A Case of Tuberculous Pericardial Effusion with Concurrent SARS-CoV-2 Infection in an Undernourished Child

Abstract

Tuberculosis (TB) continues to be a major cause of morbidity and mortality in children, especially in the endemic regions. Tuberculous pericardial effusion is a rare but severe extrapulmonary manifestation and may be further complicated by concurrent viral infections such as SARS-CoV-2. To describe a rare case of tuberculous pericardial effusion with concurrent SARS-CoV-2 infection in an undernourished child and to discuss the diagnostic challenges and clinical management. A single-center, descriptive case report from a tertiary care hospital. A 9-year-old underweight, malnourished, unvaccinated male child presenting with acute respiratory distress was evaluated clinically and with imaging. Pericardial fluid analysis, Mantoux test, Cartridge-based Nucleic Acid Amplification Test (CBNAAT), and SARS-CoV-2 RT-PCR were performed. Therapeutic pericardiocentesis and anti-tubercular treatment were administered. Investigations revealed a large pericardial effusion with early tamponade physiology. Pericardial fluid showed a lymphocytic exudate with elevated adenosine deaminase. Mantoux test was positive, supporting a diagnosis of tubercular pericarditis despite negative CBNAAT. Concurrent SARS-CoV-2 infection was confirmed on RT-PCR. The child improved significantly following pericardiocentesis, anti-tubercular therapy, corticosteroids, and supportive management, with excellent recovery at 1-month follow-up. Tuberculous pericardial effusion remains a diagnostic challenge in pediatric patients, especially when co-infected with SARS-CoV-2. A high clinical suspicion is essential in TB endemic regions. Early diagnosis and timely intervention can lead to favorable outcomes even in undernourished and unvaccinated children.

INTRODUCTION

An outbreak of an unusual respiratory illness, first identified in Wuhan, China, was determined to be caused by a novel enveloped RNA virus. The World Health Organization (WHO) designated this virus as the 2019 novel coronavirus on January 7, 2020.[1] The coronaviruses are common pathogens, with types such as 229E and NL63 being responsible for a considerable proportion of common colds in both adults and children.[2] In India, the initial coronavirus infections were linked to international travel. The first confirmed cases, detected on January 30 and February 3, 2020, reported in Kerala among individuals who had returned from Wuhan, China.[3] Early data suggested that children under ten and older adults with comorbidities were particularly susceptible to more severe infection.[4] The symptoms of COVID-19 are often similar to other respiratory diseases such as influenza and tuberculosis (TB), and co-infections with various pathogens are not uncommon, complicating diagnosis and treatment.[5,6] Before COVID-19, TB had long been the world’s most deadly infectious disease.[7]

Both COVID-19 and TB primarily spread through respiratory droplets and target the lungs, which can lead to worse health outcomes for patients with a co-infection, abbreviated as COVID-TB.[8] India carries a significant portion of the global TB burden, accounting for 26% of cases according to a 2024 WHO report, with 12% of these cases occurring in children and young adolescents. An early Indian study until October 2020, found a TB prevalence of 0.37%–4% among COVID-19 patients, and 1.14% of TB patients screened were positive for COVID-19.[9] A report from Kerala on 177 active TB-COVID-19 co-infected patients indicated a mortality rate of 15.2%, although many had other comorbidities.[9] While data remain limited, a 2023 Mumbai hospital study identified 32 pediatric coinfections.[10] Rare but serious presentations, such as tuberculous pericardial effusion alongside COVID-19, have been documented, suggesting the viral infection may trigger or reactivate TB, posing significant diagnostic and therapeutic challenges.[11]

CASE REPORT

A 9-year-old male child with no known comorbidities, presented to the emergency department with a 5-day history of high-grade fever with chills, cough, and cold and a 4-day history of progressive difficulty in breathing. The cough was nonproductive and associated with chest pain and breathlessness. The dyspnea worsened when the child was lying down (orthopnea), prompting urgent medical care.

On admission to the pediatric intensive care unit, the child was conscious and had respiratory distress. Vital signs revealed a high-grade fever (102°C), tachycardia (pulse 140/min), tachypnea (respiratory rate 42/min), and a blood pressure of 102/68 mmHg. Auscultation revealed muffled heart sounds. Anthropometric measurements (weight 18 kg, height 128 cm, and body mass index [BMI] 11.04 kg/m²) placed him below the 5^th percentile according to the WHO guidelines, indicating undernutrition.

Initial laboratory investigations showed a hemoglobin of 9.2 g/dL, suggesting mild anemia with a hypochromic, microcytic picture. The total leukocyte count was within the normal limits (8100/µL) with a neutrophilic predominance (65%). Inflammatory markers were significantly elevated, with a C-reactive protein (CRP) of 104 mg/L. A chest X-ray was suggestive of cardiomegaly [Figure 1].

Figure 1.

Chest X-ray demonstrating cardiomegaly

A subsequent 2D echocardiogram revealed a large pericardial effusion with a dilated and plethoric inferior vena cava, showing the early signs of cardiac tamponade. The left ventricular ejection fraction was preserved at 70%. The child was urgently referred to our tertiary center for further management.

Diagnostic workup and management

Upon arrival, the child was stabilized with supplemental oxygen at 4 L/min via nasal prongs. An emergency pericardiocentesis was performed, draining 300 ml of clear, yellowish, and blood-tinged fluid. Analysis of the pericardial fluid was crucial for the diagnosis:

• Microscopy: Total leukocyte count of 260/cm³ (predominantly lymphocytes, 80%) with moderate RBCs

• Biochemistry: Elevated adenosine deaminase (ADA) level of 63.49 U/L, proteins 5.6 mg/dL, and glucose 94 mg/dL.

• The absence of a cobweb coagulum was noted.

An high-resolution computed tomography thorax confirmed severe pericardial effusion (maximal thickness 24 mm), cardiomegaly, and bilateral minimal pleural effusion [Figure 2]. Blood investigations further revealed an elevated NT-pro BNP (638.7 pg/ml) and a highly elevated CRP (175 mg/L). Initially differential diagnosis of pyogenic pericarditis was considered due to the presence of hypoeichoic shadows in 2D-Echo and high-grade fever but was ruled following the pericardial fluid lab reports. Moreover, rheumatoid factor and auto-antibodies (antinuclear antibody) were negative, ruling out an autoimmune etiology for the effusion.

Figure 2.

High-resolution computed tomography reveals significant pericardial fluid separating the heart from the pericardium

Empirical broad-spectrum antibiotics (vancomycin and meropenem) were initiated to cover for bacterial pathogens, along with prednisolone (1 mg/kg) for its anti-inflammatory and beneficial role in tubercular pericarditis.

Given the endemicity of TB in India, a focused evaluation was pursued. The pericardial fluid picture (lymphocytic exudate with highly elevated ADA) was highly suggestive of tubercular pericarditis. This was supported by a positive Mantoux test, although the Cartridge-based Nucleic Acid Amplification Test (CBNAAT) on both gastric aspirate and pericardial fluid was negative. Surprisingly, an RT-PCR test for SARS-CoV-2 was also positive, confirming a concurrent COVID-19 infection.

A final diagnosis of tubercular pericardial effusion with coincident SARS-CoV-2 infection was made. The broad-spectrum antibiotics were discontinued, and the child was started on standard anti-tubercular therapy (ATT) for a planned 6-month course. The ATT included isoniazid, rifampicin, pyrazinamide, and ethambutol in the standard four drug fixed dose regimen recommended by the Government of India. Serial 2D echoes showed a gradual decrease in the effusion, with the development of fibrinous strands. The child improved clinically and was discharged after 11 days of hospitalization.

Outcome and follow-up

At discharge, the child was vitally stable. The parents were extensively counseled on the importance of ATT compliance, a high-protein diet to address undernutrition, and the need for regular monitoring for drug toxicity (liver function tests and ophthalmic examination for ethambutol-induced retinopathy) and disease progression (2D echo for constrictive pericarditis). At the 1-month follow-up, the child was asymptomatic, and a repeat 2D echocardiogram was normal, confirming an excellent initial response to therapy.

DISCUSSION

This case details the successful management of a 9-year-old, undernourished male child with a co-infection of tubercular pericardial effusion and SARS-CoV-2. The presentation highlights several critical challenges, including the overlap of symptoms with common respiratory illnesses, the diagnostic dilemma in a TB-endemic region during the COVID-19 pandemic, and the importance of a systematic workup to guide life-saving and specific therapy.

The initial symptoms of high-grade fever, cough, and respiratory distress are common to both severe COVID-19 and TB, making clinical differentiation difficult.[5,6] In our patient, the presence of orthopnea and muffled heart sounds shifted the focus toward a cardiac etiology. The diagnosis of tubercular pericarditis was primarily established by the classic pericardial fluid analysis showing a lymphocytic exudate with a markedly elevated ADA level of 63.49 U/L, supported by a positive Mantoux test. The elevated ADA is a well-recognized, highly sensitive, and specific marker for tubercular pericarditis in the endemic areas.[12] The CBNAAT (Xpert MTB/RIF) on both pericardial fluid and gastric aspirate was negative. This underscores a critical diagnostic limitation, as CBNAAT, while excellent for pulmonary TB, has variable and often lower sensitivity in paucibacillary extrapulmonary cases like pericardial TB.[12,13] Therefore, in the high-prevalence settings, a strong clinical suspicion combined with supportive evidence like elevated ADA should supersede a negative molecular test to prevent a catastrophic diagnostic mistake.

The concurrent positive RT-PCR for SARS-CoV-2 added a layer of complexity. It has been hypothesized that SARS-CoV-2 infection, through its dysregulation of immune responses, could potentially trigger the reactivation of latent TB or worsen the course of active TB, as was seen in this case.[14,15] A large cohort study by Tadolini et al. suggested that active TB is a risk factor for severe COVID-19 in adults.[15,16] However, data in children remain scarce. A study from Mumbai by Mane et al. found that while children with TB and COVID-19 co-infection had higher hospitalization rates, their mortality and final outcomes were not significantly different from children with TB alone.[17] Similarly, a case series by Leone et al. described varying severity in pediatric COVID-TB cases, with severe courses often linked to pulmonary TB involvement and possibly the SARS-CoV-2 variant, but no direct mortality from COVID-19 itself.[15] Our patient’s clinical course aligns with these observations; his respiratory distress was primarily attributable to cardiac tamponade from TB rather than a primary COVID-19 pneumonia. The SARS-CoV-2 infection in this case appeared to be coincidental and mild.

Our patient’s undernutrition (BMI <5^th percentile) is a significant comorbidity. Malnutrition is a well-established risk factor for severe TB and is highly prevalent in the Indian pediatric population.[18,19] It compromises cell-mediated immunity, increasing susceptibility to primary TB infection and progression to severe disseminated disease. While the studies by Rangarajan et al. and Mane et al. did not find specific demographic or TB-related factors that increased the risk of contracting COVID-19, the role of host immunity in determining the severity of either disease cannot be overstated.[10,17] The child’s nutritional status likely contributed to the development of severe extrapulmonary TB but did not seem to predispose him to a more severe COVID-19 course, consistent with the general trend of milder SARS-CoV-2 infection in children. Furthermore, the child being undernourished led to a prolonged clinical recovery along with delayed nutritional improvement.

The management of this co-infection required an integrated approach. The emergent pericardiocentesis was life-saving. The initiation of ATT and adjunctive corticosteroids followed the standard guidelines for tubercular pericarditis.[10,20] The use of corticosteroids as seen in our case is particularly important to reduce inflammation and the risk of constrictive pericarditis. The empirical broad-spectrum antibiotics were appropriately discontinued. For the asymptomatic/mild COVID-19, no specific antiviral therapy was deemed necessary, which is in line with national and international guidelines for pediatric management.[15,21] This case demonstrates that the core management of TB should not be compromised by the presence of COVID-19, a sentiment echoed in the observational study by Mane et al., which concluded that the management of COVID-19 is unrelated to TB status.[17]

This case adds to the existing literature and also brings to light the broader systemic challenge highlighted by Jasin et al. and others: the COVID-19 pandemic has severely disrupted TB services, leading to delayed diagnoses and presentations with advanced disease.[22,23,24] Our patient had a month-long history of symptoms before presenting in tamponade physiology, a delay potentially exacerbated by pandemic-related hesitancy in seeking care.

CONCLUSION

This case highlights that in TB-endemic regions, tubercular pericardial effusion must remain a leading differential in children presenting with cardiac tamponade and respiratory symptoms, even during the COVID-19 pandemic. A high index of suspicion, coupled with judicious use of diagnostic tools like pericardial fluid ADA and echocardiography, is crucial for timely diagnosis and management. Co-infections with SARS-CoV-2 can occur and require an integrated treatment approach to ensure a successful outcome.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his/her consent for images and other clinical information to be reported in the journal. The guardian understands that names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.