Tropical (pulmonary) eosinophilia, or TPE, is characterized by coughing, asthmatic attacks, and an enlarged spleen, and is caused by Wuchereria bancrofti, a filarial infection. It occurs most frequently in India and Southeast Asia. Tropical eosinophilia is considered a manifestation of a species of microfilaria. This disease can be confused with tuberculosis, asthma, or coughs related to roundworms.
Tropical pulmonary eosinophilia is a rare, but well recognised, syndrome characterised by pulmonary interstitial infiltrates and marked peripheral eosinophilia. 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. Chronic symptoms may delay the diagnosis by up to five years. Early recognition and treatment with the antifilarial drug, diethylcarbamazine, is important, as delay before treatment may lead to progressive interstitial fibrosis and irreversible impairment.
The condition of marked eosinophilia with pulmonary involvement was first termed tropical pulmonary eosinophilia in 1950. The syndrome is caused by a distinct hypersensitive immunological reaction to microfilariae of W. bancrofti and Brugia malayi. However, only a small percentage (< 0.5%) 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. The typical patient is a young adult man from the Indian subcontinent.
A persistent or recurrent cough that gets aggravated at night, weakness, weight loss and a low fever raises the possible diagnosis of this disease. Some children with this disease may also have enlarged lymph nodes in the neck and elsewhere. Others may cough up a little blood and may also have a wheeze.
- a history supportive of exposure to lymphatic filariasis;
- a peripheral eosinophilia count greater than 3 × 109/L);
- an elevated serum IgE levels (> 1000 kU/L);
- increased titers of antifilarial antibodies;
- peripheral blood negative for microfilariae; and
- a clinical response to diethylcarbamazine.
High antifilarial IgG titers to microfilariae often result in cross reactivity with other nonfilarial helminth antigens, such as strongyloides and schistosoma antigens, as demonstrated in reported cases. It is important to exclude other parasitic infections before tropical pulmonary eosinophilia is diagnosed, by serological tests, examination of stool specimens in a laboratory experienced in parasitic infections, or a trial of anthelminthic medication. Other parasitic infections, such as the zoonotic filariae, dirofilariasis, ascariasis, strongyloides, visceral larva migrans and hookworm disease, may also be confused with tropical pulmonary eosinophilia because of overlapping clinical features, serological profile and response to diethylcarbamazine. Radiological findings are nonspecific, with normal appearance on chest X-ray in up to 20% of patients. Lung biopsy is not part of the routine diagnostic workup of tropical pulmonary eosinophilia.
The dramatic response to a commonly used drug for filaria (diethylcarbamazine) almost confirms the diagnosis. No universal treatment guidelines have been established for tropical pulmonary eosinophilia. The antifilarial diethylcarbamazine (6 mg/kg/day in three divided doses for 21 days remains the main therapeutic agent, and is generally well tolerated. Reported side effects include headache, fever, pruritus and gastrointestinal upset. The eosinophil count often falls dramatically within 7–10 days of starting treatment.
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