Background: Globally, very few childhood deaths have been attributed to coronavirus disease 2019 . We evaluated clinical, microbiologic and postmortem histopathologic findings in childhood deaths in whom severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was identified antemortem or postmortem. Methods: Surveillance of childhood deaths was ongoing during the initial COVID-19 outbreak in South Africa from April 14, 2020, to August 31, 2020. All children hospitalized during this time had a SARS-CoV-2 test done as part of standard of care. Postmortem sampling included minimally invasive tissue sampling (MITS) of lung, liver and heart tissue; blood and lung samples for bacterial culture and molecular detection of viruses (including SARS-CoV-2) and bacteria. The cause of death attribution was undertaken by a multidisciplinary team and reported using World Health Organization framework for cause of death attribution. Results: SARS-CoV-2 was identified on antemortem and/or postmortem sampling in 11.7% (20/171) of deceased children, including 13.2% (12/91) in whom MITS was done. Eighteen (90%) of 20 deaths with SARS-CoV-2 infection were <12 months age. COVID-19 was attributed in the causal pathway to death in 91.7% (11/12) and 87.5% (7/8) cases with and without MITS, respectively. Lung histopathologic features in COVID-19-related deaths included diffuse alveolar damage (n = 6, 54.5%), type 2 pneumocyte proliferation (n = 6, 54.5%) and hyaline membrane formation (n = 5, 36.4%). Culture-confirmed invasive bacterial disease was evident in 54.5% (6/11) of COVID-19 attributed deaths investigated with MITS. Conclusions: COVID-19 was in the causal pathway of 10.5% (18/171) of all childhood deaths under surveillance. The postmortem histopathologic features in fatal COVID-19 cases in children were consistent with reports on COVID-19 deaths in adults; although there was a high prevalence of invasive bacterial disease in the children.

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The lysosomal storage disorders are a group of diseases that are typified by an accumulation of waste products in the lysosomes. Mucopolysaccharidoses are lysosomal storage disorders due to diverse lysosomal enzyme deficiencies. Ms HT was 2 years and 5 months old when she presented to our metabolic bone clinic with clinical features that were suggestive of a genetic syndrome that was associated with a metabolic bone disease. The urine GAG spot test was positive. The MPS screen identified a reduction in arylsulfatase B activity and sequencing of the ARSB gene detected a pathogenic variant, in keeping with Maroteaux-Lamy syndrome. The diagnosis of MPS is confirmed by urine GAG, enzyme activity analysis and genetic testing. The available treatments include hematopoietic stem cell transplantation, enzyme replacement therapy and surgery. MPSs are heterogeneous, progressive, multisystem diseases for which diagnosis is often delayed. Greater awareness of MPS will enable early diagnosis and treatment. Treatment is however costly and is frequently unavailable to patients in the public sector.

Cryptococcus neoformans is a yeast like fungus, which is commonly found in bird droppings, especially pigeons. Most cases of cryptococcal infections occur in immunocompromised patients or in those who are on long term immunosuppressant therapies. Cryptococcal infection usually presents as a meningoencephalitis or a pulmonary infection. Skin, bone and genital infections are very rare. We report the second case of vaginal cryptococcossis to be reported in English literature and the first to be imaged with CT and MRI.