Farmer's lung, diagnosis and symptoms. Allergic alveolitis

- is an immunologically mediated inflammatory reaction of the respiratory bronchioles and alveoli, which develops in response to the intake of inhaled allergens. Symptoms are characterized predominantly by inspiratory dyspnea, cough, chest pain, and in acute cases, a flu-like condition. Diagnosis of allergic alveolitis is based on the results of spirometry, X-ray and CT scan of the chest, bronchoalveolar lavage studies, lung tissue biopsy, and serum antibody levels. Therapy of allergic alveolitis begins with the elimination of the allergen, it is possible to prescribe glucocorticosteroids.

ICD-10

J67 Hypersensitivity pneumonitis due to organic dust

General information

Exogenous allergic alveolitis (hypersensitivity pneumonitis) is an interstitial lung disease with localization inflammatory process in the terminal sections of the respiratory tract (alveoli, bronchioles), resulting from exposure to external environmental factors. In practical pulmonology, various forms of allergic alveolitis are considered, related to occupational pathology, and also not related to professional activities. The first cases of the disease were described in 1932 among farmers ("farmer's lung"), the second most common and significant form is "bird lovers' lung", found in pigeon breeders. The overall incidence rate in the population is 42:100,000. Timely therapy of hypersensitivity pneumonitis can prevent the development of pulmonary fibrosis.

Causes

In all cases, the cause of allergic alveolitis is inhaled allergens that enter the body along with the inhaled air. At the same time, factors such as the size and concentration of inhaled particles, the characteristics of antigens and the immune response of the patient are of the greatest importance for the occurrence of the disease. It is known that in the presence of high concentrations of organic or chemical substances exogenous allergic alveolitis develops in about 5-15% of individuals. It was also found that dust particles with a diameter of up to 5 microns are able to freely penetrate into the alveoli and cause sensitization. In the pathogenesis of allergic alveolitis, repeated inhalation of antigens plays an important role.

The most common allergens are fungal spores found in hay, compost, tree bark and others. The etiological role of antigens of plant and house dust, protein antigens, bacterial spores, medicines (nitrofurans, penicillin, gold salts). Among the fungal antigens, the most common radiant fungi are thermophilic actinomycetes and aspergillus. The first of them are associated with such forms of allergic alveolitis as "farmer's lung", bagassosis, "lung of persons using air conditioners", "lung of persons growing mushrooms". Various subspecies of Aspergillus are capable of causing "malty lung", "cheesemaker's lung", suberosis, etc.

Protein antigens are commonly found in the feces of birds (parrots, pigeons, canaries, etc.) and are associated with a form of birdwatcher's lung pneumonitis. Occupational forms of allergic alveolitis can occur in people who, by the nature of their activities, are associated with the production of polyurethane, dyes and resins, in contact with metal vapors (cobalt), employed in the woodworking and wool processing industries.

Pathogenesis

Allergic alveolitis is an immunopathological disease. Type III and IV hypersensitivity reactions play a fundamental role in the development of allergic alveolitis. In this case, in response to repeated contact with an inhaled allergen, specific precipitating antibodies and CEC appear in the blood, infiltration of the alveoli with lymphocytes, neutrophils, and monocytes occurs with the development of granulomatous inflammation. The result of prolonged contact with a causally significant allergen is an intensive collagen synthesis with an outcome in pulmonary fibrosis or bronchiolitis obliterans.

Classification

Taking into account the causative factors of allergic alveolitis and the source containing antigens, the following syndromes are distinguished:

"farmer's lung" - develops upon contact with moldy hay containing thermophilic actinomycetes
"lung of bird lovers" - found in poultry farmers and persons caring for birds; the source of antigens is bird droppings, fluff, secrets of the skin glands, etc.
bagassosis - develops on contact with sugar cane microfibers
suberosis - the source of the antigen (mold fungus) is the bark of the cork tree
"malt lung" - develops in persons in contact with barley dust
"lung of persons using air conditioners" - occurs with frequent use of air conditioners, heaters and humidifiers
"Cheesemaker's lung" - the source of the antigen is cheese mold
"Lung of mushroom pickers" - develops in persons who grow mushrooms; pathogens - fungal spores contained in compost
other occupational allergic alveolitis: “lung of those producing detergents”, “lung of laboratory workers”, “lung of those employed in the production of plastics”, etc.

The course of allergic alveolitis can be acute, subacute or chronic, which is reflected in the clinical picture. The acute form develops within 4-12 hours after contact with a massive dose of antigens; chronic - with prolonged inhalation of a low dose of antigens; subacute - with a lower exposure of antigens.

Symptoms of allergic alveolitis

The clinic of the acute form of the disease is accompanied by flu-like symptoms: fever, myalgia and arthralgia, headache. A few hours after the rise in temperature, heaviness and pain in the chest, cough with scanty mucous sputum, and shortness of breath join. If contact with a causally significant allergen is excluded, all symptoms disappear within 1-3 days, but may return again after repeated inhalation of the antigen. General weakness and shortness of breath associated with physical activity, persist for several weeks.

The subacute form of allergic alveolitis, as a rule, is not caused by occupational hazards, but by exposure to antigens at home. At the onset of the disease, fever may be noted, but more often the symptoms are limited to shortness of breath during physical exertion, productive cough, and increased fatigue. Chronic allergic alveolitis can develop both as a result of repeated episodes of an acute or subacute process, and immediately on its own. The course of this form is characterized by progressive inspiratory dyspnea, persistent cough, malaise, and weight loss.

Complications

The appearance of the symptom drumsticks"- thickening of the phalanges of the fingers indicates respiratory failure and serves as an unfavorable prognostic sign. The natural outcome of the chronic form of allergic alveolitis is the development of interstitial fibrosis, pulmonary hypertension, cor pulmonale, right ventricular heart failure. Most patients develop chronic bronchitis after 10 years or more, and a quarter are diagnosed with emphysema.

Diagnostics

Forecast and prevention

A favorable outcome can be achieved only if the allergen is eliminated in a timely manner, if necessary, the active treatment of allergic alveolitis. In the case of recurrence of hypersensitivity pneumonitis, the development of cardiopulmonary insufficiency, the prognosis is relatively unfavorable. Primary prevention consists in the elimination of harmful professional and domestic factors (observance of occupational hygiene, the use of protective clothing, ventilation of industrial premises, maintenance of air conditioners, etc.), periodic medical examinations of persons with an increased risk of developing allergic alveolitis. Secondary prevention measures include cessation of contact with the allergen, if necessary, a change in professional activity.

Definition. " Farmer's Lung" is listed in the list of occupational diseases and is defined as "a lung disease caused by inhalation of rotten hay dust or other rotten plant matter, and is characterized by symptoms and signs associated with the reaction of the peripheral bronchopulmonary system, causing gas exchange disorders" .

The disease was described by Cadham in 1924 in Canada. Campbell in 1932 gave the first description in England of the disease in farm workers dealing with rotten hay in Westmerland. Radiological manifestations and most early description lung pathology in lethal outcome were the subject of Fawcitt communications in 1935 and 1938. The next great achievement was the detailed description of pulmonary pathology based on biopsy material from several authors. Discovery of precipitins to antigens in rotten hay reported by Pepys et al in 1961 and 1962. , confirmed by Kobayashi, represented a step forward in understanding the pathogenesis of the disease and stimulated interest in morbidity. This ended with the recognition of "farmer's lung" as an occupational disease in England, and since 1965, those with it have been counted for occupational hazard benefits.

The peak incidence of "farmer's lung" in England occurs from January to March, when hay supplies are used for forage in the winter. It is more common in the humid parts of the country and the incidence is higher after a rainy summer when it is more difficult to dry the hay. Hay good quality contains only about 16%; moisture and even after long-term storage, relatively little microflora develops in it.

But when harvesting wet hay (with a content of more than 29-34% water), an increase in temperature (above 60 °) causes and promotes the growth of thermophilic microorganisms, of which actinomycetes are the most important for the development of the "lung farmer". Sifting poor quality grain and sweeping barns is also associated with the danger of inhaling plant decay products and can lead to the clinical picture of "farmer's lung". The approximate incidence in England can be up to 1000 cases per year of all degrees of severity.

Pathogenesis. A joint study between the British Medical Research Council Clinical Immunology Research Group and the Rothamsted Experimental Station by Dr. Pepys and Dr. Gregory, respectively, defined what should be meant by a farmer's lung antigen complex (LF) in hay, namely a group of antigens that appears in hay only after heating and in which thermophilic actinomycetes are the main component. Abundant sources of SLF antigen are Mycropolyspora sp. (Thermopolyspora polyspora) and, to a lesser extent, Mocromonospora (Ther-moactinomyces) vulgaris. It is estimated that workers with rotten hay can ingest 3/4 million spores of Micropolyspora sp. in a minute. Spores, having only 1 micron in diameter, enter the alveoli, where the main pathological tissue reaction occurs.

In 80% of patients with "farmer's lung" caused by rotten hay, precipitins to the SFL antigen were found; precipitins to other actinomycetes were found in another 2-3%. Under the action of other dusts, such as barley and oat dust, 50% of patients found SLF precipitins. It is clear that has since been found whole line other sources of antigen and manifestations of "farmer's lung" may be present without positive serological reactions. Thus, a negative reaction does not rule out the diagnosis. 17-18% of those who have been in contact, but without clinical signs of "farmer's lung", may have precipitins to the SLF antigen. The diagnosis is therefore not based solely on a positive serological reaction, but clinical and immunological findings must also be taken into account.

Fog fever in cattle can occur after exposure to rotten hay, and 71% of affected animals show an LFS reaction on serological testing.

Pathological anatomy. Pathological anatomical manifestations depend on the stage of the disease, all degrees are possible - from an acute alveolar-interstitial reaction to diffuse pulmonary fibrosis. An acute reaction is characterized by edema and infiltration of the walls of the alveoli and interstitium of the lung by lymphocytes, plasma cells and neutrophils. The pulmonary vessels may be involved in the process. Repeated contact results in patchy foci of interstitial fibrosis and sometimes diffuse cystic changes.

Lung biopsy sometimes reveals diffuse nodular involvement of the walls of the alveoli and bronchioles throughout the lung parenchyma, in the interlobular septa, and in the subpleural regions. The lumen of affected bronchioles may be blocked by inflammatory exudate. The nodule consists of a collection of pale epithelioid cells surrounded by lymphocytes and plasma cells, and sometimes by giant cells containing pale transparent fibers, the nature of which is unknown.

When bronchoscopy in the large bronchi observed intense congestion.

And Micropolyspora sp. , and Micromonospora vulgaris have been isolated from lung biopsies from patients with farmer's lung.

Functional disorders. The nature of functional disorders is a restrictive pathology of the lungs of varying severity with a pronounced impairment of diffusion ability. Changes include a decrease in static lung volume, vital capacity, diffusing capacity, and static compliance. The amount of ventilation under load increases.

Functional disturbances are reversible in the early stages of the disease, but repeated exposure can lead to permanent lung damage and respiratory failure. Disturbances in diffusivity can persist for a long time after radiographic resorption.

Clinical and radiological manifestations. There are two main groups: a) acute and subacute, b) chronic. In the classic acute form, shortness of breath, chills, fever, and cough occur suddenly after several hours of handling rotten hay; wheezing is uncommon. Sputum scanty, occasionally stained with blood. Cyanosis is sometimes expressed even at rest. Crepitus is heard throughout the lung. The radiograph may be normal or with miliary foci, especially in the middle and lower zones or, more rarely, these areas have larger, poorly defined shadows.

Symptoms and radiological changes usually disappear spontaneously after 3–4 weeks, but repeated exposure leads to the development of a subacute form in which clinical and radiographic changes disappear much more slowly. In some cases, the disease becomes chronic and develops severe dyspnea on exertion and cough. X-ray manifestations in the chronic form are nonspecific and usually consist of heterogeneous shadows and a honeycomb pattern. Death is usually associated with cor pulmonale with right heart failure. Eosinophilia in blood, sputum, and tissue is uncommon in farmer's lung, while it is common in asthma and allergic-type pulmonary aspergillosis. There is no corresponding skin test for Farmer's Light.

differential diagnosis. Chronic bronchitis, emphysema, asthma, honeycombing, sarcoidosis, and pulmonary aspergillosis should all be considered. The diagnosis of farmer's lung is based on the history, clinical examination, radiological manifestations, functional and radiological examination. Of particular importance are the delayed onset of symptoms relative to contact, the miliary type of radiographic changes, severe diffusion disorders, and a positive precipitin test with SLF.

Prevention and treatment. Adequate drying of hay, use of open silos and increased ventilation of work areas are important preventive measures. Sensitized persons should be warned against further contact with rotten hay. If there is only one such worker on the farm, it is recommended to advise him to change jobs. As already said, wearing a mask is not a big deal. Treatment with corticosteroids in acute and subacute cases sometimes has a pronounced effect.

Farmer's Lung- diffuse granulomatous lesions of the lung parenchyma induced by inhalation of Ag spores of thermophilic actinomycetes; occurs with frequent contact with moldy hay, cheese, compost, infected grain, etc.

Code by international classification ICD-10 diseases:

J67. 0 - Lung of a farmer [agricultural worker]

Farmer's Lung: Causes

Etiology

Aspergillus clavatus. Penicillium casei. Micropolyspora faeni. Thermoactinomyces vulgaris.

Pathogenesis

Allergic reactions III (precipitating antibodies to Ag of the above microorganisms) and IV (granulomatous reaction) types.

Farmer's Lung: Signs, Symptoms

Clinical picture

Attacks of fever, dry cough, shortness of breath 4-8 hours after contact with the allergen. Chills, weakness and myalgia. Small and medium bubbling wet rales in the lungs.

Farmer's Lung: Diagnosis

Diagnostics

Precipitating antibodies to fungal Ag. The predominance of T - cells of the CD8+ subpopulation. Eosinophilia is uncharacteristic (important for differential diagnosis). X-ray of the chest organs. Bilateral spotty-focal infiltrates. Strengthening of the bronchovascular pattern. Pleural effusion and lymphadenopathy (rare). Research FVD - restrictive changes. Decrease in lung volumes. Decreased diffusing capacity of the lungs.

Farmer's Lung: Treatment Methods

Treatment

Exclusion of provoking factors. GK. Prednisolone 60 mg/day orally for 1 to 2 weeks, then tapered to 20 mg/day for 2 weeks and then reduced by 2.5 mg weekly to complete abolition. Antibiotics are not shown.
Synonym. Allergic exogenous alveolitis.

ICD-10. J67. 0 Lung farmer [agricultural worker].

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honey.
Farmer's lung - diffuse granulomatous lesion of the lung parenchyma induced by inhalation of Ag spores of thermophilic actinomycetes; occurs with frequent contact with moldy hay, cheese, compost, infected grain, etc.

Etiology

Aspergillus clavatus
Penicillium casei
Micropolyspora faeni
Thermoactinomyces vulgaris.

Pathogenesis

Allergic reactions III (AT precipitating to Ag of the above microorganisms) and IV (granulomatous reaction) types.

Clinical picture

Attacks of fever, dry cough, shortness of breath 4-8 hours after contact with the allergen
Chills, weakness and myalgia
Small and medium bubbling wet rales in the lungs.

Diagnostics

precipitating antibodies to fungal antigens
Predominance of T-cells of the CD8 subpopulation
Eosinophilia is not characteristic (important for differential diagnosis)
Chest X-ray
Bilateral macular-focal infiltrates
Strengthening of the bronchovascular pattern
Pleural effusion and lymphadenopathy (rare)
FVD studies - restrictive changes
Decrease in lung volumes
Decreased diffusing capacity of the lungs.

Treatment

Exclusion of provoking factors
Glucocorticoids
Prednisolone 60 mg/day orally for 1–2 weeks, then tapered to 20 mg/day for 2 weeks, then reduced by 2.5 mg weekly until stopped
Antibiotics are not shown.

Synonyms

Allergic exogenous alveolitis See also Pnevmosht hypersensitive. Diffuse interstitial lung disease, Atypical pneumonia, Bronchial asthma, Sarcoidosis

ICD

J67.8 Hypersensitivity pneumonitis due to other organic dusts

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Probably in Great Britain this is the most important form of exogenous allergic alveolitis. It develops when storing moist hay or grain that can grow at high temperatures(45-60 ° C) thermophilic actinomycetes. Clinical outbreaks are more common in late winter after a wet summer, especially in areas where there is usually high rainfall and where farmers work with contaminated hay, especially in enclosed spaces. Grant et al. (1972) in a sample population calculated from clinical symptoms that "farmer's lung" occurs in about 8% of Scottish farmers in the wet areas and in about 2% in the drier parts of Northern Ireland.

Staines and Forman(1961) found the incidence to be between 11.5 per 100,000 people in the East of England, 73.1 in the South West of England and up to 193.1 in Wales. The latter figure more or less corresponds to the results of somewhat different calculations: in an agricultural area where about 90 thousand people lived, 245 cases were detected over 24 years with an annual incidence of about 20 new cases. In Devonshire, Smyth et al. (1975) found 200 cases among 25,000 farmers over 32 years, corresponding to about 6 new cases per year. Farmer's Lung has a wide geographic distribution throughout the world. The first messages came from the USA.
There was a recent symposium on this subject and a review article was published by Molina (1976).

Clinical picture of farmer's lung

The illness often begins with shortness of breath, sometimes accompanied by a dry cough, with flu-like symptoms of malaise, fever, and pain in the extremities about 6 hours after intense contact. This clinical picture was observed in 32% of the 205 cases published by Pepys and Jenkins (1965). Symptoms last approximately 24-48 hours. At first they appear intermittently and only after contact, but when irreversible changes occur in the lungs, shortness of breath becomes more or less permanent. It is not uncommon (49% of cases) that symptoms are less pronounced, and thus the interval between contact and onset of symptoms cannot be clearly established. Patients may ignore symptoms for months or even years and only then see a doctor, and even then it is difficult to recognize the antigen that causes all these disorders.

less often(10% - from the material Pepys, Jenkins, patients complain of symptoms similar to asthma: about 6 hours after exposure, obstruction is more common than airway restriction. In the acute stage, thin nodular shadows are visible on the radiograph, widespread or predominantly in the middle zones. After cessation of contact, they spontaneously resolve.When compared with biopsy material, it turned out that nodular shadows are both granulomas and interstitial infiltrates.Later stages are characterized by fibrous contractions, especially of the upper lobes.Objective signs are often few.

At auscultation in the acute stage, subtle crepitations may be heard, but later signs may be very slight; neither wheezing, nor the form of deformation of the fingers in the form of drumsticks are not expressed to a large extent. In this respect, the clinic differs from crintogenic fibrosing alveolitis.

Hapke et al. (1968) and Rankin et al. (1967) also describe pathophysiological changes. As a rule, there are signs of a restrictive defect in ventilation, a decrease in static lung volumes, and the absence of airway obstruction. However, in the later stages, at least 73 patients develop irreversible airway obstruction. CO diffusion is reduced as measured at steady state or by the single breath method. If the result is corrected for alveolar lung volume (ALV), then the decrease observed in many cases can be explained by a decrease in lung ventilation and cannot be regarded as a membrane defect. However, in other cases, CSR is also reduced.

Discrepancy between ventilation and blood flow is expressed in a decrease in Po2 with a normal or even low Pco2. Initially, the norm is restored spontaneously or after treatment with corticosteroids, but as irreversible fibrosis develops, all these changes cease to respond to treatment. Cases have been described in which pathophysiological phenomena continue to progress despite the termination of contact, and the pathogenesis in these cases has not yet been elucidated. It is not known whether the progression is due to persistence of antigens in the tissue or some self-sustaining fibrosing process. Obliteration of the pulmonary vessels can lead to pulmonary hypertension and cor pulmonale.