Tropical pulmonary eosinophilia (TPE, tropical eosinophilia, or Weingarten's syndrome), is characterized by cough, bronchospasm, wheezing, abdominal pain, and an enlarged spleen. Occurring most frequently in the Indian subcontinent and Southeast Asia, TPE is a clinical manifestation of lymphatic filariasis, a parasitic infection caused by filarial roundworms that inhabit the lymphatic vessels, lymph nodes, spleen, and bloodstream. Three species of filarial roundworms, all from the Onchocercidae family, cause human lymphatic filariasis: Wuchereria bancrofti, Brugia malayi, and Brugia timori.[1]
Tropical pulmonary eosinophilia is a rare syndrome characterised by pulmonary interstitial infiltrates and marked peripheral eosinophilia.[2] This condition is more widely recognised and promptly diagnosed in filariasis-endemic regions, such as the Indian subcontinent, Africa, Asia and South America. In nonendemic countries, patients are commonly thought to have bronchial asthma.[3][4] Chronic symptoms may delay the diagnosis by up to five years.[3] Early recognition and treatment with the antifilarial drug, diethylcarbamazine, is important, as delay before treatment may lead to progressive interstitial fibrosis and irreversible impairment.[5]
The condition of marked eosinophilia with pulmonary involvement was first termed tropical pulmonary eosinophilia in 1950.[6] The syndrome is caused by a distinct hypersensitive immunological reaction to microfilariae of W. bancrofti and Brugia malayi.[5][7] However, only a small percentage (< 0.5%)[8] of the 130 million people globally who are infected with filariasis apparently develop this reaction. The clearance of rapidly opsonised microfilariae from the bloodstream results in a hypersensitive immunological process and abnormal recruitment of eosinophils, as reflected by extremely high IgE levels of over 1000 kU/L.[5][9] The typical patient is a young adult man from the Indian subcontinent.[7]