Tropical Pulmonary Eosinophilia

Abstract & Commentary

Synopsis: Tropical pulmonary eosinophilia must be considered in patients with asthma-like symptoms and significant eosinophilia, who have resided in areas endemic for lymphatic filariasis.

Source: Boggild AK, et al. Tropical Pulmonary Eosinophilia: A Case Series in a Setting of Nonendemicity. Clin Infect Dis. 2004;39:1123-1128.

Boggild and colleagues describe 17 patients with tropical pulmonary eosinophilia seen at Toronto General Hospital Tropical Disease Unit over a 13-year period. All were of South Asian ancestry, with approximately half having emigrated to Canada, where they had resided for a median of 18 months, from the Indian subcontinent, while the other half had lived in Guyana. They had resided in Canada for a median of 18 months.

The patients had been ill for as long as 60 months (median, 6 months), and had seen a median of 2 physicians each prior to referral to the Tropical Disease Unit. Shortness of breath, nocturnal cough, and wheezing were present in 88%. Three-fourths had received a diagnosis of asthma, and 15 patients received treatment for presumed asthma, including prednisone in 41%, with little or no improvement.

Chest X-ray was performed in 14 patients; 4 were normal and 10 showed interstitial patterning. Eleven of 12 had abnormal pulmonary function studies. All had eosinophilia, ranging from 2.8 × 109 to 53.3 × 109 eosinophils/L, and all had elevated serum IgE levels. Anti-filaria antibody titer, performed at the NIH in Bethesda, MD ranged from 1:4096 to1:32,678.

All patients were treated with diethylcarbamazine (DEC) for a minimum of 21 days, and follow-up information was available in 15; all but one of whom had resolution of symptoms. However, pulmonary function abnormalities returned to normal in only 1 of 4 patients.

Comment by Stan Deresinski, MD, FACP

Tropical pulmonary eosinophilia (TPE) occurs in < 0.5% of individuals infected with the agents of lymphatic filariasis, Wucheria bancrofti, and Brugia malayi.1 In contrast to other forms of filariasis, microfilariae cannot be detected in peripheral blood, although they have been found in lymph nodes and other tissue. This is consistent with TPE being the result of a hypersensitivity reaction to filarial antigens, with parasitic gamma-glutamyl transpeptidase being a likely allergen.2 Lung histopathology in the early stages of the illness are characterized by an eosionphilic alveolitis. With chronicity, however, this is gradually replaced by a fibrotic reaction.

Up to one-fifth of patients have a normal chest X-ray. Pulmonary function studies within the first month of onset of symptoms may demonstrate abnormalities dominated by obstruction to airflow, but as the disease continues, a restrictive pattern emerges, frequently leading to a mixed testing pattern.

The diagnosis of TPE depends on residence in areas endemic for lymphatic filariasis, which include many tropical and subtropical regions of South America, Africa, Asia, and Oceania. Additional criteria are listed in Table 1, below. In addition to the examinations indicated there, all patients should have stool examination for helminthes, and a sensitive test for chronic strongyloidiasis, such as an antibody test.

The differential diagnosis includes other causes of eosinophilic lung disease, including migrating intestinal parasites, such as Ascaris, Strongyloides, and Ancylostoma, as well as zoonootic infestations, such as dirofilariasis and toxocariasis. Other diagnostic considerations include drug reactions, allergic bronchopulmonary aspergillosis, vasculitides (especially Churg-Strauss syndrome, Wegener’s granulomatosis, and polyarteritis nodosa), chronic eosinophilic pneumonia, and idiopathic hypereosinophilic syndrome.

Because of the progressive fibrosis that may occur in the absence of treatment, early diagnosis and intervention is critical to assuring an optimal outcome. The treatment of choice remains DEC.

References

1. Ong RKC, et al. Tropical Pulmonary Eosinophilia. Chest. 1998;113:1673-1679.

2. Lobos E, et al. Elevated Immunoglobulin E Against Recombinant Brugia Malayi Gamma-Glutamyl Transpeptidase in Patients With Bancroftian Filariasis: Association With Tropical Pulmonary Eosiniphilia or Putative Immunity. Infect Immun. 2003;71:747-753.

3. O,Bryan L, et al. Localized Eosinophilic Degranulation Mediates Disease in Tropical Pulmonary Eosinophilia. Infect Immun. 2003;71:1337-1342.

Stan Deresinski, MD, FACP, Clinical Professor of Medicine, Stanford; Associate Chief of Infectious Diseases, Santa Clara Valley Medical Center, is Editor for Infectious Disease Alert.