Etiological factors
Exogenous allergic alveolitis develops as a hyperergic reaction to the inhalation of specific allergens. Often the specific antigen remains unidentified, but known triggers are divided into three main groups: thermophilic actinomycetes, molds, and antigens of animal origin.
Depending on the exposure conditions, occupational and domestic forms of the disease are distinguished.
Occupational factors:
- Farmer's lung — caused by hay mold spores (Micropolyspora faeni).
- Bagassosis — a reaction to sugar cane molds (Thermoactinomyces sacchari).
- Sequoiosis — a condition associated with the inhalation of wood dust mold.
- Stripper's disease (maple bark stripper's disease) — provoked by the fungus Cryptostroma corticale.
- Suberosis — the so-called «cooper's lung».
- Mushroom worker's lung and pituitary snuff-taker's lung.
Domestic factors are associated with allergens accumulating in the daily environment:
- Bird fancier's lung — a reaction to bird droppings and avian blood proteins.
- Humidifier lung — a consequence of inhaling mold from air conditioners, humidifiers, swimming pools, and central heating radiators.
- Tobacco sniffer's lung.
Pathogenesis
The mechanism of development of hyperergic alveolitis is not fully understood, but its association with immune hypersensitivity reactions has been reliably proven. The underlying damage is based on two types of reactions to inhaled allergens:
- Immune complex (type 3) — accompanied by the formation of circulating immune complexes.
- T-cytotoxic (type 4) — cell-mediated response.
An important diagnostic marker is the detection of precipitating class IgG antibodies to a specific antigen in the patient's blood serum. At the same time, the mere presence of antibodies does not guarantee the development of the disease — genetic predisposition is required for the manifestation of the pathology.
Clinical presentation and treatment approaches
Clinical manifestations directly depend on the nature of the disease course, which is determined by the dose and duration of contact with the antigen.
- Acute allergic alveolitis occurs upon exposure to high concentrations of the allergen. Symptoms (severe dyspnea, cough, chills, and fever) unfold rapidly — 4–6 hours after contact. With adequate therapy, recovery occurs within a few days, but repeated contact threatens a relapse.
- Chronic exogenous allergic alveolitis develops with prolonged inhalation of low concentrations of the antigen. It develops covertly, gradually manifesting as progressive dyspnea, cough, and generalized fatigue.
Diagnosis of the disease is complex and requires an integrated approach: assessment of the clinical picture, radiological data, and laboratory parameters. Skin tests and the detection of specific antibodies in the blood are mandatory. In diagnostically difficult cases, a lung biopsy is performed.
Basic treatment includes two stages: complete elimination of contact with the causal antigen and the administration of steroid drugs (especially effective in the acute stage).
Pathological anatomy and morphology
The morphological picture of exogenous allergic alveolitis is stereotyped. It clearly reflects the aerogenic route of antigen penetration and the immune nature of inflammation. The lesion is localized predominantly as disseminated foci around respiratory bronchioles, representing a combination of bronchiolitis and interstitial pneumonia.
Microscopic features:
- Formation of non-caseating granulomas in the interstitium (as a consequence of immune hypersensitivity). Unlike tuberculosis, foci of caseous necrosis are absent in them.
- Development of lymphocytic alveolitis — pronounced lymphohistiocytic infiltration with an admixture of plasma cells. Eosinophils may also be present in the infiltrate.
- In the acute phase of the disease, neutrophils are detected in the inflammatory infiltrates.
- Mandatory involvement of the airways in the pathological process.
In the chronic course, interstitial fibrosis steadily progresses. This leads to the appearance of foci of carnification and, ultimately, to the formation of a «honeycomb lung». At this stage, the histological picture can be extremely difficult to differentiate from usual interstitial pneumonia.
Briefly: answers to topical questions
What diagnostic criteria are used to verify the diagnosis of exogenous allergic alveolitis?
To verify the diagnosis of exogenous allergic alveolitis, a combination of clinical, radiological, and laboratory data is used.
The main diagnostic criteria include:
- Skin tests — mandatory.
- Serological testing — determination of antibodies in the blood is mandatory; precipitating IgG class antibodies to the corresponding allergens are detected in the serum.
- Lung biopsy — performed in difficult cases.
To memorize the main groups of inhaled agents, use the rule «MTA»: M — Molds, T — Thermophilic actinomycetes, A — Antigens of animal origin.
Class and exam questions
How do granulomas in allergic alveolitis differ from tuberculous ones?
In exogenous allergic alveolitis, non-caseating granulomas are formed, meaning that foci of caseous necrosis, which are typical for tuberculous inflammation, are completely absent in them.
What immunological mechanisms underlie the disease?
Pathogenesis is associated with type 3 (immune complex) and type 4 (T-cytotoxic) hypersensitivity reactions. Genetic predisposition and the production of precipitating IgG antibodies play an important role.
How does antigen concentration affect the form of the disease?
Exposure to high concentrations causes acute alveolitis with prominent clinical manifestations after 4–6 hours. Prolonged contact with low doses leads to a latent chronic course with the gradual development of fibrosis.
What else to study on this topic
- Acute interstitial pneumonia (Hamman–Rich syndrome) and diffuse alveolar damage.
- Respiratory bronchiolitis-associated interstitial lung disease in smokers.
- Morphological differences between exogenous allergic alveolitis and usual interstitial pneumonia.
- Stages of «honeycomb lung» formation and mechanisms of interstitial fibrosis.
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