Hypersensitivity pneumonitis

Hypersensitivity pneumonitis: when your lungs react to your environment

By Dr HB Lo, FACRRM 9 min read

Hypersensitivity pneumonitis (HP) is an immune-mediated lung condition triggered by repeated inhalation of organic particles — bird droppings, mould spores, or occupational antigens — in susceptible people.

Non-fibrotic HP causes flu-like episodes within hours of exposure and is often reversible with antigen avoidance. Fibrotic HP leaves permanent scarring; antifibrotic therapy (nintedanib) is PBS-listed for progressive disease. Identifying and removing the antigen source is the single most important intervention.

Hypersensitivity pneumonitis (HP) — also called extrinsic allergic alveolitis — is an immune-mediated interstitial lung disease caused by repeated inhalation of organic antigens in a susceptible person. Unlike occupational asthma, which affects the airways, HP inflames the air sacs and surrounding lung tissue. The result ranges from acute flu-like episodes that resolve when you leave the exposure, all the way to progressive irreversible lung fibrosis. In Australia, bird-keeping is the single most common trigger, but mould in damp buildings, farming exposures, and several workplace antigens all feature in the local caseload.

The condition is under-recognised in general practice because its presentations are varied — a recurrent “flu” that clears on weekends, a mysterious worsening breathlessness over months, or an incidental CT finding that looks like idiopathic pulmonary fibrosis. The key that unlocks the diagnosis is a thorough exposure history taken alongside the investigation results.

A. Core clinical — the AU general-practice framework

What the two types of HP look like

Per the ATS/JRS/ALAT 2020 HP Guideline, HP is now classified into two clinical phenotypes rather than the older acute/subacute/chronic scheme:

Non-fibrotic HP presents with recurrent acute-to-subacute episodes:

  • Fever, chills, headache, myalgia, and malaise beginning 4–12 hours after antigen exposure
  • Dry cough and breathlessness accompanying the systemic symptoms
  • Resolution over hours to days when the person leaves the exposure source
  • A highly characteristic pattern of being worse at home (→ home antigen such as birds or mould) or worse at work (→ occupational antigen), and better during holidays

Fibrotic HP presents insidiously:

  • Progressive breathlessness and dry cough over months to years
  • Weight loss and fatigue in more advanced cases
  • The acute episodic pattern may have been present earlier but is no longer obvious
  • Clinically indistinguishable from idiopathic pulmonary fibrosis without the exposure history

Exposure history — the most important part of assessment

Therapeutic Guidelines respiratory chapters and the TSANZ both emphasise that the exposure history drives the diagnosis. Ask specifically about:

  • Birds at home or work — indoor pets (parrots, cockatoos, budgerigars, finches), racing pigeons, aviaries, neighbouring birds. Also ask about feather-filled pillows, duvets, or cushions, as these can harbour bird antigens for years.
  • Indoor mould — water damage history, leaking pipes, flooding, visible mould, damp basement, old or poorly maintained ducted air conditioning
  • Farming — mouldy hay, silage, or grain (farmer’s lung); mushroom growing; malt house work
  • Industrial exposures — metal-working fluid aerosols (machining), isocyanate spray painting (polyurethane), wood dust, grain handling
  • Hot tubs and spa baths at home or commercial premises
  • Temporal clues — does it improve when the person is on leave? Does it worsen on return?

Examination findings

  • Bibasal end-inspiratory crackles on auscultation (similar to pulmonary fibrosis)
  • Finger clubbing in chronic fibrotic HP (approximately 25% of cases)
  • Occasionally inspiratory squeaks from small-airway involvement
  • The Schwartze sign — a pinkish hue visible through the tympanic membrane over the promontory — is an uncommon but specific finding of active disease

Investigations

Per eTG, a GP-initiated workup includes:

Lung-function tests (spirometry and DLCO) — typically show a restrictive pattern (reduced FVC with preserved FEV₁/FVC) and a reduced gas-transfer factor (DLCO). An obstructive component can coexist.

High-resolution CT chest (HRCT) — the key imaging study:

  • Non-fibrotic HP: diffuse centrilobular ground-glass nodules, mosaic attenuation (the “head-cheese” sign), and air-trapping on expiratory imaging
  • Fibrotic HP: upper- or mid-zone reticular pattern, traction bronchiectasis, and honeycombing — a distribution that distinguishes it from idiopathic pulmonary fibrosis (which is basal-predominant)
  • Inspiratory and expiratory CT is essential to detect air-trapping, which helps differentiate HP from other interstitial lung diseases

Serology for specific IgG antibodies against suspected antigens (avian precipitins, fungal antigens, metal-working fluid antigens) supports the diagnosis but has moderate sensitivity (~60–80%) and specificity; positive results are significant only in clinical context.

Blood tests — FBC, U&E, LFT, CRP, autoimmune screen (ANA, ENA, RF, anti-CCP, ANCA) to exclude connective tissue disease–ILD.

Bronchoalveolar lavage (BAL) via bronchoscopy (specialist) shows a lymphocyte-predominant differential (>20–30%) in most HP cases.

Lung biopsy — transbronchial cryobiopsy or surgical lung biopsy is needed when the diagnosis remains uncertain after HRCT, BAL, serology, and exposure correlation. Non-caseating granulomas in a bronchiolocentric distribution with lymphocytic infiltrate are the hallmark histological findings.

Multidisciplinary ILD team discussion is required for a confident HP diagnosis combining all of these elements.

B. Evidence — non-fibrotic vs fibrotic, and the role of antifibrotic therapy

Non-fibrotic HP

The core treatment evidence for non-fibrotic HP rests on observational and mechanistic data for antigen avoidance as the primary intervention. The ATS/JRS/ALAT 2020 guideline rates antigen avoidance as the single most important recommendation; multiple cohort studies show that strict removal of the antigen source leads to resolution or significant improvement in non-fibrotic disease.

Corticosteroids accelerate symptom resolution in acute and subacute non-fibrotic HP. Prednisolone 0.5 mg/kg/day (maximum 60 mg) tapered over 4–8 weeks is the standard course per eTG. Long-term corticosteroid use is minimised because of adverse effects and because it does not alter the natural history once fibrosis is established.

Immunosuppressants (azathioprine, mycophenolate) are used for steroid-dependent or refractory non-fibrotic HP as steroid-sparing agents. Evidence is largely observational rather than from randomised trials.

Fibrotic HP and the INBUILD trial

The INBUILD trial (Flaherty NEJM 2019) enrolled patients with progressive pulmonary fibrosis other than IPF — a group that included fibrotic HP. Nintedanib slowed the annual rate of FVC decline by approximately 50% compared with placebo across the group. Based on this evidence, nintedanib (Ofev) is PBS-listed in Australia for non-IPF progressive pulmonary fibrosis, which includes fibrotic HP meeting the progressive phenotype criteria. An Authority prescription requires specialist initiation.

Pirfenidone has been studied in non-IPF fibrotic ILD (RELIEF and RECITAL trials) but shows smaller or less consistent benefit and is not PBS-listed beyond IPF.

The paradoxical protective effect of smoking on HP incidence (~50% lower risk in smokers across multiple studies) is well-documented. This observation does not translate into a therapeutic recommendation; smoking cessation remains strongly advised to prevent additional lung damage, malignancy, and cardiovascular disease.

C. Antigen removal and environmental investigation

Identifying the antigen is straightforward when bird-keeping or a mouldy workplace is obvious, but it can require careful detective work when the trigger is diffuse or intermittent.

Birds — the entire household exposure needs addressing, not just rehoming the bird. Bird antigens (proteins from droppings, feathers, and bloom) adsorb onto soft furnishings, carpets, curtains, and ductwork and can persist for months to years. Professional cleaning and replacement of contaminated fabrics is often necessary. Feather-filled bedding should be replaced with synthetic alternatives.

Mould — professional environmental remediation is required when visible mould is extensive or when the source is within wall cavities or building structure. The Lung Foundation Australia provides guidance for patients on environmental assessment for HP. Relocation may be necessary if remediation is incomplete.

Occupational exposures — engineering controls (improved ventilation, containment of aerosols), appropriate respiratory protective equipment, and workplace redesign are coordinated through an occupational health physician. Safe Work Australia outlines the notification and compensation framework: occupational HP is notifiable under WHS legislation if it causes serious injury, and state WorkCover schemes recognise it as a compensable occupational disease.

Verifying removal — symptom improvement, the trend of serology (antigen-specific IgG levels decline over months with successful avoidance), and serial lung-function testing confirm that the exposure has been adequately removed.

D. Australian operations

Expert centres for HP and interstitial lung disease in Australia include the ILD multidisciplinary clinics at the Royal Melbourne Hospital, The Alfred Melbourne, Royal Prince Alfred Sydney, Royal North Shore Sydney, Royal Brisbane and Women’s Hospital, Sir Charles Gairdner Perth, and Royal Adelaide Hospital.

MBS items relevant to HP workup and management include:

  • GP consultation: MBS items 23, 36, and 44
  • Spirometry and DLCO: items 11500 and 11506 (specialist)
  • HRCT chest: item 56307
  • Bronchoalveolar lavage and bronchoscopy: specialist-billed items
  • Six-minute walk test: item 12203
  • Chronic condition management plan (GPCCMP): items 965 and 967 from 1 July 2025

PBS antifibrotic therapy — nintedanib (Ofev) is a Section 100 Highly Specialised Drug for non-IPF progressive pulmonary fibrosis. An Authority prescription requires specialist initiation and confirmation of progressive phenotype. It is not initiated in general practice but ongoing management is shared.

Pulmonary rehabilitation is funded through various state health networks and can be arranged via the Lung Foundation Australia referral directory. It improves exercise capacity and quality of life even in fibrotic HP.

Vaccinations — annual influenza, pneumococcal (PPV23 + PCV15/PCV20), COVID-19 boosters, and RSV vaccine (where eligible) reduce the risk of respiratory infections that can trigger acute exacerbations.

E. Special populations

Farmers and rural workers — farmer’s lung from mouldy hay and silage is a distinct HP subtype with high exposure intensity and often acute presentations during the hay season. Engineered drying systems, respiratory protection, and alternative silage management reduce re-exposure risk. WorkCover schemes across all states recognise farmer’s lung.

Industrial and office workers — metal-working fluid HP and humidifier lung can affect multiple workers in a shared environment; a cluster of similar presentations in coworkers raises the diagnostic likelihood considerably. Occupational health investigation of the workplace, rather than individual management alone, is appropriate.

Pregnant individuals — immunosuppressive therapy (corticosteroids, azathioprine) is used with caution in pregnancy; decisions should involve both the respiratory specialist and the obstetric team. Antifibrotic therapy is contraindicated in pregnancy.

Older adults — distinguishing fibrotic HP from idiopathic pulmonary fibrosis becomes more difficult with age as the episodic history may not be elicited and antigen exposure may have been remote. A thorough exposure history at every age remains essential.

Aboriginal and Torres Strait Islander peoples — the HP exposure profile in remote and regional Australia (camp dust, wood smoke, specific occupational settings) is less well characterised. Access to specialist ILD services may be limited; telehealth consultation with metropolitan ILD centres should be considered early.

When to escalate

Refer to a respiratory specialist or ILD multidisciplinary team when:

  • The diagnosis of HP is clinically suspected (exposure history + compatible symptoms + CT findings)
  • Lung-function tests show a restrictive pattern or reduced DLCO
  • Antigen removal has not produced improvement within 4–8 weeks
  • Fibrotic HP is identified on CT — antifibrotic therapy consideration requires specialist initiation
  • Pulmonary rehabilitation referral is required
  • Occupational HP is identified — occupational health physician involvement and WorkCover notification
  • Advanced disease with resting hypoxia — long-term oxygen therapy requires specialist assessment
  • Suspected acute exacerbation of HP — fever, rapidly worsening breathlessness, new radiological infiltrates despite apparent antigen avoidance

Lung transplantation assessment is appropriate for selected patients with progressive fibrotic HP not responding to antifibrotic therapy. Specialist ILD centres manage this pathway.

What this article is and is not

This is general health information drawn from current Australian respiratory guidelines — Therapeutic Guidelines, the Thoracic Society of Australia and New Zealand, Lung Foundation Australia, and Safe Work Australia — as well as the ATS/JRS/ALAT 2020 HP Guideline and the INBUILD trial. It does not constitute personal medical advice and does not create a doctor–patient relationship.

Hypersensitivity pneumonitis requires a specialist diagnosis involving imaging, lung-lavage, and expert multidisciplinary review. The information here is designed to help patients understand their condition, ask informed questions of their GP and treating teams, and engage with the antigen avoidance process — but specific treatment decisions are made with your GP and specialist.

For Australian consumer-friendly information: Lung Foundation Australia, HealthDirect, Better Health Channel, and Safe Work Australia.

Sources cited

  1. Therapeutic Guidelines — Respiratory (eTG complete)
  2. TSANZ — Thoracic Society of Australia and New Zealand
  3. Lung Foundation Australia — Pulmonary Fibrosis
  4. Safe Work Australia — Occupational Lung Disease
  5. HealthDirect
  6. Better Health Channel
  7. Raghu G et al. ATS/JRS/ALAT 2020 HP Guideline. Am J Respir Crit Care Med 2020;202:e36–e69
  8. Flaherty KR et al. INBUILD Trial. NEJM 2019;381:1718–1727

Frequently asked questions

  • What are the most common causes of HP in Australia?

    Bird-related HP is the most common cause in Australia — reactions to proteins in the droppings, feathers, and bloom of pet birds such as parrots, budgerigars, and cockatoos. Feather-filled pillows and quilts can also trigger it. Other common causes include mould in water-damaged homes or workplaces, mouldy hay or silage in farming (farmer's lung), metal-working fluid aerosols in machining, and hot-tub water. Symptoms typically worsen at the exposure site and improve when you are away from it — that pattern is a key diagnostic clue.

  • How is HP different from asthma?

    Both cause breathlessness in response to inhaled substances, but they are distinct conditions. Asthma involves airway narrowing that is typically reversible and responds well to inhalers. HP involves inflammation deep in the lung tissue itself, and it often produces flu-like symptoms — fever, chills, and muscle aches — within hours of exposure, which are not features of asthma. Lung-function tests in HP usually show a restrictive pattern rather than the reversible obstruction of asthma. A specialist assessment, including high-resolution CT and lung-lavage testing, separates them reliably.

  • Will removing the bird or fixing the mould really help my lungs?

    Yes — antigen avoidance is the most important treatment and the one most likely to lead to recovery. In non-fibrotic HP, removing the source frequently allows the lung inflammation to settle. Bird antigens can persist in carpets, soft furnishings, and ductwork for months after the bird is rehomed, so professional environmental cleaning is usually needed. In fibrotic HP, avoidance may slow further progression but cannot reverse established scarring. An occupational hygienist can help confirm that the source has been adequately dealt with, particularly in workplace-related cases.

  • What is nintedanib and who needs it?

    Nintedanib (Ofev) is an antifibrotic medicine that slows the buildup of scar tissue in the lungs. It is PBS-listed in Australia for people with progressive fibrotic HP — where lung function continues to decline despite antigen avoidance. The evidence comes from the INBUILD trial, which showed it slowed the rate of lung-function decline by roughly half in progressive pulmonary fibrosis beyond IPF. It does not reverse existing fibrosis. Side effects include diarrhoea and liver-function changes. Prescribing is managed by a specialist respiratory or ILD multidisciplinary team rather than through general practice.

  • When should I ask my GP for a referral?

    Any unexplained breathlessness or cough with a relevant exposure history warrants GP assessment. Specific triggers for timely specialist referral include a consistently worsening cough or breathlessness over weeks to months, unexpected weight loss, finger-clubbing, a restrictive pattern on lung-function tests, or a CT chest showing fibrosis. In Australia, diagnosis of HP requires an ILD multidisciplinary team combining CT findings, bronchoalveolar lavage results, and blood tests for antigen-specific antibodies with the full exposure history. Your GP initiates the investigation pathway; the ILD team confirms the diagnosis.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.