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Eosinophilic pneumonia 

Eosinophilic pneumonia

Eosinophilic pneumonia

D.J. Hendrick

and G.P. Spickett


July 30, 2015: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.


Chapter reviewed August 2013—no substantial updates required; one new reference added.

Updated on 27 Feb 2014. The previous version of this content can be found here.
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date: 29 April 2017

Eosinophilic pneumonia occurs when alveolar spaces are consolidated because of eosinophil inflammation/infiltration, usually with an accompanying eosinophilia of peripheral blood. The diagnosis should be considered when infiltrates on a chest radiograph, often migratory, are associated with blood eosinophilia, and confirmed by demonstrating an excess of eosinophils in bronchoalveolar lavage fluid.

Aetiology—before concluding that the cause is ‘idiopathic’, the following must be considered: (1) parasitic infestation; (2) adverse drug reaction; (3) asthma; (4) allergic bronchopulmonary mycosis; (5) vasculitis; (6) hypereosinophilic syndrome; and (7) other disorders known to be associated with eosinophilic pneumonia.

Acute eosinophilic pneumonia (Löffler’s syndrome)—transitory migratory pulmonary shadows associated with modest peripheral eosinophilia in patients with a mild self-limiting illness. Patients are often atopic. May be an allergic reaction to blood-borne parasites (particularly Ascaris lumbricoides) or drugs.

Chronic eosinophilic pneumonia—pulmonary shadows, typically peripheral, persist for more than 1 month and are often associated with systemic symptoms (particularly fever). May result in diffuse fibrosis or fixed airway obstruction, or both.

Eosinophilic pneumonia with asthma—may be associated with fungal hypersensitivity (commonly Aspergillus fumigatus, i.e allergic bronchopulmonary aspergillosis) or Churg–Strauss syndrome (a vasculitic and granulomatous disorder).

Tropical eosinophilia—due to migrating larvae of filarial worms (Wucheria bancrofti, Brugia malayi). Chronic cases may develop pulmonary fibrosis.

Hypereosinophilic syndrome—when eosinophilic pneumonia (and infiltrative eosinophilic disorders of other organs) is not comfortably classified by any other diagnostic category. Two mechanisms may explain many cases: (1) a genetic deletion creating a protein with tyrosine kinase activity that affects myeloid differentiation (responds to imatinib); (2) a lymphocytic variant where an abnormal clone of T-cells releases ‘eosinophilic’ cytokines.

Causal factors need to be treated, but eosinophilic pneumonia otherwise often responds well to corticosteroid medication.

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