Farmer's lung, diagnosis and symptoms. “Farmer's Lung”

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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  • - allergic exogenous alveolitis caused by the fungal flora of moldy hay; the term is used in foreign literature ...

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- is an immunologically mediated inflammatory reaction of the respiratory bronchioles and alveoli, which develops in response to the intake of inhaled allergens. The symptomatology is characterized mainly by inspiratory dyspnea, cough, chest pain, and in an acute course - 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 allergic alveolitis related to occupational pathology, as well as 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 a symptom of "drum sticks" - 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.


Exogenous allergic alveolitis is a disease caused by a diffuse lesion of the interstitial lung tissue resulting from an allergic reaction of the lung tissue. The etiological factors of this disease can be some types of organic and inorganic dust, fungi, bacteria, drugs with pronounced allergenic properties.
Exogenous allergic alveolitis is very common among agricultural workers who have to come into contact with various types of organic dust (in persons working with hay, silage, livestock; in hay processing, cheese making, woodworking, etc.).
Farmer's Lung” - a lung disease caused by inhalation of rotting plant dust (hay, grain, etc.).
In its pathogenesis, thermophilic microorganisms (especially actinomycetes) contained in decaying plants and possessing antigenic properties are important. Once in the lungs, they cause a hypersensitivity reaction of the alveolar tissue due to the production of precipins. Therefore, the "farmer's lung" according to the mechanism of occurrence can be attributed to exogenous allergic alveolitis.
According to the clinical picture, acute, subacute and chronic forms of the disease are distinguished. Acute and subacute forms develop rapidly after inhalation of dust from rotting plants. Patients develop severe shortness of breath, chills, cough with scanty sputum, which sometimes contains a small amount of blood; fever, cyanosis of visible mucous membranes and skin. Crepitus is heard in the lungs. On radiographs - a picture of fine mesh fibrosis with disseminated nodular shadows, located mainly in the middle and lower parts of the lungs.
Chronic forms of "farmer's lung" develop upon repeated contact with the dust of rotting plants, as well as during the transition of an acute form of the disease to a chronic one. In such cases, cyanosis is noted, the phenomena of diffuse emphysema of the lungs, against which crepitus is heard. Respiratory function is impaired by a restrictive type. On radiographs, the changes are the same as in the acute form of the disease.
The course of the disease depends on its form. The acute form usually ends with complete recovery after 3-4 weeks. In the chronic form, it is possible deaths due to the development of cardiac and pulmonary decompensation.
The pathoanatomical picture of the acute form is characterized by diffuse interstitial changes in the form of edema and infiltration of the alveolar walls and interstitial tissue with lymphocytes, plasma cells and neutrophils. In the chronic form, nodule-like formations may occur, consisting of epithelioid cells, around which lymphocytes, plasma and giant cells are located.
Treatment. Chronic bronchitis, bronchial asthma and pneumoconiosis due to exposure to organic dust are treated in the same way as the corresponding forms of dust lung disease. Patients with uncomplicated byssinosis in most cases do not need treatment, since after the cessation of contact with dust, a complete recovery quickly occurs. In acute and subacute forms of farmer's lung, corticosteroids are most effective.
Employability examination. The question of the working capacity of patients with lung diseases caused by exposure to various kinds organic dust is treated in the same way as in the corresponding forms of dust lung diseases caused by exposure to inorganic dust.
Prevention. Persons working in contact with dust of plant and animal origin (processing of cotton, flax, wool, kenaf, jute, grain, tobacco, wood, paper,
reed, peat, natural silk, etc.), are subject to periodic medical examinations once every 12 months. Medical examinations should be carried out with the participation of a therapist, an otorhinolaryngologist, a dermatologist. Mandatory additional research methods are chest x-ray, respiratory function, determination of the leukocyte formula.
Medical contraindications for work in contact with dust of vegetable and animal origin are the same as for work with other industrial aerosols. An additional contraindication is the presence of allergic diseases.

Exogenous allergic alveolitis is a group of diseases united by at least three common features:

  • widespread inflammation of the lung tissue itself;
  • develops in response to inhalation of polluted air and has an allergic nature;
  • allergens can be bacteria, fungi, some animal proteins.

For the first time, allergic alveolitis was described in 1932 in farmers after working with moldy hay. The workers developed respiratory symptoms. Hence the name "farmer's lung". In 1965, the "lung of bird lovers" was described - a disease that arose in pigeon breeders. This is the second most common and significant form of exogenous allergic alveolitis.
The disease occurs in approximately one in ten people who have been in contact with an allergen in a high dose. Its prognosis is uncertain: it can end in recovery, or it can lead to the development of severe. The frequency of occurrence of exogenous alveolitis reaches 42 cases per 100 thousand of the population.

The development of pathology is associated with influence, less often - a hobby. Exogenous allergic alveolitis is a group of syndromes and diseases, each of which has its own name and a specific cause.
The main syndromes in exogenous alveolitis and their causes:

V agriculture the disease is most often caused by thermophilic actinomycetes - small bacteria that resemble fungi in appearance. They live in rotting organic debris, as well as in the dust that accumulates in air conditioners. Bird and animal antigens are protein compounds. Among fungi, aspergillus is of particular importance, which often settles in warm, damp living quarters. There are cases of severe exogenous allergic alveolitis in pharmaceutical workers.
In Russia, the leading etiological factors are bird antigens and fungi. Among the professions, whose representatives are more likely to get sick with exogenous alveolitis, the following are distinguished:

  • metalworking;
  • welding and foundry works;
  • plasterers and painters;
  • mining industry;
  • medical and chemical industries;
  • woodworking and paper industry;
  • mechanical engineering.

Development mechanism

For the appearance of the disease, prolonged contact with the allergen is necessary. However, not all people who inhale mold or use air conditioners develop exogenous allergic alveolitis. Apparently, genetic predisposition and features of immunity are of great importance. These factors have been little studied.
Exogenous alveolitis of an allergic nature occurs with an altered immune response to foreign particles that have entered the respiratory tract. In the early stages of the disease, immune complexes are formed in the lung tissue, consisting of antibodies and antigens. These complexes increase vascular permeability and attract neutrophils and macrophages, cells that destroy antigens. As a result, inflammation is formed, damaging reactions are triggered, and so-called delayed-type hypersensitivity occurs.
This allergic reaction is supported by new incoming doses of antigens. As a result, chronic inflammation is formed, granulomas are formed, immature cells are activated. Due to their growth and reproduction, fibrosis of the lung tissue appears - the replacement of respiratory cells with connective tissue.

Exogenous allergic alveolitis: clinical picture

There are three types of exogenous allergic alveolitis:

  • acute;
  • subacute;
  • chronic.

Acute allergic alveolitis occurs a few hours after contact with the allergen. It is accompanied by fever with chills, cough, shortness of breath, a feeling of heaviness in the chest, joint and muscle pain. Sputum is usually absent, or there is little of it, it is light. Often the patient is bothered by a headache in the forehead.
Within two days, these signs disappear, but after a new contact with the allergen, they return. In the literature, this phenomenon is called the “Monday syndrome”: over the weekend, the allergen is removed from the respiratory tract, and on Monday all symptoms recur. For a long time, weakness persists even during exercise. A typical example of an acute current is the "farmer's lung".
There is a variant of allergic alveolitis, reminiscent of asthma: after contact with a foreign substance, after a few minutes it develops with wheezing and the release of viscous mucous sputum.
A subacute variant of exogenous alveolitis often occurs during household contact with an allergen, for example, among bird lovers. Symptoms are non-specific: with a small amount of sputum, weakness, shortness of breath on exertion. The patient's life history, his hobbies and living conditions play an important role in the diagnosis.
With improper treatment, a chronic form of exogenous allergic alveolitis develops. Its beginning is imperceptible, but shortness of breath during exercise, weight loss, cardiac and gradually appear and increase. Often the fingers take the form of "drum sticks", and the nails - "watch glasses". This symptom may indicate a poor prognosis for the patient.
The outcome of exogenous alveolitis is "" and progressive heart failure.

Diagnostics

With allergic alveolitis, the picture can be from normal to pronounced signs of pneumosclerosis. Often a decrease in the transparency of the lung fields is determined in the form of " frosted glass”, small nodules all over their surface. If contact with the allergen has not been repeated, these changes disappear after 1 to 2 months. In the chronic form, a picture of a "honeycomb lung" appears.
A more sensitive diagnostic method that allows you to recognize the manifestations of alveolitis in the early stages is the respiratory system.
V general analysis blood changes are nonspecific: there may be leukocytosis, an increase in the erythrocyte sedimentation rate, an increase in the level of total immunoglobulins.
An important sign of exogenous allergic alveolitis is the presence in the blood of specific antibodies to the "guilty" allergen. They are detected using enzyme immunoassay and other complex laboratory tests.
With functional tests, a decrease in the oxygen content in the blood and an increase in the concentration carbon dioxide. in the first hours of the disease indicates a violation of bronchial patency, which is quickly replaced by restrictive disorders, that is, a decrease in the respiratory surface of the lungs.
Functional tests with inhalation of a "suspicious" allergen are used extremely rarely. In some patients, they do not cause an increase in symptoms. In other patients, such a test provokes a sharp exacerbation of exogenous allergic alveolitis. Functional tests are not standardized, purified allergens are not available for their implementation. Therefore, it can be considered analogous to keep a patient's diary of well-being with notes on all contacts with potential etiological factors.
With an unclear diagnosis, they are used with a microscopic analysis of the resulting tissue.
The differential diagnosis of exogenous allergic alveolitis should be carried out with the following diseases:

  • lung carcinomatosis;
  • lung damage with lymphogranulomatosis and leukemia;
  • An alternative to glucocorticosteroids has not yet been developed. Sometimes with exogenous alveolitis, colchicine, D-penicillamine are used, but their effectiveness has not been proven. In some cases, patients are helped by inhaled drugs that dilate the bronchi (fenoterol, formoterol, ipratropium bromide). With the development of severe respiratory failure, oxygen therapy is prescribed if an infection joins -. Heart failure is treated according to generally accepted schemes.

    Prevention

    You can influence the incidence only in production:

    • improve technology, increase the degree of automation;
    • qualitatively conduct preliminary and current medical examinations of workers;
    • to refuse employment in hazardous working conditions for persons with allergic diseases of the upper respiratory tract, pulmonary diseases, malformations of the respiratory organs and the heart.

    Improves the prognosis of the complete cessation of contact with the allergen. In acute and subacute course, exogenous alveolitis ends in recovery, and in chronic, the prognosis is unfavorable.

Allergic alveolitis caused by exogenous environmental factors is much less common than bronchial asthma and is poorly understood, which often leads to misdiagnosis. However, this condition is important to recognize in time, since the simplest therapeutic measures often prevent the development of severe pulmonary fibrosis.

Exogenous alveolitis is an immunologically mediated response of the alveoli and peripheral bronchioles to foreign particles inhaled with air. As a rule, these are particles of avian proteins and bacterial spores, which are small enough to accumulate in the alveoli. However, there are also alveolitis of chemical etiology, which is most often due to occupational hazards (Table 1). In contrast, bronchial asthma is more common, but rarely associated with the patient's profession.

Table 1 Causes of exogenous allergic alveolitis

Disease A source Agent
Bird Lover's Lung Budgerigars, pigeons, etc. Litter, manure, fluff
Farmer's Lung Microparticles of grain, hay, straw Faenia rectivirgula (mainly Micropolyspora faeni)
and Thermoactinomycetes vulgaris
mushroom lung Compost mushroom spores
Lung air conditioned water mist bacterial spores
Bagassose Sugar cane microfiber Thermoactinomycetes sacchari
Malt light barley dust Aspergillus clavatus
Suberosis Tree bark microparticles Penicillum frequentas
  • Occupational sources of the disease

Heat-loving actinomycetes such as Faenia rectivirgula and Thermoactinomycetes vulgaris breed on decaying organic matter at 30-60°C and under appropriate working conditions cause alveolitis. For example, the process of rotting uncured hay and straw can create enough high temperature to support the growth of heat-loving strains; during subsequent work with this material are released large quantities spores that are the cause of the so-called easy farmer.

Farmer's lung is observed mainly in areas with high humidity and farms with low technical support.

Although the most common form of alveolitis, farmer's lung is still relatively rare. The overall incidence of farmers in various areas is 1 per 100-1000 people, although in some cases it can reach the state of 1 per 10 people.

Consequently, a rural general practitioner may encounter allergic alveolitis once every ten years; 1 case of farmer's lung accounts for 17 cases of occupational asthma.

Fungal spores that remain in the compost for a long time can also cause alveolitis.

Alveolitis, caused by contaminated hot water in humidifying systems in factories and public places, is common in the US but not common in Britain, where cold water is commonly used instead of hot. Occupational exposures include sauna workers and drivers (car air conditioners).

Isocyanates used in the manufacture of paints and polyurethane materials are known to cause occupational asthma, but at high concentrations can cause acute alveolitis. The same reaction sometimes develops with metal vapors, such as cobalt, which is used to produce alloys of heavy metals with tungsten carbide.

Table 2 shows the statistics of the incidence of occupational alveolitis in Britain in 1991-1997. and the reasons that caused the disease are indicated. In addition to those indicated in the table, the disease could also be caused by a number of other reasons, which now have more historical than practical value, but remind us that with a change in the production process and a deterioration in everyday life, the disease can take on new forms.

  • Non-professional causes of the disease

Keeping birds at home is one of the most common causes of allergic alveolitis. More than 80,000 pigeon owners are registered in Britain; 12% of the population keeps budgerigars at home. Alveolitis develops in 5% of domestic pigeon lovers and in 1-2% of parrot owners. Approximately one in 1,000 people has "bird-lover's lung". Thus, one or two such patients are under the supervision of a general practitioner, and allergic alveolitis is not well diagnosed everywhere.

The relevant allergen is possibly avian immunoglobulin A, found in droppings and feathers. Pigeons are exposed high levels allergens when cleaning and caring for pigeons; they develop attacks of acute alveolitis.

Table 2 Occupational alveolitis in the UK, 1991-1997

Farming, etc. 54
Communication with birds* 34
Compost recycling 12
Other microbial, excretory, fungal, etc. agents 12
Seafood proteins 2
Isocyanides 3
Metals Co, Ag/Ni 2
Rubber production 3
Chemical agents 6
unknown, others 16
*All cases are reported to the Occupational and Work-Related Disease Surveillance Service. Most cases of the disease occur in amateur owners than in professional workers.

Interaction with budgerigars at home is less intense, but longer, so the disease develops gradually and without acute manifestations.

In poultry farmers, alveolitis, oddly enough, is rare, perhaps because flightless birds have less developed feathers and fluff.

Exogenous alveolitis manifests itself in acute and chronic forms, a clear distinction between which is often not possible, and a mixed picture of the disease is often observed.

Acute alveolitis does not always develop into a chronic disease, even with continued contact with the agent. Chronic alveolitis may develop without prior acute and may progress even after cessation of contact with the agent that caused it.

Acute alveolitis is manifested by a flu-like condition with myalgia, fever, headache, and difficulty in breathing, developing several hours after the temperature rises. The examination reveals tachycardia and wheezing in the lungs during auscultation.

The study of lung function reveals a decrease in the vital capacity of the lungs and a violation of gas exchange; chest x-ray may show a small nodular or more diffuse infiltrate.

Symptoms usually resolve within 48 hours, but lung function changes and radiographic abnormalities may persist for months. Chronic alveolitis may develop after repeated attacks of acute alveolitis or de novo and begins with progressive dyspnea from exertion. Physical data may be scarce or non-existent. Clubbing fingers rarely develop and breath sounds are usually normal.

Lung ventilation is impaired in a restrictive manner, gas exchange changes, and sometimes airway obstruction occurs, which is a consequence of the involvement of bronchioles in the process. Chest x-ray shows fibrous shadows mainly in the upper regions.

Acute alveolitis is often misdiagnosed as recurrent respiratory infections, but careful history taking reveals an association with conditions. environment.

Serum IgG antibodies against the corresponding antigens are found in most cases. The presence of antibodies and symptoms such as fever, leukocytosis, and decreased lung capacity, combined with certain environmental conditions, are sufficient to make a diagnosis.

However, the specialist should always keep in mind that certain limitations are associated with this disease, both professional and related to various kinds of hobbies.

In doubtful cases, further research is carried out. Computed tomography (CT) with high resolution reveals typical features: centrilobular nodules surrounded by irregular shape areas of lung tissue of increased transparency, reflecting the obstruction of small airways. They are best seen in pictures taken at the moment of inhalation. Between acute attacks, CT scan may reveal no changes at all, or detect low-specific signs of pulmonary fibrosis. In the bronchoalveolar lavage, an increased content of CD-8 lymphocytes is found, which makes it possible to exclude infection and sarcoidosis associated with an increase in CD-4 (T-helper) lymphocytes.

Only in rare cases it is necessary to resort to a lung biopsy or provocative tests.

In allergic alveolitis, a differential diagnosis has to be made with many different conditions. Exposure to a high concentration of organic dust can cause a temperature reaction (organic dust toxic syndrome, grain fever), which may be due to direct activation of alveolar macrophages by yeast derivatives.

Adverse acute temperature reactions are caused by exposure to an infected cold water in moisturizing systems ("moisturizing fever"). Like active manifestations of buzzinosis in cotton mill workers, these symptoms do not develop until Monday morning.

Metal vapor fever occurs when exposed to zinc vapor during welding of galvanized metals and other processes; polymer fumes can also cause fever, most commonly seen in solderers whose cigarettes have solder particles sticking to them. Unlike exogenous allergic alveolitis, none of these conditions lead to progressive pulmonary fibrosis.

The diagnosis of chronic alveolitis can be very difficult, and there is often no history of symptoms due to exposure to any specific external agents. Approximately three years after cessation of contact with the agent, antibody levels become undetectable and may disappear altogether. As a rule, some signs of acute alveolitis remain, detected by CT or bronchoalveolar lavage studies.

Prednisolone therapy at a dose of 30–60 mg/day accelerates the resolution of acute alveolitis, but corticosteroids do not affect the outcome of the disease, therefore, they are indicated only for especially severe acute attacks.

Long-term treatment is aimed at reducing the time of exposure to allergens and should be carried out under close supervision. The complete cessation of contact with agents does not mean the absence of the risk of disease progression, but is often associated with loss of work. In fact, for most pigeon farmers and owners, to prevent the disease from progressing, it is enough to reduce the duration of contact with their pets, so categorical advice is not always appropriate.

Practical measures should be taken to reduce the degree of exposure to the allergen, in particular, stop cleaning the cages for pigeons, better dry the hay and wear a mask. It is necessary to continue monitoring lung function, and if there is a suspicion that the disease has begun to progress or repeated attacks of acute alveolitis have developed, the patient should be advised to completely avoid contact with allergens.

Employees who fall ill with exogenous allergic alveolitis are paid an appropriate allowance. Information leaflets on farmer's lung and occupational lung disease are available from the Health and Safety Executive and the British Lung Foundation.

Literature

1. Pickering C. A. C., Newman-Taylor A. J. Extrinic allergic bronchioloalveolitis. Occupational Lung Disorders (3rd edition). Ed Parkes WR. Butterworth Heinemann, Oxfors 1994;667-709.
2. Bourke S. J., Boyd G. Pigeon fancier "s lung. BMJ 1997; 315: 70-71.
3. Hendrick D. J., Faux J. A., Marshall R. Budgerigar fancier's lung: the common variety of allergic alveolitis in Britain. BMJ 1978;2:81-84.
4. Schuyler M. The diagnosis of hypersensitivity pneumonitis. Chest 1997; 111:534-536.
5. Kokkarien J., Tukiainen H. O., Terho E. O. Effect of corticosteroid treatment on the recovery of pulmonary function in farmer's lung. Am Rev Repir Dis 1992;145:3-5.

Note!

  • Alveolitis develops in 5% of pigeon owners and 1-2% of parrot owners. Pigeons are exposed to high levels of allergens; when cleaning and caring for pigeons, they develop attacks of acute alveolitis
  • Although occupational factors can be considered the main etiology of alveolitis, cases of farmers' disease are quite rare - one in 17 cases of occupational bronchial asthma. Basically, the disease of farmers develops in regions with high humidity and poorly equipped farms.
  • Acute alveolitis is manifested by a flu-like condition with myalgia, fever, headache, and difficulty in breathing, developing several hours after the temperature rises. The examination reveals tachycardia and wheezing in the lungs during auscultation. Symptoms usually resolve within 48 hours, but lung function and radiographic abnormalities may persist for months
  • Acute alveolitis is often misdiagnosed as recurrent respiratory infections, but careful history taking reveals occupational association
  • Therapy with prednisolone at a dose of 30–60 mg/day accelerates the resolution of acute alveolitis, but corticosteroids do not affect the outcome of the disease, therefore, they are indicated only for especially severe acute attacks. Long-term treatment is aimed at reducing the time of exposure to allergens and should be carried out under close supervision.

Secrets of the Unexplained Condition

Histological examination revealed mainly lymphocytic inflammation of the lung interstitial tissue and distal bronchioles with the formation of noncaseating sarcoid-type granulomas. The latter tend to disappear three to four months after an attack of acute alveolitis.

A chronic disease is characterized by diffuse collagenous fibrosis of the terminal bronchioles and alveoli with the formation of severe cases"cellular" lung.

Looks like lymphocytes are playing important role and in the immunological response. In the bronchoalveolar lavage, CD-8 suppressors / cytotoxic lymphocytes are found in increased numbers.

However, similar asymptomatic lymphatic alveolitis is found in pigeon owners and farmers and is more likely to be a normal protective reaction of the lungs than a pathological component.

IgG - antibodies against the etiological agent (precipitins) - are found in the serum of almost all patients, but their role is still unclear. The same antibodies are found in a significant number of clinically healthy farmers (20%) and owners of pigeons (40%) and, apparently, are markers of interaction with the allergen rather than the developed disease.

Only a few of the people in contact with the relevant agents develop alveolitis, so it can be assumed that individual sensitivity is important here. However, no association of the disease with the HLA system was found.

Antibodies are less common in smokers than in non-smokers; Thus, smoking appears to inhibit the development of allergic alveolitis, as well as sarcoidosis.