COVID-19 in 28-Week Triplets Caused by Intrauterine Transmission of SARS-CoV-2-Case Report.

Since the beginning of the COVID-19 pandemic, in-utero transmission of SARS-CoV-2 remains a rarity and only very few cases have been proven across the world. Here we depict the clinical, laboratory and radiologic findings of preterm triplets born at 28 6/7 weeks to a mother who contracted COVID-19 just 1 week before delivery. The triplets showed SARS-CoV-2 positivity right after birth, developed significant leukopenia and early-onset pulmonary interstitial emphysema. The most severely affected triplet I required 10 days of high-frequency oscillatory ventilation due to failure of conventional invasive ventilation, and circulatory support for 4 days. Despite a severe clinical course in two triplets (triplet I and II), clinical management without experimental, targeted antiviral drugs was successful. At discharge home, the triplets showed no signs of neurologic or pulmonary sequelae. Placental immunohistology with SARS-CoV-2 N-protein localized strongly to syncytiotrophoblast cells and, to a lesser extent, to fetal Hofbauer cells, proving intrauterine virus transmission. We discuss the role of maternal viremia as a potential risk factor for vertical transmission. To the best of our knowledge, our report presents the earliest unequivocally confirmed prenatal virus transmission in long-term surviving children, i.e., at the beginning of the third trimester.

First paediatric cohort for the evaluation of inflammation in endomyocardial biopsies derived from congenital heart surgery.

BACKGROUND: Endomyocardial biopsies (EMB) are the gold standard for the diagnosis of myocarditis in children and adults. The existing WHO/ISFC criteria for lymphocytic cell infiltrates by are based on the myocardium of adults. The aim of this study was to present a paediatric control cohort for the evaluation of inflammation in EMB of children. METHODS: In this study endomyocardial tissue from 62 children under 4 years of age was investigated, being collected during a planned open heart surgery with routine resection from ventricular site. Patients had no history of infection or myocardial inflammation. The heart tissue was formalin fixed and embedded in paraffin. Four µm thick tissue sections were stained with haematoxylin and eosin, Masson's trichrome, and Giemsa. Immunohistochemical stainings included quantitative evaluation of CD3+ T cells, CD20+ B cells, CD68+ macrophages and MHCII expression. RESULTS: The myocardium was obtained in 96.8% (n = 60) of the cases from the right and in 3.2% (n = 2) from the left ventricle. The median age (interquartile range) at biopsy was 0.5 years (0.3-0.9), 66.1% male. Within this cohort, a median of 2.5/mm2 (1.0-4.0) CD3+ T cells, 0.5/mm2 (0.0-0.6) CD20+ B cells and 4.0/mm2 (2.5-6.0) CD68+ macrophages were detected. The MHC II grade was 0 in 71.0% (n = 44) and 1 in 29.0% (n = 18). CONCLUSION: This is the first paediatric control cohort being relevant for the correct interpretation of inflammatory heart diseases in EMB. The lymphocytic cell numbers in children needing congenital heart surgery without myocardial inflammation are below the existing values in adults.