Background Multisystem inflammatory syndrome is a severe manifestation of SARS-CoV-2 in children. The incidence of MIS-C after infection is poorly understood. There are very few cohorts describing MIS-C in Africa despite MIS-C being more common in Black children worldwide. Methods A cohort of children with MIS-C and healthy children was recruited from May 2020 until May 2021 from the two main paediatric hospitals in Cape Town, South Africa. Clinical and demographic data were collected, and serum was tested for SARS-CoV-2 antibodies. The incidence of MIS-C was calculated using an estimation of population exposure from seroprevalence in the healthy group. Summary data, non-parametric comparisons and logistic regression analyses were performed. Results Sixty eight children with MIS-C were recruited with a median age of 7 years (3.6, 9.9). Ninety seven healthy children were recruited with a 30% seroprevalence. The estimated incidence of MIS-C was 22/100 000 exposures in the city in this time. Black children were over-represented in the MIS-C group (62% vs 37%, p = 0.002). The most common clinical features in MIS-C were fever (100%), tachycardia (98.5%), rash (85.3%), conjunctivitis (77.9%), abdominal pain (60.3%) and hypotension (60.3%). The median haemoglobin, sodium, neutrophil count, white cell count, CRP, ferritin, cardiac (pro-BNP, trop-T) and coagulation markers (D-dimer and fibrinogen) were markedly deranged in MIS-C. Cardiac, pulmonary, central nervous and renal organ systems were involved in 71%, 29.4%, 27.9% and 27.9% respectively. Ninety four percent received intravenous immune globulin, 64.7% received methylprednisolone and 61.7% received both. Forty percent required ICU admission, 38.2% required inotropic support, 38.2% required oxygen therapy, 11.8% required invasive ventilation and 6% required peritoneal dialysis. Older age was an independent predictor for the requirement for ionotropic support (OR = 1.523, CI 1.074, 2.16, p = 0.018). The median hospital stay duration was 7 days with no deaths. Conclusion The lack of reports from Southern Africa does not reflect a lack of cases of MIS-C. MIS-C poses a significant burden to children in the region as long as the pandemic continues. MIS-C disproportionately affects black children. The clinical manifestations and outcomes of MIS-C in this region highlight the need for improved surveillance, reporting and data to inform diagnosis and treatment.
Background Multisystem inflammatory syndrome is a severe manifestation of SARS-CoV-2 in children. The incidence of MIS-C after infection is poorly understood. There are very few cohorts describing MIS-C in Africa despite MIS-C being more common in Black children worldwide. Methods A cohort of children with MIS-C and healthy children was recruited from May 2020 until May 2021 from the two main paediatric hospitals in Cape Town, South Africa. Clinical and demographic data were collected, and serum was tested for SARS-CoV-2 antibodies. The incidence of MIS-C was calculated using an estimation of population exposure from seroprevalence in the healthy group. Summary data, non-parametric comparisons and logistic regression analyses were performed. Results 68 children with MIS-C were recruited with a median age of 7 years (3.6, 9.9). 97 healthy children were recruited with a 30% seroprevalence. The estimated incidence of MIS-C was 22/100 000 exposures in the city in this time. Black children were over-represented in the MIS-C group (62% vs 37%, p=0.002). The most common clinical features in MIS-C were fever (100%), tachycardia (98.5%), rash (85.3%), conjunctivitis (77.9%), abdominal pain (60.3%) and hypotension (60.3%). The median haemoglobin, sodium, neutrophil count, white cell count, CRP, ferritin, cardiac (pro-BNP, trop-T) and coagulation markers (D-dimer and fibrinogen) were markedly deranged in MIS-C. Cardiac, pulmonary, central nervous and renal organ systems were involved in 71%, 29.4%, 27.9% and 27.9% respectively. 94.1% received intravenous immune globulin, 64.7% received methylprednisolone and 61.7% received both. 39.7% required ICU admission, 38.2% required inotropic support, 38.2% required oxygen therapy, 11.8% required invasive ventilation and 6% required peritoneal dialysis. Older age was an independent predictor for the requirement for ionotropic support (OR=1.523, CI 1.074, 2.16, p=0.018). The median hospital stay duration was 7 days with no deaths. Conclusion The lack of reports from Southern Africa does not reflect a lack of cases of MIS-C. MIS-C poses a significant burden to children in the region as long as the pandemic continues. MIS-C disproportionately affects black children. The clinical manifestations and outcomes of MIS-C in this region highlight the need for improved surveillance, reporting and data to inform diagnosis and treatment.
Immunodeficiency, whether primary or secondary, results in the disruption of normal immune response and function. Typical presentations of immune deficiency are increased susceptibility to infection, usually in a specific class depending on the immune pathway or cell affected. [1,2] The phenotype is broad, and autoimmunity, immune dysregulation and increased risk for malignancy may also be hallmarks of the immunodeficiency. [2,3] In the absence of secondary immunodeficiency, severe infections in otherwise healthy children can alert clinicians to single-gene inborn errors of immunity or primary immunodeficiency disorders (PIDDs). [1,4] In tuberculosis (TB)-hyperendemic settings such as South Africa (SA), the risk for infection with TB cumulates with exposure, which provides an interesting context for the study of PIDD, in particular Mendelian susceptibility to mycobacterial disease (MSMD). [5][6][7][8] MSMD is molecularly characterised by errors in the interleukin 12 (IL-12) and interferon gamma (IFN-γ) pathway. [9] IFN-γ is a key cytokine in both innate and adaptive responses against viruses and intracellular bacteria, namely mycobacteria. [9][10][11] There is a dynamic balance between the host and the organism that determines the course of TB infection. [4,[12][13][14][15] The risk of progression to active disease is highest in infants aged <12 months and lowest in children aged 5 -10 years, the 'wonder years' . [6] Severe disease implies that there is either poor host control of the infection, i.e. dissemination, or a complex disease manifestation, often with severe sequelae such as TB empyema or pericarditis. [15] Non-severe disease implies that the host has managed to control the pathogen, resulting in contained disease. [15] Impaired response to IFN-γ is caused by mutations in the IFNGR1, IFNGR2, STAT1, CYBB, IRF8 and NEMO genes. [9,10] Deficient production of IFN-γ is associated with mutations in IL12B, IL12RB1, IL12RB2, TYK2, SPPL2a and ISG15. [9,10] MSMD is a PIDD characterised by selective predisposition to infections, typically with BCG or poorly pathogenic mycobacteria (e.g. Mycobacterium avium complex, M. kansasii, M. ghodii). [10,12] Individuals with MSMD are also predisposed to infection with M. tuberculosis complex (MTBC), Salmonella species, Listeria, Candida species, Toxoplasma species, and This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.
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