Pediatrics, Perinatology and Child Health, Neurology (clinical), Infectious Diseases, Endocrinology
29
Scopus Publications
Scopus Publications
Comparison of Clinical Profile and Outcomes Associated with Adenovirus and Non-adenovirus Viral Pneumonia in Children Admitted to a Pediatric Intensive Care Unit: A Single-center Retrospective Study Sheetal Agarwal, Bijoy Patra, Nishtha Goyal, Suchismita Nanda, Sneh Yadav, Aarzoo Malik, Vishal Kumar Indian Journal of Critical Care Medicine, 2026 Background: Severe adenovirus (AdV) pneumonia is a significant cause of morbidity and mortality in pediatric intensive care units (PICUs).This study aims to compare the clinical profile, laboratory parameters, radiological findings, and outcomes of children with severe AdV pneumonia with non-AdV viral pneumonia.Patients and methods: We conducted a retrospective review of case records of children diagnosed with viral pneumonia through PCR analysis of nasopharyngeal/throat swabs or bronchoalveolar lavage.Outcomes assessed included all-cause mortality, need for mechanical ventilation, duration of PICU and hospital stay, and incidence of bronchiolitis obliterans (BO) in each group.Univariate and multivariate logistic regression analyses were performed to identify risk factors for mortality and BO in the entire cohort.Results: Among 148 children with severe pneumonia, 63 (42.5%) had one or more viral isolates: AdV (31, 49.2%) and non-AdV viruses (32, 50.7%).The clinical profiles of the AdV and non-AdV viral pneumonia groups were comparable, except that all children in the AdV group were under 5 years of age [32 (100%) vs 26 (81.2%), (p = 0.02)].Leukopenia was more common in the AdV group (16.1 vs 0%, p = 0.01).Short-term outcomes, including mortality, length of PICU and hospital stay, and duration of mechanical ventilation, were similar between the groups.However, BO incidence was significantly higher in AdV cases (22.5 vs 3.1%, p = 0.02).Multivariate analysis identified acute respiratory distress syndrome (ARDS) and acute kidney injury (AKI) as independent risk factors for mortality, while prolonged PICU and hospital stay were linked to BO development.Conclusion: While the overall clinical profile and short-term outcomes of severe AdV and non-AdV viral pneumonia are similar, children with AdV pneumonia are younger, more prone to leukopenia, and at a higher risk of developing BO.
An Unusual Case of Cryptococcal Meningitis in an Immunocompetent 5-Year-Old: A Case Report Kritika Goel, Subhalaxmi Behera, Bijoy Patra, Hema Gupta Mittal, Shardul Tyagi, Supriya Sachan Annals of Child Neurology, 2026 Cryptococcal meningitis is a life-threatening fungal infection primarily caused by Cryptococcus neoformans [1], typically affecting immunocompromised individuals, particularly those with human immunodeficiency virus (HIV)/acquired 1 www.annchildneurol.org
Severe Pneumonia and Pediatric Acute Respiratory Distress Syndrome Caused by HCoV NL 63 and Respiratory Syncytial Virus Coinfection With Favorable Outcome Priyanka Verma, Sudha Chandelia, Sachin Bhagat, Selvakumar R, Sonali Kumari, Swati Mahich, Bijoy Patra Pediatric Infectious Disease Journal, 2025 To the Editors: NL63 coronavirus (HCoV NL63) was first described during the SARS-CoV outbreak in 2004, since then it has been reported infrequently in children. Data on coinfection with human covid NL 63 and respiratory syncytial virus (RSV) is sparse. We report 2 cases of HCoV NL63 and RSV coinfection causing pediatric acute respiratory distress syndrome (PARDS). Case 1: A 10-month-old baby, immunized for age, predominantly breastfed, wt-6 kg, who was admitted for pneumonia and PARDS. For worsening respiratory distress and impending failure, he had to be intubated and ventilated. His initial oxygenation index (OI) was 12 and progressed to 22 (severe PARDS). Chest radiograph showed bilateral heterogeneous opacities (Fig. 1). Respiratory viral panel showed coinfection of RSV and human covid NL 63 virus. In view of severe viral pneumonia and severe PARDS, we started him on intravenous dexamethasone @0.15 mg per kg and tapered over 3 weeks. The child responded and showed clinical and radiological improvement (OI decreased from 22→16→8→5→4). The child also had multiple organ dysfunction syndrome (MODS) (shock, acute kidney injury, transaminitis, all were managed conservatively and improved).FIGURE 1.: Admission chest x-ray of case 1 showing bilateral haziness (left >> right lung).Case 2: An 8-month-old girl, immunized for age, presented with fever, cough and fast breathing for 5 days. She was initially put on CPAP. In view of worsening distress, she was intubated within 24 hours and shifted to PICU and mechanically ventilated. She received IV ceftriaxone and ribavirin. She developed transudative pleural effusion on day 2 of admission. She was classified as a case of moderate PARDS. She also developed MODS (AKI, transaminitis) which were managed conservatively. Her respiratory viral panel showed coinfection with RSV and HCov NL 63 virus. Gradually, her OI decreased from 8→5→below 4 over a week, and MODS also resolved. She was successfully extubated after 8 days. HCoV NL 63 was first isolated during 2004. By, 2006, the incidence had decreased to 6% of all respiratory cases, RSV being the most common (48% cases).1 It occurs predominantly in the winter season.2 In children, it causes self-limiting mild to moderate respiratory disease, but has the potential to cause severe disease in immunocompromised children.1,3 Recently, there have been no cases of severe pneumonia ARDS published due to HCoV NL 63. The epidemic potential remains unclear. In a recent study, the incidence was estimated to be 21% among all corona virus, Coinfection with other viruses is common.3 In case 1 with severe pneumonia, severe PARDS and MODS, complicated with underlying vitamin-D deficiency, anemia and undernutrition, having a successful patient outcome was a challenging task. To our best knowledge, there have been no case reports on severe infection and disease caused by HCoV NL 63 in children recently. The child showed improvement with the addition of steroids, prone positioning and other supportive care. In contrast, case 2 improved without steroids. Adult case reports in HCoV NL 63 induced pneumonia, seen in immunocompromised patients have shown adverse outcomes despite the usage of steroids.4 Little is known about the consequences of RSV-HCoV NL 63 coinfection. Li et al5 concluded that there was no difference in the severity of illness in RSV infection vs RSV-HCoV NL 63 coinfection but in RSV-metapneumovirus coinfection severity of illness was high. We noticed that coinfection with RSV and human covid NL 63 virus resulted in increased severity of respiratory illness. ACKNOWLEDGMENTS We acknowledge the contribution of our nursing staff in the management of these cases and successful outcome.
Fulminant Parvovirus B-19 Infection Manifesting as Acute Encephalitis Syndrome and Myocarditis in a 10-Year-old Boy Iqra Khan, Nimisha Sharma, Kiran Kumar Banothu, Sakshi Sachdeva, Ira Agarwal, Kavita Vani, Bijoy Patra, Sheetal Agarwal Pediatric Infectious Disease Journal, 2025 To the Editor: Parvovirus B-19 infection commonly presents with skin, joint and hematological manifestations. Acute encephalitis and myocarditis are rare presentations and concurrent manifestation of both is extremely rare. We report a case of 10-year-old boy presenting as acute encephalitis syndrome (AES) with recurrent episodes of cardiac arrhythmias and myocardial dysfunction without any other identifiable underlying cause. Parvovirus B-19 DNA polymerase chain reaction was positive in cerebrospinal fluid (CSF). Administration of intravenous immunoglobulin (IVIg) possibly led to improvement in cardiac function; however, improvement in sensorium was modest. A 10-year-old boy presented with fever, vomiting and headache for 2 days and altered sensorium with left eye ptosis for 12 hours. At the presentation, the vitals were normal. On central nervous system (CNS) examination, the Glasgow Coma Scale was 8/15, pupils were mid-dilated, reactive to light and there was no papilledema. There was left eye ptosis, deep tendon reflexes were brisk and meningeal signs were positive. He was managed as a case of AES with raised intracranial pressure and required mechanical ventilation. The initial computed tomography scan was normal. CSF examination demonstrated 40 cells (50% neutrophils), increased proteins (140 mg/dL) and low sugar levels (30 mg/dL). On day 2, he developed wide complex ventricular tachycardia requiring synchronized cardioversion, intravenous metoprolol, lidocaine and amiodarone infusion. The ejection fraction was 35% and cardiac enzymes were raised (Creatinine Kinase-MB-1075 IU/L, positive Troponin I). He was administered IVIg along with intravenous corticosteroids. Cardiac manifestations resolved in 3 days but encephalopathy persisted. The CSF viral panel was positive for parvovirus B-19 DNA polymerase chain reaction. Contrast-enhanced magnetic resonance imaging brain revealed involvement of multiple areas of brain including bilateral temporal lobes, right parietal lobe and bilateral cerebellar hemisphere showing diffusion restriction and post-contrast enhancement suggestive of encephalitis and cerebellitis (Fig. 1). Tracheostomy was done and child was weaned off from ventilator. However, severe neurologic sequelae persisted at discharge.FIGURE 1.: Magnetic resonance imaging (MRI) brain showing. A: Gyral thickening involving bilateral temporal lobes showing hyperintense signal on FLAIR images. B: Diffusion restriction in DWI. C: Patchy FLAIR hyperintensities in bilateral cerebellar lobes. D: Diffusion restriction in DWI. E: Dependent debris in lateral ventricles showing diffusion restriction in DWI. F: Lacunar infarcts showing diffusion restriction in DWI involving splenium of corpus callosum. G: Leptomeningeal enhancement along ventral aspect of brainstem and spinal cord (white arrows). H: Nodular enhancement in left external capsule (white arrows). DWI indicates diffusion-weighted images; FLAIR, fluid-attenuated inversion recovery.The classical manifestation of B19V infection includes erythema infectiosum, multisystem involvement with anemia, thrombocytopenia, hepatitis, arthropathy and transient aplastic crisis. Serious manifestations of B19V infection include neurological and cardiac dysfunction owing to its viral cytopathic effect. The data regarding CNS manifestations of B19V infection in children is scarce.1 Acute encephalitis and encephalopathy are the most common neurological manifestations, accounting for 33.8% of B19V-associated CNS infections.2 The outcomes of B19V encephalitis are often poor and 31% patients of all age groups were reported to have persistent neurologic defects. There was no statistically significant difference in the rates of sequelae or death between those who received IVIg and/or steroids and those who were not treated with any immunomodulatory therapy.3 B19V myocarditis is a life-threatening manifestation in children with arrhythmias occurring in 15.6% children.4 The administration of immunosuppressive drugs and immunoglobulin administration is correlated with good outcomes in pediatric patients with B19V-associated myocarditis.5 However, B19V myocarditis also causes significant mortality and morbidity with 37.5% deaths and only 26% children having complete recovery of cardiac function.4,6 Fulminant presentation of human Parvovirus B-19 virus causing simultaneous acute encephalitis with myocardial dysfunction is extremely rare. Still, it is important to consider Parvovirus B-19 as a cause of pediatric AES and myocardial dysfunction. Administration of IVIg along with supportive management may reduce the morbidity and mortality.
Missed Diagnosis of Cystic Fibrosis in Developing Countries—Need to Raise the Awareness! Komal Attri, Kiran Kumar Banothu, Arun K, Suchismita Nanda, Manju Nimesh, Bijoy Patra, Sheetal Agarwal Pediatric Pulmonology, 2025 Cystic fibrosis (CF) is a multi-system, autosomal recessive, life-limiting disorder characterized by variants in the CFTR gene, leading to defective chloride transport across epithelial cells. This results in the production of thick, viscous secretions affecting multiple organ systems, primarily the respiratory, gastrointestinal, and reproductive tracts. While CF has erroneously been associated with European ancestry, recent data suggest that its prevalence in non-European populations, including Asian and African groups, is underrecognized and potentially underestimated. In India, the estimated prevalence of CF is approximately 1 in 40,000 live births, although this figure is likely conservative due to limited awareness and diagnostic challenges [1]. The clinical presentation of CF is highly variable and can manifest at any age, often mimicking more common respiratory and gastrointestinal conditions such as asthma, tuberculosis, or malabsorption syndromes. This phenotypic variability contributes to delays in diagnosis, particularly in regions where CF is not traditionally considered in differential diagnoses. We report two cases of CF; an infant and an adolescent girl who were misdiagnosed as post infectious bronchiolitis obliterans (PIBO) and tuberculosis (TB) respectively, highlighting the diagnostic challenges and the need for increased awareness of CF in low and middle income countries (LMICs). An informed written consent was obtained from the parents for publication. An 11-month-old boy presented with a 1-month history of intermittent wet cough and fast breathing, with symptoms more pronounced after waking. He had experienced recurrent respiratory infections since 20 days of age, requiring multiple hospital admissions. Each episode responded to antibiotics and nebulized salbutamol, with symptom resolution within 5–6 days. There was no history of regurgitation of feeds, coughing or choking during feeding, suck-rest cycles, vomiting, diarrhoea, oily or bulky stools, pustular skin lesions, or rash. The child was born full-term to a primiparous mother with a birth weight of 2.7 kg. There was no history of delayed passage of meconium, neonatal jaundice, or other perinatal complications. Family history was noncontributory. On presentation, the child was undernourished, with weight-for-height below the 3rd centile. His heart rate was 132 beats per minute, and his respiratory rate was 42 breaths per minute, accompanied by subcostal and intercostal retractions. Oxygen saturation was 91% on room air, necessitating high-flow oxygen support. Grade 1 digital clubbing was noted. There was no pallor, lymphadenopathy, or peripheral oedema. Respiratory examination revealed hyperinflation of the chest with diffuse fine crackles auscultated bilaterally. Examination of other systems was unremarkable. The initial blood tests revealed hemoglobin of 10.6 g/dL, total leukocyte count of 10,700/mm³ (neutrophils 50%, lymphocytes 36%, eosinophils 1%, monocytes 11%), and a platelet count of 250,000/mm³. Serum electrolytes, including sodium (135 mmol/L), potassium (4.1 mmol/L), and chloride (96 mmol/L), were within normal limits. Arterial blood gas analysis was also unremarkable. A chest radiograph demonstrated diffuse bilateral infiltrates, peribronchial thickening, and hyperinflation (Figure 1A). A computed tomography (CT) scan performed 3 months before admission showed bronchial dilatation with wall thickening (Figure 1B,C). Based on these findings, the child was initially managed at another institution as a case of post-infectious bronchiolitis obliterans (PIBO), receiving treatment with fluticasone metered-dose inhaler, azithromycin, and montelukast. Given the early onset of symptoms in the neonatal period, recurrent pneumonia, failure to thrive, and the CT scan findings of peribronchial thickening with early bronchiectasis (in the absence of mosaic attenuation), alternative diagnoses such as CF or primary immunodeficiency were considered. Due to the unavailability of sweat chloride testing at our institution, whole exome sequencing was performed. This revealed a compound homozygous CFTR variant (Phe508del), confirming the diagnosis of cystic fibrosis (Figure 1D). The child was initiated on CF specific treatment, including pancreatic enzyme replacement therapy (PERT), airway clearance therapies, and nutritional support. After 4 months, he demonstrated significant clinical improvement with a reduction in respiratory symptoms and a weight gain of two kilogram. A 9-year-old girl, born full-term to a primiparous mother with a birth weight of 3.1 kg, presented with a 6-month history of fever, wet cough and exertional dyspnea. She was initially diagnosed with tuberculosis based on clinical and radiological findings and started on antitubercular therapy. However, due to the lack of symptom improvement, multidrug-resistant tuberculosis was suspected, and she was referred to our center for further evaluation. On admission, her heart rate was 135 beats per minute, respiratory rate was 44 breaths per minute, and oxygen saturation was 88% on room air, improving to 98% with oxygen delivered via a non-rebreathing mask. She exhibited no pallor, cyanosis, or lymphadenopathy. Grade II digital clubbing was present. Both her weight and height were below the 3rd centile, and her BMI was 11.5 (Z-score < −3). Respiratory examination revealed pectus carinatum and Harrison's sulcus, with equal breath sounds bilaterally and diffuse coarse crepitations. On the third day of admission, the patient developed type 2 respiratory failure and required intubation. Arterial blood gas analysis showed severe respiratory acidosis (pH 7.1, pCO₂ 102 mmHg, paO2- 55 mmHg, HCO₃⁻ 46 mEq/L). Copious, thick secretions were frequently suctioned from the endotracheal tube. Chest radiograph revealed hyperinflated lungs with peribronchial thickening, cystic changes, and mucus plugging (Figure 2A). A previously performed CT scan of the chest demonstrated tubular bronchiectasis and cystic changes predominantly in the bilateral upper lobes (Figure 2B,C). Review of prior investigations revealed hyponatremia (128 mmol/L), hypokalemia (3.2 mmol/L), hypochloremia (71 mmol/L), and metabolic alkalosis. Cartridge-Based Nucleic Acid Amplification Test (CBNAAT) was negative for Mycobacterium tuberculosis, prompting consideration of an alternative diagnosis. On further review, the patient's history included prolonged neonatal jaundice but no delay in meconium passage. Since 4 months of age, she experienced recurrent episodes of wet cough and dyspnea, which temporarily resolved with antibiotics and nebulized salbutamol, although she was never entirely asymptomatic between episodes. Additionally, there was a history of occasional oily, sticky stools and poor weight gain despite a good appetite. The clinical picture raised suspicion for CF. This was confirmed by an elevated sweat chloride level (92 mEq/L) and genetic analysis identifying CFTR variant (Figure 2D). The patient was extubated to high-flow nasal cannula support and gradually weaned to room air. She was discharged with a comprehensive management plan, including fat-soluble vitamin supplementation (A, D, E, K), a high-calorie diet, azithromycin (5 mg/kg/day), airway clearance therapies and PERT. Over the following 3 months, the patient gained 2 kg weight, showed significant clinical recovery and demonstrated radiological improvement (Figure 2E). CF commonly presents with recurrent pneumonia, failure to thrive, chronic cough, intestinal obstruction, and salt-losing syndrome. However, these clinical manifestations are nonspecific, especially in LMICs where malnutrition, pneumonia, diarrhea and tropical infections are highly prevalent. This overlap often leads to CF being misdiagnosed or underdiagnosed, mistaken for conditions such as protein-energy malnutrition, tuberculosis, bronchiolitis, or asthma. Ranjous et al. described a delayed CF diagnosis in a 7-year-old girl from Syria who had been treated for celiac disease since infancy [2]. Similarly, in a Chinese cohort of CF patients, delayed diagnosis was common, likely due to limited physician awareness [3]. In India, a recent study estimated that while only 600 CF patients have been diagnosed, approximately 31,000 cases remain undiagnosed, highlighting the significant gap between disease prevalence and diagnosis [4]. Newborn screening is valuable for early CF diagnosis, while sweat chloride testing and/or mutation analysis are the primary diagnostic tools. However, in densely populated and LMIC like India, with a relatively low incidence of CF, newborn screening is challenging to implement due to limited public health resources and infrastructure availability. The availability of sweat chloride testing is limited to a few centers, and establishing a common genetic mutation panel is challenging due to the wide variety of common, rare, and novel CFTR mutations with diverse genotype-phenotype correlations found in the population [5, 6]. Moreover, genetic tests involving whole exome sequencing are costly. Given these challenges, a targeted diagnostic algorithm proposed by Sahoo et al. offers a pragmatic alternative. This algorithm incorporates simple clinical factors such as family history of sibling deaths, serum electrolyte imbalances, aquagenic wrinkling of the skin, fat globules in the stool, and Pseudomonas detection in sputum cultures for patients with recurrent pneumonia and failure to thrive [7]. In both our cases, this diagnostic algorithm was instrumental in guiding further testing. Early detection of CF enables timely treatment and significantly enhances quality of life. In conclusion, CF is often considered rare in developing countries and is frequently misdiagnosed. The diagnosis remains challenging due to limited awareness, insufficient training of healthcare providers, and restricted availability or high costs of diagnostic tools. Maintaining a high index of suspicion, conducting detailed patient histories, utilizing simple investigations, and employing algorithmic diagnostic approaches can aid in the timely identification of CF. There is an urgent need to improve diagnostic capabilities and raise awareness of this life-limiting disease in developing countries. Komal Attri: writing – original draft, investigation. Kiran Kumar Banothu: conceptualization, writing – review and editing. Arun K: writing – original draft. Suchismita Nanda: investigation. Manju Nimesh: investigation. Bijoy Patra: investigation. Sheetal Agarwal: conceptualization, writing – review and editing, investigation. This manuscript was assisted by ChatGPT, an AI language model developed by OpenAI, which helped in refining the language. The authors received no specific funding for this work. The ethical clearance is waived off for case reports by institutional ethics committee of Atal Bihari Vajpayee Institute of Medical Sciences and Dr. Ram Manohar Lohia Hospital, New Delhi as per the Indian Council of Medical Research guidelines. The authors declare no conflicts of interest. Data sharing is not applicable to this article as no new data were created or analyzed in this study.
Purpura Fulminans and Transient Nephrotic Range Proteinuria: Rare Manifestation of Leptospirosis Sumiti Banga, Sudha Chandelia, Bijoy Patra Pediatric Infectious Disease Journal, 2024 To the Editors: An 11-year-old male child presented to the emergency department in a state of septic shock. He complained of high-grade fever, purpura fulminans, altered sensorium and seizures for the last 5 days (Fig. 1). He was immediately stabilized, intubated for poor Glass Gow Coma scale (E2V1M5) and other supportive care was started. Empirical antimicrobials included ceftriaxone and vancomycin. He had leukocytosis (20 × 103/L; neutrophils 80%, lymphocytes 18%), thrombocytopenia (60 × 103/L) and elevated C-reactive protein (21.9 mg/dL). Malaria, scrub typhus and blood cultures were negative. Punch biopsy from skin lesions and cerebrospinal fluid latex agglutination studies ruled out meningococcemia. The patient developed nonoliguric acute kidney injury (AKI, stage 3; estimated glomerular filtration rate, 46 mL/min/1.73m2; blood urea, 11.15 mmol/L and serum creatinine, 0.11 mmol/L). Urine examination revealed proteinuria (3+), but no hematuria. Spot urine protein creatinine ratio was highly raised (6.35). He also developed transaminitis (serum glutamic-oxaloacetic transaminase, 6.71 µkat/L, serum glutamic pyruvic transaminase, 7.91µkat/L), without jaundice. Serum IgM antibodies by enzyme-linked immunosorbent assay for leptospirosis were positive (National Centre for Disease Control). He was then started on intravenous doxycycline. AKI was managed conservatively. He improved subsequently, was extubated successfully on day 7 of intensive care unit admission, and was shifted to the ward.Figure 1.: Left panel shows purpura fulminans during active infection. Right panel shows purpura fulminans during recoveryLeptospirosis is an infectious and emerging public health zoonotic disease caused by the spirochetes bacteria Leptospira spp. The clinical course of leptospirosis is variable. Most cases are mild and self-limited or subclinical, while some are severe and potentially fatal, such as aseptic meningitis and hepatorenal dysfunction.1 Rash in leptospirosis may be transient truncal maculopapular erythematous, lasting for a day. But frank purpura fulminans is not described (Fig. 1).2 At admission, Purpura fulminans rash was violaceous in color, irregular margins and was present mainly over lower limbs. Over the next 10 days, the rash became darker and blackish, coalesced and grew. Its progress halted only after 2 weeks. Purpura is frequently caused by meningococcus, streptococcus and staphylococcus infections.3 Pathophysiology includes consumption of protein C, S and antithrombin III, creating a prothrombotic state. Thrombosis of dermal vessels ensues, along with hemorrhagic necrosis.3 In this case, purpura involved all 4 limbs and started fading after 3 weeks. AKI (in about 60% of cases) is known in leptospirosis along with mild proteinuria. Urinalysis may show pyuria, granular casts and occasionally microscopic hematuria. The case fatality rate of AKI due to leptospirosis is approximately 22%. Heavy proteinuria in the nephrotic range is rare. Our patient had a very high urine protein/urine creatinine ratio of 6.35. This persisted even when the child became afebrile. Improvement in proteinuria started after 2 weeks of illness. We could find only 1 case report of nephrotic range proteinuria (9 g/day).4 We kept meningococcemia as the first possibility in view of acute meningoencephalitis, septic shock, thrombocytopenia and purpura fulminans but workup for the same was negative. Leptospira contains endotoxins in its outer membrane in the form of lipopolysaccharides, lipoproteins and peptidoglycans. These antigenic irritants can potentially cause vasculitis and renal tubular, glomerular inflammation, and dysfunction.5
