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International School of Medicine
Presented BY:-
Dharmavarapu Swapna Reddy
4th Group
8th Semester
Topic:- Farmer’s Lung Diseases
Definition
 It is a group of lung diseases caused by inhalation of organic antigen
to which the individual has been previously sensitized to. It is often
divided into ‘ acute ‘ and ‘ chronic ‘ forms based on the time course
of presentation.
 Acute form often follows a short period of exposure to a high
concentration of antigen, and is usually reversible.
 Chronic form typically follows a period of chronic exposure to a low
antigen dose and is less reversible.
 These two presentations may overlap and ‘ subacute ‘ form of the
disease is recognized.
Aetiology
 The disease is usually named colourfully after the environment
in which it occurs (e.g. farmer’s lung and bird fancier’s lung )
Some etiologic agents in Hypersensitivity Pneumonitis
Major antigen or
microbe
Source of exposureDisease
MicropolysporafaeniMoldy hayFarmer's lung
Micropolysporafaeni,
Thermoactinomyces vulgaris
Moldy grainGrain handler's lung
ThermoactinomycessacchariMoldy sugar cane fiberBagassosis
TrichosporoncutaneumHouse dust or bird
droppings
Summer type
hypersensitivity
M. faeni, Tvulgaris, occasionally
amoebae are implicated
Contaminated forced-air
system, heated water
reservoir
Humidifier or air-
conditioner lung
CryptostromacorticaleMoldy barkMaple bark stripper's lung
AspergillusclavatusMoldy maltMalt worker's lung
Aureobasidiumpullalans and
Graphium spp.
Moldy redwood dustSequoiosis
SitophilusgranariusWheat weevilWheat weevil disease
PenicilliumcaseiiCheese moldCheese worker's lung
PenicilliumfrequentansMoldy cork dustSuberosis
Avian or animal proteins (in
excreta)
Pigeons, parakeets, fowl,
rodents
Bird breeder's lung
Trimellitic anhydride,
diisocyanate, methylene
diisocyanate
Manufacture of plastics,
polyurethane foam, or
rubber
Chemical workers lung
Pathophysiology
 The pathogenesis is not fully understood, and may involve T-
cell mediated immunity and granuloma formation ( type IV
hypersensitivity ) and/or antibody-antigen immune complex
formation ( type III hypersensitivity ).
 It is not an atopic disease, and is not characterized by a rise
in tissue eosinophils or Ig E ( type I hypersensitivity ); this may
in part be due to the small particle size of offending antigens
which tend to be deposited more distally in the air spaces than
the larger particles associated with asthma.
Clinical picture
• Breathlessness, dry cough, and systemic symptoms ( fever, chills,
arthralgia, myalgia, headache ) occur 4-8 hours after exposure to
antigen.
• Examination : crackles and squeaks on auscultation, fever.
• In the absence of ongoing exposure, symptoms settle spontaneously
within 1-3 days.
• Episodes may be recurrent.
Investigations
 Chest X ray
 Diffuse small (1-3 mm) nodules or infiltrates, sometimes ground
glass change, apical sparing.
 Normal in up to 20% of cases.
 High resolution CT
 Patchy ground glass change and poorly defined nodules.
 Areas of increased lucency ( enhanced in expiratory HRCT ) occur
due to air trapping from bronchiolar involvement.
Investigations
 Pulmonary function tests
• Typically restrictive pattern with reduced gas transfer and lung volumes.
• Mild obstruction is also sometimes observed.
• Hypoxia may occur.
• Inhalation antigen challenge may be unpleasant, and it is not recommended
routinely.
 Blood picture
 Acute form associated with neutrophilia but not eosinophilia.
 Inflammatory markers are often increased.
 Bronchoalveolar lavage
 A lymphocytic alveolitis characterizes the BAL fluid of patients. In fact, a
BAL lymphocytic count of less than 30% makes the diagnosis unlikely, except
in smokers and more chronic forms in which lymphocytosis is less
prominent.
 However, a BAL lymphocytosis is not specific because it may be present in
many other conditions, including sarcoidosis, chronic beryllium disease, and
several autoimmune lung diseases.
Differential diagnosis
•Atypical pneumonia.
•Idiopathic interstitial pneumonia ( particularly
UIP and COP )
•Sarcoidosis.
•Vasculitis.
•Occupational asthma.
•Drug induced lung disease ( including
pesticides).
•Organic Dust Toxic Syndrome ( follow very high
levels of exposure to agricultural dusts,
symptoms transient, benign course ).
Treatment
 The only treatment for allergic diseases is to avoid exposure to the
offending allergen.
 Respiratory protection can be used to minimize the exposure as much as
possible.
 Systemic glucocorticosteroids are usually required to treat severely
symptomatic patients, although there is no formal evidence that such
treatment is associated with long term abatement of symptoms or
radiologic or pulmonary function tests abnormalities.
 The usual treatment is prednisone or prednisolone, 40 to 60 mg a day for
2 weeks, followed by a gradual decrease over 2 to 4 weeks.
Prognosis
 The natural history of the disease is variable and probably depends
on the type and duration of antigen exposure and the host immune
response.
 Acute form generally resolves within several weeks with
corticosteroid therapy and removal from antigen exposure.
 Continued symptoms and progressive lung impairment have been
reported after recurrent acute attacks and even after a single acute
attack. Additionally, progressive persistent airway hyper
responsiveness and emphysema may impact long term recovery.
=:Thank You For your attention:=

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farmer's lung disease

  • 1. International School of Medicine Presented BY:- Dharmavarapu Swapna Reddy 4th Group 8th Semester Topic:- Farmer’s Lung Diseases
  • 2. Definition  It is a group of lung diseases caused by inhalation of organic antigen to which the individual has been previously sensitized to. It is often divided into ‘ acute ‘ and ‘ chronic ‘ forms based on the time course of presentation.  Acute form often follows a short period of exposure to a high concentration of antigen, and is usually reversible.  Chronic form typically follows a period of chronic exposure to a low antigen dose and is less reversible.  These two presentations may overlap and ‘ subacute ‘ form of the disease is recognized.
  • 3. Aetiology  The disease is usually named colourfully after the environment in which it occurs (e.g. farmer’s lung and bird fancier’s lung ) Some etiologic agents in Hypersensitivity Pneumonitis Major antigen or microbe Source of exposureDisease MicropolysporafaeniMoldy hayFarmer's lung Micropolysporafaeni, Thermoactinomyces vulgaris Moldy grainGrain handler's lung ThermoactinomycessacchariMoldy sugar cane fiberBagassosis TrichosporoncutaneumHouse dust or bird droppings Summer type hypersensitivity M. faeni, Tvulgaris, occasionally amoebae are implicated Contaminated forced-air system, heated water reservoir Humidifier or air- conditioner lung CryptostromacorticaleMoldy barkMaple bark stripper's lung AspergillusclavatusMoldy maltMalt worker's lung Aureobasidiumpullalans and Graphium spp. Moldy redwood dustSequoiosis SitophilusgranariusWheat weevilWheat weevil disease PenicilliumcaseiiCheese moldCheese worker's lung PenicilliumfrequentansMoldy cork dustSuberosis Avian or animal proteins (in excreta) Pigeons, parakeets, fowl, rodents Bird breeder's lung Trimellitic anhydride, diisocyanate, methylene diisocyanate Manufacture of plastics, polyurethane foam, or rubber Chemical workers lung
  • 4. Pathophysiology  The pathogenesis is not fully understood, and may involve T- cell mediated immunity and granuloma formation ( type IV hypersensitivity ) and/or antibody-antigen immune complex formation ( type III hypersensitivity ).  It is not an atopic disease, and is not characterized by a rise in tissue eosinophils or Ig E ( type I hypersensitivity ); this may in part be due to the small particle size of offending antigens which tend to be deposited more distally in the air spaces than the larger particles associated with asthma.
  • 5. Clinical picture • Breathlessness, dry cough, and systemic symptoms ( fever, chills, arthralgia, myalgia, headache ) occur 4-8 hours after exposure to antigen. • Examination : crackles and squeaks on auscultation, fever. • In the absence of ongoing exposure, symptoms settle spontaneously within 1-3 days. • Episodes may be recurrent.
  • 6. Investigations  Chest X ray  Diffuse small (1-3 mm) nodules or infiltrates, sometimes ground glass change, apical sparing.  Normal in up to 20% of cases.  High resolution CT  Patchy ground glass change and poorly defined nodules.  Areas of increased lucency ( enhanced in expiratory HRCT ) occur due to air trapping from bronchiolar involvement.
  • 7. Investigations  Pulmonary function tests • Typically restrictive pattern with reduced gas transfer and lung volumes. • Mild obstruction is also sometimes observed. • Hypoxia may occur. • Inhalation antigen challenge may be unpleasant, and it is not recommended routinely.  Blood picture  Acute form associated with neutrophilia but not eosinophilia.  Inflammatory markers are often increased.  Bronchoalveolar lavage  A lymphocytic alveolitis characterizes the BAL fluid of patients. In fact, a BAL lymphocytic count of less than 30% makes the diagnosis unlikely, except in smokers and more chronic forms in which lymphocytosis is less prominent.  However, a BAL lymphocytosis is not specific because it may be present in many other conditions, including sarcoidosis, chronic beryllium disease, and several autoimmune lung diseases.
  • 8. Differential diagnosis •Atypical pneumonia. •Idiopathic interstitial pneumonia ( particularly UIP and COP ) •Sarcoidosis. •Vasculitis. •Occupational asthma. •Drug induced lung disease ( including pesticides). •Organic Dust Toxic Syndrome ( follow very high levels of exposure to agricultural dusts, symptoms transient, benign course ).
  • 9. Treatment  The only treatment for allergic diseases is to avoid exposure to the offending allergen.  Respiratory protection can be used to minimize the exposure as much as possible.  Systemic glucocorticosteroids are usually required to treat severely symptomatic patients, although there is no formal evidence that such treatment is associated with long term abatement of symptoms or radiologic or pulmonary function tests abnormalities.  The usual treatment is prednisone or prednisolone, 40 to 60 mg a day for 2 weeks, followed by a gradual decrease over 2 to 4 weeks.
  • 10. Prognosis  The natural history of the disease is variable and probably depends on the type and duration of antigen exposure and the host immune response.  Acute form generally resolves within several weeks with corticosteroid therapy and removal from antigen exposure.  Continued symptoms and progressive lung impairment have been reported after recurrent acute attacks and even after a single acute attack. Additionally, progressive persistent airway hyper responsiveness and emphysema may impact long term recovery.
  • 11. =:Thank You For your attention:=