Bronchopulmonary allergic aspergillosis

Bronchopulmonary allergic aspergillosis is an allergic disease manifested by migratory pulmonary infiltrates, bronchospasm, pulmonary eosinophilia, peripheral blood eosinophilia, increased levels of immunoglobulin E and the presence of antibodies. For the first time, bronchopulmonary allergic aspergillosis was described in 1952 by Hinsonoi. Often develops in people with atopy, allergic rhinitis and bronchial asthma. The occurrence of bronchopulmonary allergic aspergillosis is promoted by chronic inflammation and sputum retention in the distal bronchi. The development of bronchopulmonary allergic aspergillosis is possible with prolonged treatment with glucocorticosteroid drugs and antibiotics for severe bronchial asthma. Most often found in the winter months, when the number of fungal spores in the environment increases. 

Etiology of bronchopulmonary allergic aspergillosis

Bronchopulmonary allergic aspergillosis is caused by spores of fungi of the genus Aspergillus, which are a ubiquitous microorganism, the source of which can be air, fertile soil, rotting plants, flour, water in the swimming pool. Mushrooms often breed in homes, especially in basements, bedding, house dust, and indoor plants. Many species of Aspergillus (A. fumigatus, A. clavatus, A. terreus, A. fischeri, A. niger, A. amstelodani, etc.) can infect humans, but A. fumigatus is the most common cause of bronchopulmonary allergic aspergillosis. Along with bronchopulmonary allergic aspergillosis, other types of respiratory diseases caused by A. fumigatus arise, depending on immunological reactivity and contact conditions : invasive, or septicemic, aspergillosis; saprophytic aspergillosis or aspergilloma; aspergillosis bronchial asthma; bronchioloalveolitis allergic exogenous. The nature of the damage depends on the biological characteristics of the pathogen. In particular, Aspergillus spores with a diameter of 1-2 microns penetrate the periphery of the lung, causing allergic bronchioloalveolitis; spores with a diameter of 10-12 microns remain in the proximal bronchi, causing bronchopulmonary allergic aspergillosis. Aspergillus can also be randomly detected in the sputum of individuals without signs of pulmonary disease (saprophytes).

Pathogenesis of bronchopulmonary allergic aspergillosis

The cardinal sign of bronchopulmonary allergic aspergillosis, which distinguishes it from other diseases, is that the inhaled Aspergillus spores grow well at body temperature and form mycelium in the lumen of subsegmental bronchi, as a result of which the amount of antigen increases and its constant entry into the tissue occurs. It is believed that the leading factors in the pathogenesis of bronchopulmonary allergic aspergillosis are immunological damage of types I and III, possibly also the participation of delayed-type hypersensitivity. The pathogenetic role of type III immunological damage is confirmed by the following facts: constant detection of large amounts of precipitating antibodies related to immunoglobulins G in blood serum; development of late type allergic reactions to A. fumigatus (after 4-10 hours); detection of mononuclear infiltration in skin biopsies at the site of a late reaction; detection of deposits of immunoglobulins and component C3 of the complement of the system in the vascular endothelium of the lungs; the possibility of transferring late skin reactions and lung damage from a person to a monkey using the serum of a patient with bronchopulmonary allergic aspergillosis, followed by inhalation of Aspergillus antigen. The involvement of immediate allergic reactions is confirmed by the occurrence of immediate skin reactions to the antigen, a high level of total immunoglobulin E and antibodies related to immunoglobulins E. It is believed that GNT stimulates the attraction of antigen-antibody immune complexes (or their products) to vascular endothelial cells. Pathogenetic significance is also associated with reactive airway obstruction. The peripheral blood leukocytes of patients with bronchopulmonary allergic aspergillosis in contact with a specific antigen and antibodies against immunoglobulin E and immunoglobulin G of various subclasses (Iig, I3, HGt) secrete a significant amount of histamine. Based on these facts, it is believed that specific cytophilic antibodies related to immunoglobulin E, as well as immunoglobulin G, some of which belong to thermostable immunoglobulin G2, are found on leukocytes. HRT is allowed, as sensitized lymphocytes are detected (inhibition of leukocyte migration, lymphocyte proliferation under the influence of a specific antigen). There are reports of complement activation in both the classical and alternative ways in the acute phase of the disease.

Pathomorphology of bronchopulmonary allergic aspergillosis

In lung biopsy specimens, predominantly mononuclear infiltration is determined with the presence of eosinophils. The bronchi are dilated and filled with thick mucus and exudate, in which fungal hyphae can be found. A large number of granulomas with central necrosis, multinuclear giant cells and eosinophilic infiltration are detected in the parenchyma . The alveoli are thickened, significant deposits of immune complexes are not detected. In case of bronchopulmonary allergic aspergillosis, which developed against the background of asthma, bronchial steroid-dependent, desquamative alveolitis and fibrinous thrombosis of small vessels without signs of eosinophilia and vasculitis are noted in lung biopsies.

Clinic of bronchopulmonary allergic aspergillosis

Patients complain of weakness, anorexia, headache, chest pain, fever, asthma attacks, cough with brown sputum, bronchial casts similar to rubber. 50% of patients have hemoptysis.
Inhalation of A. fumigatus antigen can cause both early bronchospasm and late (after 4-8 hours). In these cases, shortness of breath is not episodic, but prolonged. Crepitating wet or dry wheezing is often heard over the area of ​​the lung lesion. Bronchospasm is resistant to bronchodilators. Although the lungs are most often affected, other organs (skin, eyes, meningeal membranes) may be involved in the pathological process.
The course of bronchopulmonary allergic aspergillosis is variable. Some patients have one or two episodes of bronchopulmonary allergic aspergillosis, while others (in the absence of glucocorticosteroid therapy) have frequent relapses. There is evidence that irreversible airway obstruction in patients with long-term asthma (more than 30 years) was most often observed with a combination of asthma and bronchopulmonary allergic aspergillosis. The forecast is serious. In many cases of bronchopulmonary allergic aspergillosis, severe pulmonary destruction develops. With unrecognized bronchopulmonary allergic aspergillosis, lung damage progresses.

local_offerevent_note November 4, 2019

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