Background Limited evidence exists on perinatal transmission and outcomes of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection in neonates. Objective To describe clinical outcomes and risk factors for transmission in neonates born to mothers with perinatal SARS-CoV-2 infection. Design Prospective cohort of suspected and confirmed SARS-CoV-2 infected neonates entered in National Neonatology Forum (NNF) of India registry. Subjects Neonates born to women with SARS-CoV-2 infection within two weeks before or two days after birth and neonates with SARS-CoV-2 infection. Outcomes Incidence and risk factors of perinatal transmission. Results Among 1713 neonates, SARS-CoV-2 infection status was available for 1330 intramural and 104 extramural neonates. SARS-CoV-2 positivity was reported in 144 intramural and 39 extramural neonates. Perinatal transmission occurred in 106 (8%) and horizontal transmission in 21 (1.5%) intramural neonates. Neonates roomed-in with mother had higher transmission risk (RR1.16, 95% CI 1.1 to 2.4; P =0.01). No association was noted with the mode of delivery or type of feeding. The majority of neonates positive for SARS-CoV2 were asymptomatic. Intramural SARS-CoV-2 positive neonates were more likely to be symptomatic (RR 5, 95%CI 3.3 to 7.7; P <0.0001) and need resuscitation (RR 2, 95%CI 1.0 to 3.9; P =0.05) compared to SARS-CoV-2 negative neonates. Amongst symptomatic neonates, most morbidities were related to prematurity and perinatal events. Conclusion Data from a large cohort suggests perinatal transmission of SARS-CoV-2 infection and increased morbidity in infected infants.

Introduction There is a lack of large multicentric studies in children with COVID-19 from developing countries. We aimed to describe the clinical profile and risk factors for severe disease in children hospitalized with COVID-19 from India. Methods In this multicentric retrospective study, we retrieved data related to demographic details, clinical features, including the severity of disease, laboratory investigations, and outcome. Results We included 402 children with a median (IQR) age of 7 (2,11) years. Fever was the most common symptom, present in 38.2% of children. About 44% had underlying comorbidity. The majority were asymptomatic (144, 35.8%) or mildly symptomatic (219, 54.5%). There were 39 (9.7%) moderate-severe cases and 13 (3.2%) deaths. The laboratory abnormalities included lymphopenia 25.4%; thrombocytopenia 22.1%; transaminitis 26.4%; low total serum protein 34.7%; low serum albumin 37.9%; and, and low alkaline phosphatase 40%. Out of those who were tested, raised inflammatory markers were ferritin 58.9% (56/95); c-reactive protein 33.3% (41/123); procalcitonin 53.5% (46/86); and interleukin-6 (IL-6) 76%. The presence of fever, rash, vomiting, underlying comorbidity, increased total leucocyte count, thrombocytopenia, high urea, low total serum protein, and raised c-reactive protein were factors associated with moderate to severe disease. Conclusion Fever was the commonest symptom. We identified additional laboratory abnormalities, namely lymphopenia, low total serum protein and albumin, and low alkaline phosphatase. The majority of the children were asymptomatic or mildly symptomatic. We found high urea and low total serum protein as risk factors for moderate to severe disease for the first time.

AIMS AND OBJECTIVE:Evaluation of C677T polymorphisms of the methylenetetra hydrofolate reductase (MTHFR) gene and its association with level of serum homocysteine, folate, and vitamin B12 as possible maternal risk factors for Down syndrome.DESIGN:This was a case–control study.MATERIAL AND METHODSFifty-two mothers (mean age 27.6 years) with babies having free trisomy 21 of North Indian ethnicity and 52 control nonlactating mothers (mean age 24.9 years) of same ethnicity attending services of genetic lab for bloodletting for other causes were enrolled after informed written consent. Fasting blood was collected and was used for determination of plasma homocysteine, vitamin B12, and folate (serum and RBC), and for PCR amplification of the MTHFR gene.RESULTS:The prevalence of MTHFR C677T polymorphism in north Indian mothers of babies with trisomy 21 Down syndrome was 15.38% compared to 5.88 % in controls. The difference between two groups was not statistically significant (P = 0.124). Low serum folate was demonstrated in 34.62% of cases vs. 11.54% in controls, which was significant (P = 0.005). Low RBC folate was found in 30.7% of cases versus 11.53% in controls, which was not significant (P = 0.059), when analyzed independently. But on multiple regression analysis the difference was statistically significant. Low serum vitamin B12 was found in 42.31% of cases versus 34.62% in controls, which was not significant (P = 0.118). The mean serum homocysteine in cases was 10.35 ± 0.68 while controls were 9.02 ± 0.535.CONCLUSION:Serum levels of folate were low in cases. The RBC folate levels were comparable in both groups. However the combined serum folate and RBC folate were low in cases compared to control groups. Homocysteine levels in our study were higher in Down syndrome mothers compared to controls; however high-serum level of Homocysteine had no association with MTHFR polymorphism. No association of serum vitamin B12 with MTHFR polymorphism in occurrence of Down syndrome births was found. Peri- or preconceptional folate supplementation may therefore lead to a decline in DS births, if supported by larger studies.

Difficult intubation in neonates has innumerable aetiologies. It especially poses a formidable challenge to save a newborn baby immediately after birth where antenatal details are unavailable. A late preterm neonate was born limp and apnoeic. Several attempts to intubate the baby were unsuccessful. Possibility of subglottic obstruction was considered. The baby died of severe perinatal asphyxia. Autopsy showed a mass around the airway which turned out to be ectopic thymus on histopathology. Ectopic thymus can present as periglottic mass without externally visible cervical swelling and can cause difficult intubation which may lead to serious adverse outcome including death if not anticipated early and managed accordingly.

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SUMMARYCardiac tamponade is a clinical emergency. Detection of a swinging heart rate is one of the earliest markers of large pericardial effusion, in which the four cardiac chambers are free to float in a phasic manner. We present a case of a preterm baby, one of the twins, who developed sudden onset of deterioration in the form of swinging heart rate, fluctuation in blood pressure and desaturation, requiring emergency intubation and inotropic support. Bedside functional echo was performed, which demonstrated cardiac tamponade; an immediate echocardiography-guided tap was initiated and fluid was aspirated from the pericardial space. BACKGROUND

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Lymphatic filariasis is a major health problem in India with a large number of patients tending to be asymptomatic. In the Southeast and South Asian regions, Wuchereria bancrofti is the most prevalent parasite, causing filariasis in 99.4% of cases. While kidney involvement is a rare event in chronic filariasis, this case is unique because AA-type renal amyloidosis occurs in chronic W. bancrofti infection. We present here a unique case of lymphatic filariasis. The patient, a 25-year-old male who was previously diagnosed with right lower limb filarial lymphedema and had undergone lymphovenous anastomosis, was admitted for evaluation of persistent nephrotic-range proteinuria. Autoimmune markers in the form of anti-nuclear antibodies, anti-double-stranded DNA and anti-neutrophil cytoplasmic antibody were negative; C3 was normal. Urine analysis revealed inactive sediment with moderate proteinuria. Both serum and urine electrophoresis were negative for paraproteins and bone marrow aspirate and biopsy were normal. Evidence of active filarial infection was established on the basis of microfilariae in the peripheral smear and a positive W. bancrofti antigen test. Kidney biopsy revealed renal amyloidosis when stained with Congo red and anti-AA immunostain. The patient's proteinuria improved on conservative management with angiotensin-converting enzyme inhibitors and a course of antifilarial drugs. His proteinuria returned to <1 g/24 h with normalization of renal function and no significant proteinuria on periodic follow-up at 6-month and 1-year intervals. Repeat kidney biopsy after 1.5 years showed regression of amyloidosis. Repeat demonstration of filarial antigen and microfilariae in the peripheral smear were negative on multiple occasions during the follow-up period. Although various chronic infections can lead to secondary renal amyloidosis, this is the first case reported in world literature where secondary amyloidosis developed as a complication of chronic filarial infection due to W. bancrofti. This is probably also the first case reported in world literature where renal amyloidosis has an etiological association with W. bancrofti infection and where patient symptoms improved with antifilarial and antiproteinuric management.