Unmasking the Masquerader: A Case of Tropical Pulmonary Eosinophilia-mimicking Tuberculosis

Sir, Pulmonary infiltrates with eosinophilia (PIE) encompass a diverse group of disorders characterized by the accumulation of eosinophils in the lung parenchyma, often resulting in respiratory symptoms such as cough, wheezing, and breathlessness.[1] Tropical pulmonary eosinophilia (TPE), a parasitic lung disease caused by filarial infections, particularly Wuchereria bancrofti and Brugia malayi, is a well-recognized but often underdiagnosed cause of PIE. The pathophysiology of TPE involves the immune response to microfilariae trapped within the pulmonary microcirculation.[2,3] TPE remains a challenge to diagnose due to its rarity and the nonspecific nature of its symptoms and imaging findings. Here, we present a compelling case of a young male with persistent cough and fever, initially misdiagnosed as pulmonary tuberculosis, ultimately diagnosed with TPE. A 28-year-old male with no known comorbidities, a resident of Bihar currently working in Mumbai, presented to a peripheral hospital with a 20-day history of cough and a 5-day history of fever. The cough was productive, yielding yellow mucopurulent expectoration, and exhibited nocturnal exacerbation. The fever was associated with chills and rigors, with a nocturnal rise in temperature. Chest radiography performed at the peripheral hospital revealed nonhomogeneous patchy airspace opacities in the bilateral lower zones [Figure 1a]. Given the clinical and radiological findings, pulmonary tuberculosis was suspected, and the patient was referred to our center for further evaluation and management. On presentation, the patient remained symptomatic, his vital signs were stable, and chest auscultation revealed bilateral polyphonic wheezing.Figure 1: (a) Initial chest radiography of patient revealing nonhomogeneous patchy airspace opacities in the bilateral lower zones (as denoted by arrows), (b) Chest radiography after 1 week showing bilateral reticulonodular opacities with lower zone predominance, (c) Follow-up chest radiography after 2 weeks of treatment demonstrating near complete resolutionHematological evaluation revealed a total leukocyte count of 27,000 cells/mm3 (neutrophils 25%, lymphocytes 12%, and eosinophils 59%), and a platelet count of 255,000/mm3. His absolute eosinophil count was markedly elevated at 15,930 cells/mm3. Other metabolic parameters were within normal limits. A peripheral blood smear demonstrated normocytic, normochromic red blood cells along with significant eosinophilia without evidence of atypical cells. Chest radiography performed at our center revealed bilateral diffuse reticulonodular opacities [Figure 1b]. High-resolution computed tomography (HRCT) of the chest demonstrated multiple tiny centrilobular nodules with adjacent ground–glass opacities, randomly distributed across both lung fields. The patient underwent a video bronchoscopy, which revealed erythematous tracheobronchial mucosa with areas of desquamation. Bronchoalveolar lavage (BAL) was sent for Gram stain, aerobic and anaerobic cultures, Ziehl–Neelsen stain, nucleic acid amplification testing for Mycobacterium tuberculosis, and fungal culture – all of which returned negative. BAL cytology demonstrated a predominance of eosinophils (>70%), interspersed with alveolar macrophages and bronchial epithelial cells, with no evidence of malignancy [Figure 2]. Further evaluation revealed markedly elevated serum total IgE levels (23,692 kU/L; reference range: 0–114) and a positive qualitative test for serum anti-filarial IgG antibodies. A diagnosis of TPE was established, and the patient was initiated on diethylcarbamazine (DEC) (6 mg/kg/day in three divided doses) for 21 days, along with bronchodilator nebulization and supportive care.Figure 2: Bronchoalveolar lavage stained with Leishman stain, under ×40, demonstrating a predominance of eosinophils (>70%), interspersed with alveolar macrophages and bronchial epithelial cellsHe responded well to treatment, with significant symptom resolution within 1 week of therapy initiation. Follow-up chest radiography performed after 2 weeks demonstrated near-complete radiological resolution [Figure 1c]. Repeat hematological evaluation at 2 weeks showed a reduced eosinophil differential count of 27% and an absolute eosinophil count of 2900 cells/mm3. The patient was discharged in stable condition after making a full recovery. TPE is an infrequent yet frequently underdiagnosed complication of filarial infection. It often presents with clinical features that closely mimic more prevalent pulmonary conditions, such as tuberculosis or pneumonia. Despite the endemic prevalence of filarial infections, fewer than 1% of those infected develop TPE, though the exact reasons for this rare and selective presentation remain unclear.[3] Endemic regions primarily include parts of India, sub-Saharan Africa, and Southeast Asia. However, the appearance of TPE in nonendemic areas warrants a detailed history of travel to endemic regions to guide diagnostic consideration. Transmission occurs through mosquito bites that introduce the filarial larvae into the bloodstream, where they migrate to the lymphatics. Female filarial worms release microfilariae, which then become trapped in the pulmonary microcirculation. The subsequent degradation of these microfilariae within the lungs leads to the release of antigens that provoke a profound immune response, characterized by parasite-specific antibodies and a marked eosinophilic infiltration. While the precise factors that predispose certain individuals to this intense inflammatory response remain unidentified, genetic or immune system-based factors may play a role.[3] The clinical presentation of TPE is highly variable and can be easily confused with other diseases. Symptoms include fever, malaise, anorexia, weight loss, and cough, with nocturnal exacerbation of symptoms, resembling common pulmonary disorders such as tuberculosis. The associated breathlessness, wheezing, and elevated eosinophil count often result in mismanagement as asthma exacerbations. Less frequently, patients may exhibit generalized lymphadenopathy, hepatosplenomegaly, pericarditis, and musculoskeletal or central nervous system involvement.[3] The hallmark laboratory findings of TPE include marked peripheral eosinophilia (typically >3000 cells/mm3), elevated serum total immunoglobulin E (IgE) levels (often >1000 U/ml), and BAL eosinophilia (>50%). Notably, microfilariae are often absent from peripheral blood or sputum, and the diagnosis is solidified through the detection of high titers of filarial-specific immunoglobulin (Ig) G and IgE antibodies, particularly in the appropriate clinical setting.[4] Imaging findings in TPE are typically nonspecific. The most frequent radiographic feature is the presence of bilateral, diffuse, ill-defined reticulonodular opacities, most often located in the mid and lower lung zones. In approximately 20% of cases, chest radiography may appear normal, though occasional patients may show hilar lymphadenopathy or pleural effusion. typically reveals widespread ill-defined nodules, with long-standing cases sometimes demonstrating bronchiectasis and calcific foci.[5] Diagnosis is primarily clinical, supported by laboratory findings such as elevated eosinophil count, serum Ig E levels, and specific anti-filarial IgG and IgE antibodies. The treatment of choice for TPE is DEC, a micro- and macrofilaricidal agent.[6] The recommended dosage is 6 mg/kg/day, administered in three divided doses for 14–21 days.[2] Clinical improvement, as well as resolution of peripheral eosinophilia, is typically observed within 2 weeks of initiating therapy. However, BAL eosinophilia and reductions in filarial IgG and IgE levels may take up to 4 weeks to normalize. Although spontaneous remission is possible, the risk of relapse is significant in approximately 20% of cases, often requiring retreatment with DEC.[2] If left untreated, TPE can result in persistent mild chronic lung inflammation, potentially progressing to fibrosis.[4] The systematic evaluation and management of this condition underscores the critical importance of considering TPE in patients from endemic regions and highlights the diagnostic challenges posed by its overlapping clinical and radiological features. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.