Secondary Hemophagocytic Lymphohistiocytosis in a Neonate with SARS-CoV-2 Infection.

BACKGROUND Infants born to mothers with Coronavirus disease (COVID-19) are susceptible to infection, either vertically or horizontally. The mechanism is not completely understood. Regardless, it is rare that an infant with COVID-19 suffers from serious, life-threatening complications. We speculate that one of these complications can be hemophagocytic lymphohistiocytosis (HLH), a dysregulated hyperinflammatory response that leads to multi-organ failure. CASE REPORT We describe a case of a female newborn, born to a SARS-CoV-2-positive mother via cesarean section delivery at 35 weeks of gestation, that tested positive for SARS-CoV-2 on the first day after birth. The patient presented with progressive respiratory distress, intermittent fever, splenomegaly, and cytopenia. Hemophagocytic lymphohistiocytosis (HLH) work-up was done, which showed hyperferritinemia, hypofibrinogenemia, and hypertriglyceridemia. Bone marrow aspirate showed hemophagocytic activity of both red blood cells and platelets. We suspect that the virus triggered HLH, which led to the patient's death at 51 days of age due to severe respiratory failure. CONCLUSIONS Infants and children suffer from milder symptoms than adults when infected with SARS-CoV-2, for reasons not well understood, although multiple hypotheses have been proposed, which are discussed in this paper. However, there is a possibility that the severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) virus can cause HLH and multi-system inflammatory syndrome in children (MIS-C).

Coronaviruses in children: A review of potential mechanisms of childhood protection.

AIM: The 2019 coronavirus disease (COVID-19) has spread worldwide and the number of cases continues to rise exponentially. Epidemiologic reports indicate that severity of illness increases with age. However, the reasons behind the relative protection of children and infants are unclear. Whether the rationale is host-related or virus dependent is important to determine since the latter could change with viral mutations. We review factors that could affect the susceptibility of children to the novel coronavirus. METHODS: We search publications indexed on PUBMED. RESULTS: Descriptions of the pathophysiology of current and previous coronavirus infections suggest several viral targets and immunomodulatory pathways affecting the severity of illness. There is limited evidence to suggest age-variability of viral cell receptors and transmembrane co-factors required for coronavirus entry and replication. However, the ensuing cytokine storm and the effect of higher melatonin in children are age-dependent and could explain decreased disease variability in children. CONCLUSION: We believe that current evidence suggests host factors can play a role in disease severity in children and thus may remain protective despite potential virus mutation in the future. However, we recognise and discuss avenues of future research that can further illuminate the reasons children are protected from severe COVID-19 illness.