Hypersensitivity Pneumonitis
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Direct answer
Fever, cough and breathlessness arriving four to eight hours after exposure — pigeon loft, mouldy hay, humidifier or air-conditioning — and resolving by the next day is acute hypersensitivity pneumonitis, a combined type III and IV immunological reaction to inhaled organic antigens in a sensitised host. Recurrent or continuous exposure instead produces chronic disease: insidious dyspnoea, clubbing and fibrotic interstitial lung disease that can become irreversible. HRCT shows centrilobular ground-glass nodules with mosaic attenuation and air trapping — the three-density "headcheese" sign — typically upper-zone predominant; bronchoalveolar lavage yields marked lymphocytosis, and biopsy shows small-airway-centred inflammation with poorly formed non-caseating granulomas. Antigen avoidance is the only disease-modifying treatment; corticosteroids accelerate recovery in severe cases.
What you must remember
- Antigen map: bird fancier's disease (avian serum proteins from droppings and feather dust), farmer's lung (thermophilic actinomycetes such as Saccharopolyspora rectivirgula in mouldy hay), mushroom-worker's and malt-worker's lung, humidifier and air-conditioner lung, hot-tub lung (Mycobacterium avium), and isocyanate chemicals.
- Timing is the diagnosis: symptoms four to eight hours post-exposure, settling within 12-72 hours away from it; fever with inspiratory crackles without wheeze distinguishes it from occupational asthma's immediate bronchospasm.
- Imaging triad: centrilobular ground-glass nodules, mosaic attenuation with expiratory air trapping, three-density headcheese sign; chronic disease adds traction bronchiectasis and fibrosis with relative upper-zone predominance and basal sparing.
- BAL signature: lymphocytosis above roughly 30-40 percent, usually CD8-predominant, dropping the CD4:CD8 ratio — the mirror image of sarcoidosis.
- Histology: bronchiolocentric interstitial infiltrate with poorly formed, loose non-caseating granulomas and giant cells — "small airway on fire".
- Management hierarchy: antigen avoidance is definitive — rehome birds (including feather pillows and duvets), remediate mould, service water systems; respirators for unavoidable exposure; prednisolone taper for severe acute or progressive disease; oxygen and transplant assessment for end-stage fibrosis.
- Serology: precipitating antibodies or specific IgG document exposure, not disease — many exposed individuals carry antibodies without illness.
- Prognosis pivot: outcome tracks exposure recognition and removal; fibrotic chronic disease at diagnosis is the strongest adverse predictor.
An exposure history worth more than a biopsy
A 52-year-old woman has six months of exertional breathlessness with two "pneumonia-like" episodes; HRCT shows mosaic attenuation with centrilobular nodules sparing the bases. Interrogate the environment in order: birds — balcony pigeon feeders, a budgie, feather pillows and quilts; damp — monsoon-stained walls, water-leaked ceilings, room coolers; systems — home and office air-conditioning and humidifiers kept unserviced; occupation — farming, mushroom sheds, grain stores. She keeps pigeons on her balcony and sleeps under a feather quilt. Confirm with avian precipitins or specific IgG and bronchoscopy: BAL lymphocytosis with a low CD4:CD8 ratio fits hypersensitivity pneumonitis; transbronchial biopsy showing loose peribronchiolar granulomas seals it where doubt persists. Then act on the only treatment that works — remove the birds, discard the feather bedding, remediate the damp — and re-evaluate lung function at three and six months, adding prednisolone for residual impairment or progression.
The reasoning to articulate: unlike most interstitial lung disease, this diagnosis is made at the front door of the house rather than in the pathology laboratory — the CT pattern opens the question and the environment closes it.
The Indian context
Indian exposure sources are distinctive and rarely on Western checklists: temple and terrace pigeon populations fed by devotees, feather mattresses and pillows in ordinary households, room coolers and poorly maintained air-conditioners in sealed offices, grain and spice godowns, mushroom cultivation and farm mould during the monsoon. Two practice points earn marks. First, the TB trap: upper-zone fibrotic changes on HRCT in India reflexively attract an empirical antitubercular therapy label — the headcheese sign with mosaic attenuation and exposure history redirects toward hypersensitivity pneumonitis and prevents months of wrongful ATT. Second, access: bronchoscopy and specific IgG panels cluster in metros, so a meticulously documented exposure diary and the physiology (restrictive PFTs with low DLCO) carry the referral. Prevention counselling — enclosing bird-feeding, servicing coolers, discarding old feather bedding — is cheap and, unlike steroids, changes the disease's natural history.
Frequently asked questions
What timing of symptoms suggests acute hypersensitivity pneumonitis?
Onset four to eight hours after exposure with resolution over 12-72 hours away from the antigen — a pattern distinct from the immediate wheeze of occupational asthma.
What is the headcheese sign?
The HRCT coexistence of normal lung, ground-glass and low-density mosaic attenuation in adjacent regions, from mixed infiltrative and obstructive small-airway disease.
What BAL profile supports hypersensitivity pneumonitis?
Marked lymphocytosis, typically above 30-40 percent, CD8-predominant and lowering the CD4:CD8 ratio — opposite to sarcoidosis.
What is the only disease-modifying treatment?
Complete antigen avoidance — removing birds and feather bedding, remediating mould and servicing water systems; steroids only accelerate recovery.
Which exposures dominate Indian practice?
Pigeon keeping and temple feeding, feather bedding, room coolers and air-conditioners, monsoon-damp housing and agricultural mould.