Tropical Pulmonary Eosinophilia

While I was spending time in the TB clinic at the CHAD clinic, I kept hearing about a disease that I had never encountered before in the U.S. Many patients would come into the clinic for sputum sample collections for presumed TB, but one of the residents kept ordering CBCs to work up for a disease entity called "TPE." TPE, as it turns out, stands for Tropical Pulmonary Eosinophilia. He told me that TPE is very common in Vellore and other parts of Asia and this is something they often check for when a patient comes to TB clinic with because the disease is endemic to south India and so prevalent there.

TPE is the result of an immune hypersensitivity reaction to human filarial parasites, Wuchereria bancrofti and Brugia malayi, is characterized by cough, dyspnea and nocturnal wheezing, diffuse reticulonodular infiltrates in chest radiographs, and marked peripheral blood eosinophilia. The criteria used for the diagnosis of TPE are: (1) appropriate exposure history (mosquito bite) in an endemic area of filariasis, (2) a history of paroxysmal nocturnal cough and breathlessness, (3) chest radiographic evidence of pulmonary infiltrations, (4) leucocytosis in blood, (5) peripheral blood eosinophils more than 3000 cells/mm3, (6) elevated serum IgE levels, (7) elevated serum antifilarial antibodies (IgG and/or IgE), and (8) a clinical response to diethylcarbamazine.
TPE) usually affects people living in the tropics, especially those in Southeast Asia, India, and certain parts of China and Africa. However, due to increasing global travel and the migration, this disease is increasinglyseen in the West, where the diagnosis can be easily missed since it is rarely encountered and can mimic many other conditions. Most typically, TPE can mimic acuteor refractory bronchial asthma

Leucocytosis with an absolute increase in eosinophils in the peripheral blood is the hallmark of TPE. Lung function tests reveal mainly a restrictive ventilation defect with superimposed airway obstruction.

Typically, microfilariae circulate in the blood of patients with lymphatic filariasis without significant clinical consequences. In the case of TPE, however, these microfilariae appear to be trapped in the lung on their first pass through the circulation, where they are presumed to initiate an inflammatory response.

In contrast to the majority of people with lymphatic filariasis, who have a downregulated response to the parasites, patients with TPE mount a robust systemic and localized immune response that includes elevations of both polyclonal and filaria-specific IgE and IgG. The very high levels of eosinophils found in the peripheral blood of TPE patients (>3,000/µl) are surpassed in the lungs: levels have been determined to be 12-fold more concentrated in the epithelial lining fluid of the lungs than in the systemic circulation.

A mild form of interstitial lung disease persists in the majority of patients treated for TPE. For the untreated TPE patient, the outcome is more extreme and could lead to a progressive interstitial fibrosis.