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Pulmonary eosinophilia with asthmatic syndrome: causes, symptoms, diagnosis, treatment

 
, medical expert
Last reviewed: 06.07.2025
 
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Bronchial asthma

Bronchial asthma (as an independent nosological form) can occur with blood eosinophilia (usually no more than 15-20%) and “flying” pulmonary infiltrates, sometimes with other clinical manifestations of allergy ( urticaria, Quincke's edema, vasomotor rhinitis ).

The examination program is the same as for simple pulmonary eosinophilia.

Bronchopulmonary aspergillosis

Aspergillosis is caused by fungi of the genus Aspergillus. They are widespread in the environment - in the soil, in the air, on plants, vegetables, fruits, in grain, flour and other products, especially if they are stored in a warm and humid environment. In addition, aspergilli saprophyte on the skin and mucous membranes of healthy people, can significantly multiply and cause severe disease in conditions of reduced body defenses.

Aspergillosis is more common among people of certain professions: pigeon breeders, workers on plantations growing and processing red pepper, hemp, barley; workers in factories producing alcohol, beer, and the bakery industry (saccharifying enzymes of some types of aspergillus are used in the form of fungal malt); in fish factories (fermentation of fish for canning); in the manufacture of soy sauce, as well as in wool and hair carders. The specified nature of the professions should be taken into account when diagnosing aspergillosis.

Currently, about 300 species of aspergillus have been described. The most reliable causative agents of aspergillosis in humans and animals are the following species of aspergillus: A. fumigatus, A. niger, A. clavatus, A. flavus, A. candidus, A. nidulans, A. glaucus, A. versicolor.

Human infection occurs most often through inhalation and partly through the alimentary route, less often as a result of direct contact (during damage and maceration of the mucous membranes and skin) with fungal spores, as well as through autoinfection as a result of biological activation of aspergilli living on human skin.

When entering the human body, aspergilli release a number of substances that have a toxic effect. Aflatoxins are the most important. They suppress DNA synthesis, cell mitosis, affect the hematopoiesis system, and cause thrombocytopenia, leukopenia, and anemia. Aflatoxin also causes significant damage to the liver and other organs.

The following types of aspergillosis are distinguished depending on the location of the lesions:

  • bronchopulmonary aspergillosis;
  • extrapulmonary visceral systemic organ aspergillosis;
  • aspergillosis of ENT organs;
  • aspergillosis of the eye;
  • bone aspergillosis;
  • aspergillosis of the skin and nails;
  • aspergillosis of the mucous membranes;
  • other manifestations of aspergillosis.

Bronchopulmonary aspergillosis is the most common form of aspergillosis in humans.

Allergic bronchopulmonary aspergillosis

In the pathogenesis of bronchial asthma in aspergillosis, the development of an immediate-type allergic reaction caused by the production of IgE reagins and degranulation of mast cells is of primary importance. The affected alveoli are filled with eosinophils, followed by granulomatous interstitial pneumonitis with pronounced infiltration of the peribronchial tissue and interalveolar septa with plasma cells, monocytes, lymphocytes, and a large number of eosinophils. With steady progression of the disease, proximal bronchiectasis is formed. Hyperplasia of the mucous glands and goblet cells in the bronchi and bronchioles is also characteristic.

Allergic bronchopulmonary aspergillosis is characterized by attacks of bronchial asthma, the clinical picture of which corresponds to ordinary bronchial asthma, however, in addition, the patient may have intermittent fever. Also characteristic is the separation of sputum containing brownish or yellowish grains or plugs.

Aspergillosis bronchitis, tracheobronchitis

The clinical picture of aspergillosis bronchitis and tracheobronchitis is similar to the clinical picture of banal inflammation of the bronchi and trachea. But unlike them, aspergillosis bronchitis and tracheobronchitis are characterized by the release of gray lumps resembling cotton wool, sometimes purulent sputum with blood streaks, when coughing. The aspergillosis nature of the disease can only be proven by detecting aspergilli in the sputum.

Aspergillus bronchopneumonia

Small focal disseminated processes in the lungs are most often observed, and extensive pneumonic foci are less common.

Aspergillosis bronchopneumonia clinically occurs as bronchopneumonia of a different etiology.

X-ray examination reveals foci of inflammatory infiltration mainly in the middle-lower parts of the lung, more often the right one. In this case, the sputum contains grayish-green flakes. The diagnosis is confirmed by the detection of aspergillus in the sputum. It should be taken into account that some patients may develop abscessing and necrotic aspergillosis pneumonia, in which case hemoptysis and severe chills appear, and infiltration foci with cavities of decay are revealed on chest X-rays.

Aspergilloma of the lungs

Aspergilloma is a unique tumor-like form of aspergillosis, characterized by the presence of a cavity in the lungs lined with epithelium with varying amounts of granulation tissue. The cavity usually communicates with the bronchus, and contains fungal masses inside - byssus. The cavity is easily damaged by byssus during movement, which leads to bleeding of the aspergilloma.

The diagnosis of aspergilloma is based on the following signs:

  • repeated hemoptysis (sometimes bleeding);
  • chronic wave-like course (febrile and subfebrile with periods of remission);
  • a characteristic radiological picture is the presence, most often in the apical segments of the upper lobes, of an “elite round thin-walled cavity without perifocal infiltration with a central darkening in the form of a ball and marginal enlightenment in the form of a crescent;
  • positive serological reactions with specific antigens from aspergilli;
  • repeated isolation of the same species of aspergillus from sputum, biopsy materials or bronchial washings.

Diagnostic criteria

The main diagnostic criteria for allergic bronchopulmonary aspergillosis are:

  • recurrent attacks of atopic bronchial asthma;
  • proximal bronchiectasis (detected by radiography or computed tomography, bronchography is not recommended);
  • high percentage of eosinophils in peripheral blood; sputum eosinophilia;
  • high levels of IgE in the blood;
  • recurrent pulmonary infiltrates (detected by X-ray examination); they can move from one lobe to another;
  • detection of precipitating antibodies to aspergillus antigen;
  • growth of aspergilli in sputum culture;
  • detection of calcium oxalate crystals in sputum - a metabolite of aspergillus;
  • increased levels of uric acid in bronchial lavage;
  • positive skin tests with a specific allergen. The skin test can give a two-phase positive reaction: first, an immediate type with a papule and erythema, and then a delayed type in the form of erythema, edema and soreness, which are maximally manifested after 6-8 hours.

Laboratory data

In aspergillosis, sputum analysis is performed, bronchial lavage waters, and mucus from the pharynx are examined. The material to be examined is treated with a 20% KOH solution, then microscopy of native unstained preparations is performed, and the septate mycelium of aspergillus is already visible at low magnification, but especially well - at high magnification. Often, along with the mycelium, convdial heads of aspergillus are found.

To identify the type of aspergillus, as well as to isolate a pure culture, pathological material is sown on Chapek nutrient media, wort agar, and Sabouraud glucose agar.

Determination of serum precipitating antibodies to the aspergillus antigen and papular-erythematous skin reaction to the aspergillus antigen are also of great diagnostic significance.

Survey program

  1. Analysis of subjective manifestations of the disease and professional history.
  2. General blood and urine tests.
  3. Sputum analysis - physical properties (color, odor, transparency, presence of yellow and brown lumps), cytological examination (number of eosinophils, neutrophils, lymphocytes, atypical cells), examination for the presence of aspergillus mycelium, sputum culture on special nutrient media.
  4. Immunological studies - content of T- and B-lymphocytes, subpopulations of T-lymphocytes, circulating immune complexes, immunoglobulins, including IgE.
  5. Determination of serum precipitating antibodies to aspergillus antigen.
  6. Skin test with aspergillus antigen.
  7. X-ray examination of the lungs.
  8. ECG.
  9. Spirometry.
  10. Computed tomography of the lungs.
  11. Consultation with a phthisiologist, oncologist, allergist.

Tropical pulmonary eosinophilia

Tropical pulmonary eosinophilia (Weingarten syndrome) is caused by invasion and subsequent migration of larval forms of microfilaria helminths. The main manifestations of the disease are:

  • severe attacks of bronchial asthma;
  • increase in body temperature to 38°C, sometimes up to 39°C;
  • symptoms of intoxication (headache, loss of appetite, weight loss, sweating);
  • cough with difficult to separate mucous sputum;
  • aching, sometimes paroxysmal pain in the abdomen without clear localization;
  • systemic manifestations of the disease - enlargement of peripheral lymph nodes, various skin rashes, polyarthralgia (less often - transient polyarthritis), splenomegaly;
  • focal infiltrative, often disseminated, miliary radiological changes in the lungs;
  • characteristic laboratory data - high eosinophilia (60-80%) in the peripheral blood, high IgE levels in the blood, false positive Wasserman reaction (a frequent but not constant symptom).

When diagnosing this disease, great importance is attached to the epidemiological history (the disease is most often observed in residents of Southeast Asia, India, Pakistan), the detection of microfilariae in a thick drop of blood and the detection of antifilariasis antibodies in the blood using the complement fixation reaction.

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