Write a short note on eosinophilic lung disease — ABPA, hypersensitivity pneumonitis and tropical pulmonary eosinophilia.

Allergic Bronchopulmonary Aspergillosis (abpa)

Definition: a hypersensitivity reaction to airway colonisation by *Aspergillus fumigatus*, occurring almost exclusively in asthma (1–2% of asthmatics) or cystic fibrosis. India has one of the highest reported burdens in the world, and it is a major under-diagnosed cause of "difficult" asthma.

Pathogenesis: *Aspergillus* colonises bronchial mucus without invading tissue, provoking combined type I (IgE) and type III (immune complex) hypersensitivity → eosinophilic inflammation, mucoid impaction, bronchial wall damage and CENTRAL BRONCHIECTASIS, progressing to fibrosis.

Clinical features:

• poorly controlled asthma despite adequate therapy
• recurrent wheeze, fever and weight loss
• expectoration of thick brown or blackish MUCUS PLUGS — highly characteristic
• haemoptysis
• recurrent "pneumonia" with fleeting infiltrates.

Diagnostic criteria (ISHAM): predisposing condition (asthma or CF) plus both obligatory criteria — positive *Aspergillus*-specific IgE and raised TOTAL SERUM IgE (typically > 1000 IU/mL) — plus at least two of: *Aspergillus* precipitins/IgG, compatible radiographic opacities, and eosinophils > 500/µL.

Radiology: fleeting infiltrates; CENTRAL (proximal) BRONCHIECTASIS with normal distal airways — highly characteristic; mucoid impaction with "FINGER-IN-GLOVE" opacities; HIGH-ATTENUATION MUCUS on CT (pathognomonic).

Management:

• ORAL CORTICOSTEROIDS — the mainstay, tapered over months, to control the immunological response and prevent bronchiectasis
• itraconazole or voriconazole to reduce fungal burden and spare steroids
• optimise asthma therapy
• omalizumab in refractory disease.
• Monitor total serum IgE — a fall of 25–50% indicates response and a rise heralds relapse.

Hypersensitivity Pneumonitis

Definition: immune-mediated inflammation of the lung PARENCHYMA and small airways from repeated inhalation of an organic antigen. Despite being allergic, peripheral eosinophilia is characteristically ABSENT — it is a type III and IV reaction with non-caseating granulomas and a lymphocytic alveolitis.

Clinical forms: ACUTE — 4–8 hours after heavy exposure, with fever, chills, dry cough and dyspnoea, mistaken for pneumonia or influenza, resolving in 24–72 hours if exposure ceases and recurring on re-exposure (the temporal relation to work or hobby is the key). CHRONIC — insidious dyspnoea, cough and weight loss from continuous low-level exposure, progressing to irreversible FIBROSIS.

Investigations:

• HRCT — ground-glass, centrilobular nodules and MOSAIC ATTENUATION with AIR TRAPPING
• chronic disease shows upper and mid-zone fibrosis (a useful contrast with the basal predominance of IPF).
• RESTRICTIVE spirometry with reduced DLCO.
• Serum precipitins indicate exposure, not disease.
• BAL: marked LYMPHOCYTOSIS (often > 50%).

Management:

• ANTIGEN AVOIDANCE IS THE DEFINITIVE TREATMENT — which may mean changing occupation or giving up birds.
• Corticosteroids hasten recovery in acute disease and are used in progressive chronic disease
• immunosuppressants and antifibrotics (nintedanib) for progressive fibrosis.

Tropical Pulmonary Eosinophilia (tpe)

Definition: a hypersensitivity response to microfilariae of *Wuchereria bancrofti* or *Brugia malayi* trapped and destroyed in the lungs — a distinctly Indian and South Asian diagnosis, repeatedly misdiagnosed and treated as asthma or tuberculosis for months or years.

Features: paroxysmal NOCTURNAL cough and wheeze (mirroring microfilarial periodicity), breathlessness, low-grade fever, weight loss.

Diagnostic combination — highly characteristic:

• MARKED EOSINOPHILIA — absolute count > 3000/µL
• VERY HIGH TOTAL IgE (> 1000 IU/mL)
• High antifilarial antibody titres
• ABSENCE of microfilariae in peripheral blood — they are sequestered and destroyed in the lung
• Diffuse bilateral reticulonodular shadowing on chest X-ray
• DRAMATIC RESPONSE TO DIETHYLCARBAMAZINE — both therapeutic and diagnostic

Management: diethylcarbamazine for 3 weeks; relapse in up to 20% may need repeat courses. Untreated, it progresses to interstitial fibrosis.

Other Pulmonary Eosinophilias

• LÖFFLER'S SYNDROME — transient migratory infiltrates with eosinophilia during pulmonary migration of *Ascaris*, hookworm, *Strongyloides*; self-limiting, treated with an anthelmintic
• Drug-induced — nitrofurantoin, sulphonamides, NSAIDs, phenytoin; resolves on withdrawal
• Eosinophilic granulomatosis with polyangiitis (Churg–Strauss) — asthma, eosinophilia and vasculitis; p-ANCA/MPO positive
• Chronic eosinophilic pneumonia — the "photographic negative of pulmonary oedema", responding dramatically to steroids