Biology:Tropical eosinophilia

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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. The filariasis is transmitted by a vector, specifically the bite of a Culex, Anopheles, or Aedes mosquito, and the microfilariae (larvae) take up residence in the lung tissue, hindering respiration and causing chest pain as the disease progresses.[1]This disease can be confused with tuberculosis,[2] asthma, or coughs related to roundworms.[3] Tropical pulmonary eosinophilia is a rare, but well recognised, syndrome characterised by pulmonary interstitial infiltrates and marked peripheral eosinophilia.[4] 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.[5][6] Chronic symptoms may delay the diagnosis by up to five years.[5] Early recognition and treatment with the antifilarial drug, diethylcarbamazine, is important, as delay before treatment may lead to progressive interstitial fibrosis and irreversible impairment.[7]

The condition of marked eosinophilia with pulmonary involvement was first termed tropical pulmonary eosinophilia in 1950.[8] The syndrome is caused by a distinct hypersensitive immunological reaction to microfilariae of W. bancrofti and Brugia malayi.[7][9] However, only a small percentage (< 0.5%)[10] 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.[7][11] The typical patient is a young adult man from the Indian subcontinent.[9]

Symptoms and signs

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.[2]

Diagnosis

The diagnostic criteria for tropical pulmonary eosinophilia[11] include:

  • 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,[12][13] 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 anthelmintic medication. Other parasitic infections, such as the zoonotic filariae, dirofilariasis, ascariasis, strongyloidiasis, 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.[7][11][13][14] Radiological findings are nonspecific, with normal appearance on chest X-ray in up to 20% of patients.[9] Lung biopsy is not part of the routine diagnostic workup of tropical pulmonary eosinophilia.[4]

Treatment

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.[5] The antifilarial diethylcarbamazine (6 mg/kg/day in three divided doses[4] for 21 days[10] remains the main therapeutic agent, and is generally well tolerated. Reported side effects include headache, fever, pruritus and gastrointestinal upset.[15] The eosinophil count often falls dramatically within 7–10 days of starting treatment.[4][7]

References

  1. ↑ Jha, Suman K.; Karna, Bibek; Mahajan, Kunal (2020), "Tropical Pulmonary Eosinophilia", StatPearls (Treasure Island (FL): StatPearls Publishing), PMID 32491456, http://www.ncbi.nlm.nih.gov/books/NBK557524/, retrieved 2020-12-01 
  2. ↑ 2.0 2.1 "Pulmonary Eosinophilia". http://emedicine.medscape.com/article/301070-overview. Retrieved 2011-04-16. 
  3. ↑ "ICD-10 Classification". http://apps.who.int/classifications/apps/icd/icd10online/?gj80.htm+j82. Retrieved 2011-04-16. 
  4. ↑ 4.0 4.1 4.2 4.3 Yong, M.; Marshall, C.; Eisen, D. (2007). "Tropical pulmonary eosinophilia: A rare cause of cough in immigrants to Australia". The Medical Journal of Australia 187 (7): 416–418. doi:10.5694/j.1326-5377.2007.tb01316.x. PMID 17908009. 
  5. ↑ 5.0 5.1 5.2 Boggild, A. K.; Keystone, J. S.; Kain, K. C. (2004). "Tropical Pulmonary Eosinophilia: A Case Series in a Setting of Nonendemicity". Clinical Infectious Diseases 39 (8): 1123–1128. doi:10.1086/423964. PMID 15486834. 
  6. ↑ Jiva, T.; Israel, R.; Poe, R. (1996). "Tropical pulmonary eosinophilia masquerading as acute bronchial asthma". Respiration; International Review of Thoracic Diseases 63 (1): 55–58. doi:10.1159/000196517. PMID 8833995. 
  7. ↑ 7.0 7.1 7.2 7.3 7.4 Ong, R.; Doyle, R. (1998). "Tropical pulmonary eosinophilia". Chest 113 (6): 1673–1679. doi:10.1378/chest.113.6.1673. PMID 9631810. 
  8. ↑ Ball, J. (1950). "Tropical pulmonary eosinophilia". Transactions of the Royal Society of Tropical Medicine and Hygiene 44 (3): 237–258. doi:10.1016/0035-9203(50)90053-8. PMID 14809749. 
  9. ↑ 9.0 9.1 9.2 Udwaida F. (1975). "Tropical eosinophilia". in Herzog H. Pulmonary eosinophilia: progress in respiration research. Basel, Switzerland: Karger. pp. 35–155. 
  10. ↑ 10.0 10.1 "Lymphatic filariasis: The disease and its control. Fifth report of the WHO Expert Committee on Filariasis". World Health Organization Technical Report Series 821: 1–71. 1992. PMID 1441569. 
  11. ↑ 11.0 11.1 11.2 Ottesen, E. A.; Nutman, T. B. (1992). "Tropical Pulmonary Eosinophilia". Annual Review of Medicine 43: 417–424. doi:10.1146/annurev.me.43.020192.002221. PMID 1580599. 
  12. ↑ Muck, A.; Pires, M.; Lammie, P. (2003). "Influence of infection with non-filarial helminths on the specificity of serological assays for antifilarial immunoglobulin G4". Transactions of the Royal Society of Tropical Medicine and Hygiene 97 (1): 88–90. doi:10.1016/s0035-9203(03)90033-2. PMID 12886811. https://zenodo.org/record/1259701. 
  13. ↑ 13.0 13.1 Magnaval, J. -F.; Berry, A. (2005). "Tropical Pulmonary Eosinophilia". Clinical Infectious Diseases 40 (4): 635–636. doi:10.1086/427755. PMID 15712096. 
  14. ↑ Kuzucu, A. (2006). "Parasitic diseases of the respiratory tract". Current Opinion in Pulmonary Medicine 12 (3): 212–221. doi:10.1097/01.mcp.0000219271.80804.9e. PMID 16582677. 
  15. ↑ McLaughlin, S.; Radday, J.; Michel, M.; Addiss, D.; Beach, M.; Lammie, P.; Lammie, J.; Rheingans, R. et al. (2003). "Frequency, severity, and costs of adverse reactions following mass treatment for lymphatic filariasis using diethylcarbamazine and albendazole in Leogane, Haiti, 2000". The American Journal of Tropical Medicine and Hygiene 68 (5): 568–573. doi:10.4269/ajtmh.2003.68.568. PMID 12812348. 




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