Tropical pulmonary eosinophilia (TPE) is a clinical manifestation of lymphatic filariasis caused by filarial nematodes transmitted by mosquitoes. It results from an immune response to microfilariae trapped in the lungs. Patients present with nocturnal cough, fever, weight loss and marked eosinophilia. Chest imaging may show reticulonodular opacities. Treatment involves diethylcarbamazine to kill the filarial worms along with bronchodilators and corticosteroids for symptoms. TPE must be differentiated from other causes of eosinophilia such as chronic eosinophilic pneumonia.

1. Tropical Pulmonary Eosinophilia
DR. MD. SHAFIQUL ISLAM DEWAN
RESIDENT (PULMONOLOGY)
DHAKA MEDICAL COLLEGE HOSPITAL
4/27/2023 1

2. Tropical pulmonary eosinophilia (TPE)
Tropical pulmonary eosinophilia (TPE) is a clinical manifestation of lymphatic filariasis, a
parasitic infection caused by filarial nematodes (roundworms) that inhabit the lymphatics and
bloodstream.
Three species cause human lymphatic filariasis: Wuchereria bancrofti, Brugia malayi, and
Brugia timori.
Infection is transmitted by mosquito vectors; humans are definitive hosts.
TPE is caused by an immune hyper-responsiveness to microfilariae that become trapped in the
lungs
4/27/2023 DR. MD. SHAFIQUL ISLAM DEWAN, RESIDENT (PULMONOLOGY), DMCH 2

3. Filariae
Filariae have five morphologic stages.
Humans are infected with third-stage larvae transmitted by mosquitoes.
Infective larvae molt twice and develop into adults that survive in a
human host for up to 20 years.
The first-stage larvae, or microfilariae, are released into the circulation
by female adult worms.
4/27/2023 DR. MD. SHAFIQUL ISLAM DEWAN, RESIDENT (PULMONOLOGY), DMCH 3

4. Epidemiology
TPE can occur in any tropical area where filariasis occurs and is most common among
young adults.
It is more common in individuals from the indian subcontinent and occurs four to
seven times more frequently in males than in females.
Rare cases have been described in children.
The majority of cases of TPE occur in endemic areas; cases in nonendemic settings
have also been described.
4/27/2023 DR. MD. SHAFIQUL ISLAM DEWAN, RESIDENT (PULMONOLOGY), DMCH 4

5. Pathogenesis
Pulmonary disease reflects a robust immunologic response against blood borne microfilariae
that become trapped within the lung and reticuloendothelial organs.
TPE develops in less than 0.5 percent of patients with lymphatic filariasis;
The earliest histopathologic finding is histiocytic infiltration.
Approximately one month following infection, an eosinophilic interstitial infiltrate develops.
In more severe cases, eosinophilic abscesses, eosinophilic bronchopneumonia, or eosinophilic
granulomas may be observed.
With chronic disease, there is an ongoing eosinophil interstitial infiltration and increasing
pulmonary fibrosis.
Occasionally, microfilarial fragments may be identifiable in biopsied lung or reticuloendothelial
tissues.
4/27/2023 DR. MD. SHAFIQUL ISLAM DEWAN, RESIDENT (PULMONOLOGY), DMCH 5

6. Clinical Features
Clinical manifestations is usually gradual.
TPE is seen predominantly (80%) in men, usually in middle age.
Nocturnal paroxysmal cough and bronchospasm
Low-grade fever
Weight loss
Lymphadenopathy
Some patients also have hepatosplenomegaly.
4/27/2023 DR. MD. SHAFIQUL ISLAM DEWAN, RESIDENT (PULMONOLOGY), DMCH 6

7. Physical Examination
Chest findings are minimal or absent in most patients.
In some cases, rhonchi, crepitations(especially over the midzones and
bases).
Lymphadenopathy, hepatomegaly, and/or splenomegaly are observed in
approximately 15percent of patients.
Cor pulmonale is a rare complication.
4/27/2023 DR. MD. SHAFIQUL ISLAM DEWAN, RESIDENT (PULMONOLOGY), DMCH 7

8. Investigation
Complete blood count (Leukocytosis, marked eosinophilia,usually above
3000/microL)
Serum igE level (marked increased, often above 1000units/mL)
Antibodies to filarial antigens (Diagnostic)
CXR, CT scan
Spirometry (Restrictive & Obstructive)
Sputum examination (Eosinophil)
BAL (Increased eosinophil)
**Although TPE is caused by filaria, patients with TPE do not have detectable
microfilaremia.
4/27/2023 DR. MD. SHAFIQUL ISLAM DEWAN, RESIDENT (PULMONOLOGY), DMCH 8

9. Chest Radiographs
Usually increased bilateral bronchovascular markings and
reticulonodular opacities or diffuse miliary lesions, or opacities in
the middle and lower lung fields.
Cavitation, bronchiectasis, and pleural effusion have been
reported but are uncommon;
Chest radiographs may also be normal.
4/27/2023 DR. MD. SHAFIQUL ISLAM DEWAN, RESIDENT (PULMONOLOGY), DMCH 9

10. Treatment of TPE
Specific treatment: Diethylcarbamazine (6 mg/kg/day in three doses for12 to
21 days) (Grade 1B).
Bronchospasm: Managed with bronchodilators and in severe cases, short-
term corticosteroids.
Relapses: Treated with a repeat course of the same treatment regimen.
**Corticosteroid therapy has been used as adjunctive therapy to reduce
inflammation in the acute setting but is not definitive therapy for TPE.
4/27/2023 DR. MD. SHAFIQUL ISLAM DEWAN, RESIDENT (PULMONOLOGY), DMCH 10

11. Differential Diagnosis
Chronic eosinophilic pneumonia,
Drug hypersensitivity reactions,
Fungal pneumonia,
Pulmonary syndromes associated with other helminths (most commonly
toxocara hookworm, ascaris, and strongyloides).
**Among these, strongyloidiasis is most important to exclude since
corticosteroid administration can lead to fatal dissemination o finfection.
**Although the imaging studies in TPE can mimic miliary tuberculosis the
presence of marked eosinophilia in TPE is an important distinguishing feature.
4/27/2023 DR. MD. SHAFIQUL ISLAM DEWAN, RESIDENT (PULMONOLOGY), DMCH 11

12. (A) Chest radiograph of a patient with confirmed tropical pulmonary eosinophilia
shows subpleural rightlung consolidation, subpleuralleft midlung opacity,and
bilateral perihilar interstitial thickening.
(B) Chest radiograph of the same patient after treatment with diethylcarbamazine.
Note the improved opacities.
4/27/2023 DR. MD. SHAFIQUL ISLAM DEWAN, RESIDENT (PULMONOLOGY), DMCH 12

13. Thank You
4/27/2023 DR. MD. SHAFIQUL ISLAM DEWAN, RESIDENT (PULMONOLOGY), DMCH 13