Eosinophilic pleural effusion as a manifestation of taeniasis
Synrang Batngen Warjri; Tony Ete; Habung Mobing; Narang Naku; Vanlalmawsawmdawngliana Fanai; Shakeel Ahamad Khan; Arun Kumar; Animesh Mishra
A 21-year-old male patient presented with a history of low-grade fever, non-productive cough, and generalized weakness of one-month duration. On examination, he was conscious, oriented, and afebrile with the blood pressure of 120/80 mm of Hg, a pulse rate of 68 beats per min, and a respiratory rate of 20 per minute. There was no pallor, clubbing, icterus, or any enlarged lymph nodes. On the chest examination, respiratory sounds were absent on the bilateral infra-scapular and infra-axillary regions, where a stony dullness was achieved on percussion. Cardiac and neurological examination revealed no significant abnormalities. His abdomen was soft, with no organomegaly. Bowel sounds were normal on auscultation. Laboratory workup revealed a total leukocyte count of 38,500 cells/mL (reference range [RR]; 4000-11000 cells/ml) with a differential count showing 76% eosinophils, 14% neutrophils and 8% lymphocytes. Liver, thyroid, and renal function tests were within normal limits. p-ANCA (perinuclear anti-neutrophil cytoplasmic antibody), c-ANCA (cytoplasmic anti-neutrophil cytoplasmic antibody), rheumatoid factor and ANA (anti-nuclear antibodies) were all negative. Erythrocyte sedimentation rate (ESR) was 25 mm (RR; 0-22 mm/hr) after the first hour. Urinalysis was normal.
Bone marrow examination revealed a hypercellular marrow with increased eosinophilic cells (33%). No atypical or neoplastic cells were seen in the bone marrow study. Chest roentgenogram showed bilateral pleural effusions confirmed by the thoracic contrast-enhanced computed tomography (
|Cell count||6200 cells/mL|
|adenosine deaminase (ADA)||39 U/L|
The pulmonary manifestations of parasitic infections in humans are diverse and include transient pulmonary infiltrates, focal lung cysts, pneumothorax, consolidations, eosinophilic pneumonia, and pleural effusions. In 1932, the Swiss doctor Wilhelm Löffler described a syndrome of acute transient respiratory illness associated with blood eosinophilia and radiographic shadowing. This was attributed to the pulmonary migration of the larvae of Ascaris lumbricoides.
Eosinophilic pleural effusion (EPE) is characterized by an eosinophil count of ≥ 10% in the pleural fluid. It has been estimated to occur in 5-16% of all pleural effusions.
The pathogenesis of pulmonary eosinophilia due to parasitic infections is uncertain. Parasites such as Ascaris lumbricoides, Necator americanus, Ancylostoma duodenale, and Strongyloides stercoralis, whose life cycle in the human host includes the passage through the lung, can possibly induce an eosinophilic immune response leading to pulmonary eosinophilia. Other parasites such as toxocara, echinococcus, and paragonimus can penetrate the intestinal wall and spread to various tissues (including the lung), leading to local and systemic allergic and inflammatory responses. The life cycle of both Taenia saginata (beef tapeworm) and Taenia solium (pork tapeworm) in the human host does not involve migration through the lung. However, the Taenia solium eggs can penetrate the intestinal wall and develop cysticerci in any organ, typically in muscles, subcutaneous tissues, brain, and eyes.
The precise mechanism of EPEs in intestinal taeniasis remains speculative and most likely results from increased production and migration of eosinophils from the bone marrow into the pleural space in response to secretion of Interleukin (IL)-5 and Interleukin-4 by T-helper2 (Th2) lymphocytes. This response is similar to a Th2-type hypersensitivity reaction leading to tissue eosinophilia in allergic diseases. EPEs due to parasitic infestations also have higher levels of thymus and activation-regulated chemokine (TCAR), which is a selective chemoattractant for Th2 cells.
Even taking into account this background of uncertain pathogenesis of EPEs, we believe that the association of the Taenia sp infestation was related to the EPE, in our patient. A retrospective study by Wang et al.
The initial diagnostic workup of patients with EPEs should be directed towards identifying the likely responsible etiology. Malignancies are the most common causes of EPEs, and a thorough search for any neoplastic disease is always warranted. Proper drug history is essential to rule out drug-induced reactions. Drugs that have been implicated in EPEs include dantrolene, nitrofurantoin, bromocriptine, methotrexate, methysergide, amiodarone, bleomycin, procarbazine, procainamide, isotretinoin, valproic acid and fluoxetine.
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