Background: Tropical pulmonary eosinophilia (TPE) is a rare, immunologically mediated hypersensitivity reaction to microfilarial antigens, primarily caused by Wuchereria bancrofti and Brugia species. It manifests with nocturnal cough, dyspnea, wheezing, and marked peripheral eosinophilia, and may progress to fibrosis without early treatment.

Aim: This review aims to summarize current knowledge on the clinical characteristics, diagnosis, pathophysiology, and management of TPE, highlighting its relevance in both endemic and non‑endemic regions.

Methods: The article synthesizes historical descriptions, epidemiological data, immunopathological insights, diagnostic criteria, and therapeutic strategies for TPE, drawing from contemporary literature and clinical experience.

Results: TPE results from an exaggerated type I hypersensitivity response to microfilariae trapped in the pulmonary vasculature, triggering intense eosinophilic inflammation and elevated IgE. Although endemic to tropical regions, increased global travel has expanded its geographic distribution. Diagnosis relies on characteristic symptoms, eosinophilia often >3,000/µL, elevated IgE, radiologic infiltrates, positive antifilarial antibodies, and marked clinical response to diethylcarbamazine (DEC). DEC at 6 mg/kg/day for 21 days remains the treatment of choice, producing rapid clinical improvement, though relapse occurs in up to 20% of patients. Adjunct corticosteroids may be required for persistent inflammation. Untreated disease risks progression to chronic fibrosis and pulmonary hypertension.

Conclusion: Early diagnosis and prompt DEC therapy result in excellent outcomes for most patients. Failure to treat can lead to irreversible structural lung changes, highlighting the need for clinical vigilance—especially in non‑endemic regions where cases may be missed.