eMedicine Specialties > Pulmonology > Interstitial Lung Diseases

Hypersensitivity Pneumonitis

Author: Marine Demirjian, MD, Resident Physician, Department of Internal Medicine, Ronald Reagan University of California in Los Angeles Medical Center
Coauthor(s): Nader Kamangar, MD, FACP, FCCP, FAASM,, Associate Professor of Clinical Medicine, Director of Hospitalist/Intensivist Program, Division of Pulmonary, Critical Care and Sleep Medicine, David Geffen School of Medicine at University of California Los Angeles; Associate Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA/West Los Angeles Veterans Affairs Medical Center; Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Contributor Information and Disclosures

Updated: Jul 24, 2009

Introduction

Background

Hypersensitivity pneumonitis (HP), also called extrinsic allergic alveolitis, is a complex syndrome of varying intensity, clinical presentation, and natural history, rather than a single uniform disease.

First described in Iceland in 1874 and termed heykatarr, hypersensitivity pneumonitis is caused by sensitization to repeated inhalation of dusts containing organic antigens. These dusts can be derived from a variety of sources, such as dairy and grain products, animal dander and protein, wood bark, and water reservoir vaporizers. The most common antigens are thermophilic Actinomycetes species and avian proteins; the most common diseases are farmer's lung and bird fancier's lung.

Hypersensitivity pneumonitis is characterized by diffuse inflammation of lung parenchyma and airways in previously sensitized patients. Based on the length and intensity of exposure and subsequent duration of illness, clinical presentations of hypersensitivity pneumonitis are categorized as acute, subacute (intermittent), and chronic progressive.

Pathophysiology

Pathologically, acute hypersensitivity pneumonitis is characterized by poorly formed noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution with prominent giant cells.

The subacute, or intermittent, form produces more well-formed noncaseating granulomas, bronchiolitis with or without organizing pneumonia, and interstitial fibrosis.

Chronic forms reveal additional findings of chronic interstitial inflammation and alveolar destruction (honeycombing). Cholesterol clefts or asteroid bodies are present within or outside granulomas. Additionally, centrilobular fibrosis and bridging fibrosis are important hallmarks of chronic hypersensitivity pneumonitis.1

The pathologic features of chronic hypersensitivity pneumonitis, often associated with a poor prognosis, have the following 3 patterns of fibrosis.

  • Predominantly peripheral fibrosis in a patchy pattern with architectural distortion and fibroblast foci similar to usual interstitial pneumonia (UIP)
  • Homogeneous linear fibrosis similar to fibrotic nonspecific interstitial pneumonia (NSIP)
  • Irregular predominantly peribronchiolar fibrosis

Thus, chronic hypersensitivity pneumonitis may mimic usual interstitial pneumonia or fibrotic nonspecific interstitial pneumonia. To diagnose chronic hypersensitivity pneumonitis in a case with features resembling usual interstitial pneumonia, identifying areas of cellular interstitial pneumonia with giant cells or granulomas situated around bronchioles may lead to the correct diagnosis.2 The finding of peribronchiolar fibrosis also may be helpful.3

Pathogenesis

Most patients have circulating immunoglobulin G antibodies that are specific for the offending antigen. The antibody (called precipitating antibody) reacts with a specific antigen to form a precipitation. However, approximately 50% of asymptomatic persons exposed to the sensitizing antigen also have these antibodies.

Although initially thought to be an immunocomplex-mediated process, subsequent studies showed that cell-mediated immunity is more important.4

Early response to the antigen is characterized by an increase in neutrophils in the alveoli and small airways followed by an influx of mononuclear cells. These cells release proteolytic enzymes, prostaglandins, and leukotrienes. The production and release of interleukins, cytokines, growth factors, and various other mediators from T lymphocytes and macrophages play important roles in hypersensitivity pneumonitis pathogenesis.

Frequency

United States

Resistance or susceptibility to infection following exposure varies. Incidence also varies considerably. Studies document 8-540 cases per 100,000 persons per year for farmers and 6,000-21,000 cases per 100,000 persons per year for pigeon breeders. High attack rates are documented in sporadic outbreaks. Approximately 52% of office workers exposed to an infected humidifier were infected, and 27% of workers at a molding plant for polyurethane foam parts were infected.

Prevalence varies by region, climate, and farming practices. Hypersensitivity pneumonitis affects 0.4-7% of the farming population. Reported prevalence among bird fanciers is estimated to be 20-20,000 cases per 100,000 persons at risk.

International

The prevalence of farmer's lung in the United Kingdom is reported to be 420-3,000 cases per 100,000 persons at risk, in France is 4,370 cases per 100,000 persons at risk,5,6 and in Finland is 1,400-1,700 cases per 100,000 persons at risk.7

One epidemiologic study revealed that the estimated incidence of interstitial lung disease was 7.6 cases per 100,000 persons per year. Of all interstitial lung diseases, the most common was idiopathic pulmonary fibrosis (38.6%), followed by sarcoidosis (14.9%), cryptogenic organizing pneumonia (10.4%), interstitial lung disease associated with collagen-vascular diseases (9.9%), hypersensitivity pneumonitis (6.6%), and unclassified in 5.1% of cases.8

Mortality/Morbidity

  • Most patients recover completely after the inciting exposure ceases.
  • Bird fancier's disease has a worse prognosis than farmer's lung.
  • The outcomes of other varieties of hypersensitivity pneumonitis are more variable.

Sex

One epidemiological study revealed a male to female ratio of 1.2:1.

Age

Hypersensitivity pneumonitis is usually seen in the fourth to sixth decade of life. One study looking at 85 consecutive patients with hypersensitivity pneumonitis found a mean age of 53 +14 years.9

Clinical

History

The clinical presentation of hypersensitivity pneumonitis is categorized as acute, subacute, or chronic, according to duration of illness.

  • Acute hypersensitivity pneumonitis
    • The acute form may develop 4-6 hours following heavy exposure to an inciting agent. Symptoms often resolve spontaneously within 12 hours to several days upon cessation of exposure.
    • Patients abruptly develop fever, chills, malaise, cough, chest tightness, dyspnea, headache, and malaise.
  • Subacute (intermittent) hypersensitivity pneumonitis
    • Patients may gradually develop a productive cough, dyspnea, fatigue, anorexia, and weight loss.
    • Findings may be present in patients who experience repeated acute attacks.
  • Chronic hypersensitivity pneumonitis
    • Patients often lack a history of acute episodes.
    • They have an insidious onset of cough, progressive dyspnea, fatigue, and weight loss.
    • Removing exposure results in only partial improvement.

Physical

Physical examination findings of hypersensitivity pneumonitis vary according to clinical presentation.

  • Patients with acute hypersensitivity pneumonitis present with fever, tachypnea, and diffuse fine bibasilar crackles upon auscultation.
  • Patients with subacute hypersensitivity pneumonitis present similarly to patients with acute disease, but symptoms are less severe and last longer.
  • Patients with chronic hypersensitivity pneumonitis present with muscle wasting and weight loss. Clubbing is observed in 50% of patients. Tachypnea, respiratory distress, and inspiratory crackles over lower lung fields often are present.

Causes

More than 300 etiologies of hypersensitivity pneumonitis have been reported from a wide range of exposures involving airborne antigens.

Selected Etiological Agents for Hypersensitivity Pneumonitis

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Table
DiseaseSource of ExposureMajor Antigen

Farmer's lung

Moldy haySaccharopolyspora rectivirgula
(Micropolyspora faeni)
BagassosisMoldy sugar cane fiberThermoactinomyces sacchari
Grain handler's lungMoldy grainS rectivirgula, Thermoactinomyces vulgaris
Humidifier/air-conditioner lungContaminated forced-air systems, heated water reservoirsS rectivirgula, T vulgaris
Bird breeder's lungPigeons, parakeets, fowl, rodentsAvian or animal proteins

Cheese worker's lung

Cheese moldPenicillium casei

Malt worker's lung

Moldy maltAspergillus clavatus
Paprika splitter's lungPaprika dustMucor stolonifer
Wheat weevilInfested wheatSitophilus granarius
Mollusk shell hypersensitivityShell dustSea snail shells
Chemical worker's lungManufacture of plastics, polyurethane foam, rubberTrimellitic anhydride, diisocyanate, methylene diisocyanate
DiseaseSource of ExposureMajor Antigen

Farmer's lung

Moldy haySaccharopolyspora rectivirgula
(Micropolyspora faeni)
BagassosisMoldy sugar cane fiberThermoactinomyces sacchari
Grain handler's lungMoldy grainS rectivirgula, Thermoactinomyces vulgaris
Humidifier/air-conditioner lungContaminated forced-air systems, heated water reservoirsS rectivirgula, T vulgaris
Bird breeder's lungPigeons, parakeets, fowl, rodentsAvian or animal proteins

Cheese worker's lung

Cheese moldPenicillium casei

Malt worker's lung

Moldy maltAspergillus clavatus
Paprika splitter's lungPaprika dustMucor stolonifer
Wheat weevilInfested wheatSitophilus granarius
Mollusk shell hypersensitivityShell dustSea snail shells
Chemical worker's lungManufacture of plastics, polyurethane foam, rubberTrimellitic anhydride, diisocyanate, methylene diisocyanate

Reported occupations and major causative antigens are as follows:

  • Farmers and cattle workers develop the most common form of hypersensitivity pneumonitis.
    • The major causative antigen is thermophilic Actinomycetes species.
    • Farmer's lung must be distinguished from febrile toxic reactions to inhaled mold dusts (organic dust toxic syndrome). This nonimmunologic reaction occurs 30-50 times more commonly than hypersensitivity pneumonitis.
  • Ventilation workers and those exposed to water-related contamination may be exposed to microorganism-colonized forced-air systems, humidifiers, whirlpools, hot tubs, and spas.10,11,12 Antigens are various species of Thermoactinomyces, Cladosporium, or Mycobacterium avium complex (MAC).
  • Poultry and other bird handlers are commonly exposed to droppings, feathers, and serum proteins of pigeons, other birds, and fowl.
  • Veterinarians and animal handlers have significant contact with animals and organic antigens.
  • Grain and flour processors and loaders are exposed to grain that may become colonized with a variety of microorganisms that are easily aerosolized. Exposure may lead to hypersensitivity pneumonitis.
  • Lumber mill workers and paper and wallboard manufacturers are exposed to wood products colonized with molds.13,14
  • Plastic manufacturers, painters, and electronics industry workers may be exposed to inciting agents that are synthetic in origin, possibly including diphenylmethane diisocyanate or toluene diisocyanate.
  • Metalworking fluid handlers, including those involved in the shaping of metal parts, are at risk of developing hypersensitivity pneumonitis from microbial contamination of metalworking fluids, frequently with Mycobacterium immunogenum.15
  • Textile workers may have exposures that lead to lung injury characterized by diffuse alveolar damage or airway dysfunction (eg, byssinosis, nylon worker's lung). This is not a true form of hypersensitivity pneumonitis.
  • Conditions that mimic hypersensitivity pneumonitis that occur from inhalation of organic agents but are not true forms of hypersensitivity pneumonitis are as follows:  
    • Patients with inhalation fever present with fever, chills, headaches, and myalgias without pulmonary findings (although mild dyspnea may occur). Onset is 4-8 hours following exposure, but no long-term sequelae occur.
    • Organic dust toxic syndrome results from exposure to bioaerosols contaminated with toxin-producing fungi (mycotoxins). Fever, chills, and myalgias occur 4-6 hours after exposure, and chest radiographs may show diffuse opacities. Bronchiolitis or diffuse alveolar damage may be present on lung biopsy specimens. These are not true forms of hypersensitivity pneumonitis because no prior sensitization is required.
    • Chronic bronchitis can result from chronic obstructive pulmonary disease, which is the most common respiratory syndrome among agricultural workers. The prevalence of chronic bronchitis is 10%, compared with 1.4% for hypersensitivity pneumonitis. Smoking and atopy have additive effects.16,17 An association may exist between chronic bronchitis and hypersensitivity pneumonitis.
    • A case-control study investigated the agricultural practices and the microbiological composition of hay handled in patients with farmer's lung disease. The location, type of farm, and working conditions were similar to those of the control farms. However, the microbiological composition of hay differed. Significantly higher amounts of Eurotium amstelodami, Absidia corymbifera, mesophilic Streptomyces, thermophilic Streptomyces, and Saccharomonospora viridis were present in the hay. Farmer's lung resulted from handling hay with high amounts of these 5 microorganisms.18
    • Hypersensitivity pneumonitis–like syndrome in patients exposed to aerosolized MAC has been described. Hot-tub lung is a term used to describe these hypersensitivity pneumonitis–like cases because they have generally been associated with hot tub use (linked to the high levels of infectious aerosols containing organisms found in the water).19,20,21,22,23,24 Whether this pulmonary response to MAC represents true infection or classic hypersensitivity pneumonitis remains controversial.25

More on Hypersensitivity Pneumonitis

Overview: Hypersensitivity Pneumonitis
Differential Diagnoses & Workup: Hypersensitivity Pneumonitis
Treatment & Medication: Hypersensitivity Pneumonitis
Follow-up: Hypersensitivity Pneumonitis
Multimedia: Hypersensitivity Pneumonitis
References
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Further Reading

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Keywords

hypersensitivity pneumonitis, HP, bird fancier's lung, extrinsic allergic alveolitis, farmer's lung, Saccharopolyspora rectivirgula, S rectivirgula, Micropolyspora faeni, M faeni, Thermoactinomyces sacchari, T sacchari, Thermoactinomyces vulgaris, T vulgaris, Penicillium casei, P casei, Aspergillus clavatus, A clavatus, Mucor stolonifer, M stolonifer, Sitophilus granarius, S granarius, Cladosporium, heykatarr, bagassosis, grain handler's lung, humidifier lung, air-conditioner lung, bird breeder's lung, cheese worker's lung, malt worker's lung, paprika splitter's lung, mollusk shell hypersensitivity, chemical worker's lung, pulmonary disease, lung disease

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Contributor Information and Disclosures

Author

Marine Demirjian, MD, Resident Physician, Department of Internal Medicine, Ronald Reagan University of California in Los Angeles Medical Center
Marine Demirjian, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Medical Women's Association, and California Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Nader Kamangar, MD, FACP, FCCP, FAASM,, Associate Professor of Clinical Medicine, Director of Hospitalist/Intensivist Program, Division of Pulmonary, Critical Care and Sleep Medicine, David Geffen School of Medicine at University of California Los Angeles; Associate Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA/West Los Angeles Veterans Affairs Medical Center
Nader Kamangar, MD, FACP, FCCP, FAASM, is a member of the following medical societies: American Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Michael Peterson, MD, Chief of Medicine, Vice-Chair of Medicine, University of California at San Francisco; Endowed Professor of Medicine, University of California at San Francisco-Fresno
Michael Peterson, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Daniel R Ouellette, MD, FCCP, Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Pulmonary Disease and Critical Care Medicine Service, Henry Ford Health System
Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society
Disclosure: Boehringer Ingleheim Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

 
 
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