological and clinical-morphological features:

  • Nosological forms: The disease can present as a primary independent nosology or act as a secondary pathological process.
  • Designations in literature: In scientific publications and guidelines, this pathology is often called "atypical pneumonia". This name is explained by the fact that the disease differs significantly from classical pneumonias in its clinical presentation and the therapeutic methods used.
  • Features of the clinical course: The pathogenetic profile of this condition is characterized by the prolonged presence (persistence) of the pathogen in the human body.

Macroscopic picture of lung pathology

During post-mortem examination and visual inspection of the organ, a complex of characteristic changes in the lung tissue and adjacent structures is revealed:

  • Bronchopneumonic pattern: A picture of bronchopneumonia is observed, spreading to involve several lobes of the lung simultaneously.
  • Similarity to lobar involvement: In a certain proportion of cases, the macroscopic appearance of the organ bears noticeable similarities to lobar pneumonia in the stage of gray hepatization.
  • Pleural involvement: A reactive process—fibrinous pleurisy—is recorded in the pleural leaves.
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Microscopic features and histopathology

Histological examination of sections of the affected lung tissue reveals the following key microscopic changes:

  1. Vascular and tissue disorders: Pronounced hemorrhagic edema of the respiratory divisions is revealed.
  2. Cellular infiltrate: Massive infiltration by cellular elements—macrophages and polymorphonuclear leukocytes—is traced in the alveolar septa.
  3. Primary and secondary nature of changes: Primary acute inflammation is localized in the interalveolar septa and the interstitium of the respiratory divisions, while the formation of exudate inside the lumens of the alveoli and bronchioles is secondary in nature.

Summary characteristics of the pneumonia form

Terminological variant | Morphological essence | Morphogenetic features --- | --- | --- Acute interstitial pneumonia | Primary inflammation of the alveolar wall and interstitium | Secondary exudate in alveoli and bronchioles Acute pneumonitis | Synonym for interstitial pneumonia | Prolonged persistence of the infectious agent in the body Atypical pneumonia | Designation due to clinical presentation and treatment | Resembles gray hepatization, produces fibrinous pleurisy

Briefly: answers to topical questions

Which microorganisms are the most frequent causative agents of acute interstitial pneumonia?

Etiological factors of acute interstitial pneumonia include viruses, mycoplasmas, chlamydia, legionella, rickettsia, the causative agent of ornithosis, fungi, and pneumocystis. Viral variants can be caused by influenza viruses, parainfluenza viruses, and adenoviruses; among influenza viruses, the H1N1 strain poses a particular danger. In some cases, the etiology remains undetermined, as in Hamman-Rich disease. A viral-bacterial nature of the disease is also possible.

What are the typical morphological outcomes of acute interstitial pneumonia?

Morphological outcomes include the formation of moderately pronounced pulmonary interstitial fibrosis in the late stage and septoalveolar sclerosis with the progression of productive inflammation. Nonspecific interstitial pneumonia is characterized by a relatively favorable clinical course and a sufficiently high survival rate. Hamman-Rich disease represents an acute interstitial pneumonia of undetermined etiology resulting in death within 2–4 months from acute cor pulmonale and heart failure.

What pulmonary and extrapulmonary complications can develop in acute interstitial pneumonia?

Complications of usual interstitial pneumonia include the development of cor pulmonale and progressive cardiopulmonary failure.

How to memorize

INTERSTITIUM — Infiltration by macrophages and leukocytes, Alveolar wall initiation, Persistence of the pathogen during the course, Unified process with secondary exudate in bronchioles, Sdevelopment of fibrinous pleurisy.

Class and exam questions

Which lung structure is primarily affected in acute interstitial pneumonia?

Primary acute inflammation is localized in the interstitium of the respiratory divisions of the lung and directly in the alveolar walls. The formation of inflammatory exudate within the lumens of the alveoli and bronchioles occurs secondarily.

Why is acute interstitial pneumonia called "atypical"?

The term "atypical pneumonia" is used in the literature due to the characteristic features of the clinical picture of the disease and the use of specific treatment methods that differ from the therapy of classical pneumonias.

What are the key macroscopic manifestations of the pathology?

Macroscopically, bronchopneumonia involving multiple lobes is revealed, in some cases resembling lobar pneumonia in the stage of gray hepatization, as well as fibrinous inflammation of the pleura (fibrinous pleurisy).

Which cells infiltrate the alveolar septa upon microscopy?

Histological microscopic examination reveals hemorrhagic edema, and infiltration by macrophages and polymorphonuclear leukocytes is determined in the alveolar septa.

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What else to study on this topic

  • Secondary nature of acute interstitial pneumonia in concomitant pathologies
  • The stage of gray hepatization in lobar pneumonia and its morphological similarity to interstitial pneumonia
  • Mechanisms of prolonged persistence of pathogens in lung tissue
  • Features of therapy in the atypical course of acute pneumonitides

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