, more than 25.1 million confirmed cases of coronavirus disease (COVID-19) including more than 844,000 deaths have been reported worldwide [1]. Limited data describe clinical manifestations of COVID-19 generally milder in children compared with adults but also show that some children do require hospitalization and intensive care support. Recently, a limited number of children with exposure to COVID-19 virus who developed significant systemic inflammatory response syndrome with clinical features overlapping with Kawasaki disease (KD) and toxic shock syndrome have been identified from Europe, North America, and various parts of the world [2]. This syndrome has been described in children after 2-4 weeks of exposure to COVID-19 virus suggesting aberrant cellular and humoral immune response to the virus [3]. This syndrome has been labeled by different terminologies such as multisystem inflammatory syndrome in children (MIS-C) associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [4], pediatric multisystem inflammatory syndrome temporally associated with SARS-CoV-2 (PIM-TS) [5], and hyperinflammatory shock during COVID-19 pandemic [6]. Clinical and laboratory manifestations of MIS-C have been attributed to the antibodies produced against SARS-CoV-2. It has been postulated that these antibodies enhance the severity of infection by triggering inflammation or mediating organ damage [3]. Clinical similarity between KD and MIS-C implies a related underlying genetic architecture, supporting the hypothesis that the new disorder arises from aberrant T-or B-cell responses to SARS-CoV-2 [7]. MIS-C shares overlapping clinical features with KD such as conjunctival injection, oropharyngeal findings (red and/ or cracked lips and strawberry tongue), rash, swollen and/or erythematous hands and feet, and cervical lymphadenopathy. However, some notable differences from KD include broader age range of presentation, more prominent gastrointestinal and neurological symptoms, more frequent presentation with shock, and more likely to display cardiac dysfunction (arrhythmias and ventricular dysfunction) [8]. Here, we report a case of a previously well 4-year-old female child who presented to us with MIS-C following exposure to SARS-CoV-2 and was successfully managed with intravenous immunoglobulin (IVIG) and intravenous (IV) steroids. CASE REPORT A 4-year-old female child who was previously well was brought with complaints of high-grade fever (>39°C), vomiting, and loose motions for 4 days. She developed a non-itchy, generalized rash all over the body 2 days before admission. It initially started

cute necrotizing encephalopathy of childhood (ANEC) is a rare, severe atypical encephalopathy of para infectious etiology usually triggered by viral infections and is associated with rapid deterioration of sensorium and seizures [1]. It was first described by Mizuguchi from Japan in 1995 [1]. It is seen predominantly in previously healthy young children or infants of East Asian countries such as Japan and Taiwan. However, sporadic cases of this illness have been reported from all around the globe [1,2]. Influenza virus, human herpes virus 6 (HHV-6), herpes simplex virus, mycoplasma, and dengue viruses are among the most common infections causing ANEC [3-5]. Recently, acute hemorrhagic necrotizing encephalitis was observed in a young adult due to coronavirus disease-19 infection [6]. The elevation of hepatic enzymes is unique without hyperammonemia [7]. A recurrent or familial form is associated with mutations in the RANBP2 gene and is noted as ANE1 [7,8]. Classical magnetic resonance imaging (MRI) findings include multifocal symmetrical lesions in thalami, brainstem, and cerebellum [3,9]. The physicians should rule out other causes of encephalopathies such as fulminant hepatitis, Reye's syndrome, toxic shock syndrome, Leigh encephalopathy, organic academia, hypoxic brain insult, acute disseminated encephalomyelitis, venous and arterial infarcts in children, and occasionally heatstroke [10]. The prognosis is poor in most cases. We report a case of ANEC following HHV-6 infection in a previously healthy 9-month-old infant. CASE REPORT A previously healthy 9-month-old female infant presented to us with fever for 4 days, loose stools for 2 days, and decreased activity for 1 day. At the time of admission, she was irritable, drowsy and her deep tendon reflexes were brisk with the Glasgow Coma Scale of 13/15. Her pupils were equal and reacting to direct light and the hydration status of the child was good. However, after 1 h of admission in the pediatric intensive care unit (PICU), she developed right-sided focal seizure, which was aborted with short-acting benzodiazepine injection midazolam, and later, she was loaded with inj. levetiracetam 20 mg/kg IV route over 20 min. The seizure got controlled but encephalopathy with signs of meningitis (neck stiffness, Kernig's sign, and Brudzinski signs) persisted. Hence, an initial provisional diagnosis of acute meningoencephalitis was made. Other differential diagnoses kept in mind were metabolic encephalopathy with sepsis, hypoxicischemic encephalopathy (HIE) due to status epilepticus, and Reye's syndrome, respectively. She was given O 2 therapy, intravenous (IV) fluids, IV thirdgeneration cephalosporins, and IV acyclovir initially for 5 days. After stabilizing the airway, breathing, circulation, and neurological status of the child, a lumbar puncture was done after ruling out optic disc edema by fundoscopy. The cerebrospinal fluid (CSF) report revealed total two cells with 100% lymphocytes, CSF glucose was 38 mg/dl, and CSF total protein was 44 mg/dl. Thus, there was neither C...

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