Allergic predisposition factors in patients with exogenous allergic bronchioalveolitis have not been established, although HLA-BW40 and HLA-B8 are more common. Immunological and non-immunological mechanisms are involved in the development of the disease. Allergic reactions of various types are expected to be involved: delayed-type hypersensitivity, immune complexes, immediate-type allergic reactions caused by antibodies related to immunoglobulin E, mediated by cytotoxicity antibodies. There is currently no evidence of a predominance of a particular type of immunological reaction.
Existing ideas about exogenous allergic bronchioloalveolitis as a disease caused by the immune complex are questioned for the following reasons: there is no parallelism between the level of precipitating antibodies related to immunoglobulin G and the severity of the disease; precipitins are found in a large number of healthy individuals in contact with the antigen; in the acute period of the disease, granulomas are formed that are uncharacteristic of the Arthus phenomenon; skin reactions according to the type of Arthus phenomenon to specific antigens are not constantly detected in patients;
deposits of immune complexes in biopsies of human lungs are noted only at an early stage of the process; histological signs with exogenous allergic bronchioalveolitis are more characteristic of cellular reactions, fibrinoid necrosis of the vascular walls and perivascular infiltration by segmented cells. Many authors assign the leading role of HRT. The role of GNT due to immunoglobulin E is not clear, antibodies related to immunoglobulin E have not been identified, although certain antigens (pigeon proteins, pituitary powder) can cause GNT. It is assumed that immunoglobulin E does not participate in the development of a typical granulomatous lesion, but can mediate GNT. The question of the role of immunoglobulin E needs to be studied in connection with recent data on late-type allergic reactions caused by immunoglobulin E and characterized by mononuclear cell infiltration without the presence of vasculitis. Perhaps the participation of a secondary autoimmune cytotoxic mechanism associated with chronic inflammation and tissue destruction. Non-immunological mechanisms are associated with the characteristics of disease-causing antigens that are resistant to lysosomal enzymes, are not destroyed by alveolar macrophages, are able to activate the complement system in an alternative way and have a nonspecific adjuvant effect on the induction of cell-mediated reactions and activation of alveolar macrophages. Immuno-non-immunological mechanisms activate alveolar macrophages, which, through soluble mediators, induce inflammation and stimulate the activity of fibroblasts, which leads to fibrosis. There is an opinion that it is activated alveolar macrophages that occupy a central place in the pathogenesis of exogenous allergic bronchioloalveolitis.
With the fulminant form of exogenous allergic bronchioalveolitis, ending with the rapid death of the patient, intense inflammatory exudate in the alveolar septa, hemorrhagic edema inside the alveoli, necrosis of the bronchioles with obliteration are detected. In the acute period, infiltration of the alveoli and bronchioles with lymphocytes, plasma cells and a large number of alveolar macrophages is detected. Noncaseating sarcoid-like granulomas, consisting of lymphocytes, activated macrophages, epithelioid and giant cells, are characteristic. In a very early period of the disease, deposits of immune complexes on the alveolar membrane and necrotizing vasculitis are found. In the chronic form, infiltration by lymphocytes and plasma cells is less pronounced, granulomas are scattered in areas of interstitial fibrosis, destruction of the bronchioles mural structure with macrophage obliteration of the lumen, hypertrophy of the cuboid epithelium of the alveoli, and sometimes of the “emphysema” zone due to uneven destruction of the alveoli are observed. At the final stage, destruction of the alveoli, fibrosis, and the picture of the “cell lung” develop.
Clinical signs of the disease depend on the nature of the organic particles, the intensity and frequency of inhalation, and the characteristics of the immunological response of the patient. The allergy period is different – from several months to several years. Usually, 4-6 hours after inhalation of organic dust, a cough appears, dry or with viscous yellow sputum, which may contain blood; there is an increase in temperature to 38-40 ° C, heavy sweat, chills, myalgia, weakness, retrosternal pain. Inspiratory dyspnea progresses rapidly. Over the lungs, dullness of the sound and crepitus are determined. In the acute period, tachycardia and bronchial obstruction resistant to the action of bronchodilators may occur, which indicates the prevalence of inflammation over increased bronchial tone. Fever lasts up to 24 hours, shortness of breath and weakness sometimes lasts up to several weeks. In other cases, the symptoms spontaneously disappear within a day. Upon contact with certain antigens (pigeon proteins, pituitary powder), HNT can occur, which occurs rarely if actinomycetes are the cause of exogenous allergic bronchioloalveolitis. With repeated exposures of the antigen, shortness of breath intensifies, anorexia, weight loss are noted – the disease acquires a chronic course, which can develop without an acute attack – in cases of prolonged contact with small stumps of antigen. This form is formed by bird lovers, especially budgerigar owners, workers in contact with heating and conditioning systems, and is characterized by progressive shortness of breath, coughing, weakness, malaise, and emaciation. Wet cracking rales (“cracking cellophane”) are heard over the lungs, but this is less typical of a disease than an idiopathic fibrosing alveolitis; in 10% of patients, after a gradual onset, subsequent antigen inhalations cause acute symptoms and GNT. Rare clinical signs of exogenous allergic allergic bronchioalveolitis are also described: chest tightness, impaired consciousness, changes in sensitivity and paralysis of the facial nerve.
The course of the disease is usually acute or subacute when inhaled enough antigen; with massive inhalation, the disease can last no more than a day. In cases of prolonged exposure to small doses of antigen, the disease progresses with the development of fibrosis.
The prognosis for acute and subacute currents is favorable, elimination of antigen and glucocorticosteroid therapy lead to the reverse development of the process. The prognosis is less favorable if the disease lasts several years, especially in the elderly.