The clinical presentation of our patient associating fever, hypotension, diffuse skin rash, and multisystem organ dysfunction was initially suggestive of septic shock complicated by TSS. After having had negative results from the bacteriological analysis and having considered the COVID 19 pandemic, however, we have raised concerns for serious syndromes caused by this virus such as MIS-C. The patient fulfilled MIS-C criteria and showed overlapping features with Kawasaki disease shock syndrome (KDSS) and toxic shock syndrome. We finally retained the diagnosis of MIS-C with features of TSS secondary to COVID19 considering the normal heart function and the absence of coronary lesions. TSS is a severe syndrome secondary to the uncontrolled activation of the immune system by “superantigens”, proteins that stimulate T cells, leading to a massive production and release of cytokines [
3,
6]. Bacterial species, such as
Staphylococcus aureus and
Streptococcus pyogenes, are well-known to produce exotoxins that can function as superantigens. Interestingly, some viruses including SARS-CoV-1 can also act as superantigens [
3,
6]. As for SARS-CoV-2 this “superantigen” role has not yet been proved. However, the hyperinflammatory state and cytokine storm noticed in patients, who are infected by SARS-CoV-2 may suggest the existence of a similar immunological phenomenon to the one described in TSS [
1,
3,
7‐
9]. As in the majority of patients having MIS-C, patient presenting features of TSS due to COVID19, usually had a negative RT-PCR test, while the serologic testing for SARS-CoV-2 reported positive in many cases [
1,
3,
7‐
9]. In our case, 2 weeks after being tested positive for SARS-CoV-2 by RT-PCR, the patient developed symptoms and biological abnormalities fulfilling the definition of MIS-C. Her negative second test by RT-PCR elucidate the post-infectious MIS-C’s pathogenesis’s theory. Typical treatment for TSS includes fluid resuscitation and pressor support [
10]. The majority of reported children responded well to those treatments with the resolution of hypotension after volume resuscitation and only a few cases required the use of inotropes. The use of IVIG and corticosteroids in TSS remains controversial. Chen et al. [
11] reported 62 children with TSS, 24 of them received corticosteroid. In this study, the residual morbidity was higher in patients who received IVIG or steroids. The authors explained that these results may be due to the fact that these treatments were given to more seriously ill patients. However, others authors reported that the use of IVIG has improved the outcome of patients with TSS [
12]. In patients with MIS-C, the optimal therapy remains unknown [
13]. Empirical treatment with IVIG alone or associated with corticosteroids has been received by many children with MIS-C based on Kawasaki disease guidelines [
13‐
16]. Previously, In patients with MIS-C, corticosteroid has been provided as a second-line therapy for children who remain unwell 24 h after infusion of IVIG or in those with severe symptoms [
3,
17,
18]. Actually, steroids such as methylprednisolone may not be used as rescue therapy but rather as a first line therapy for MIS-C. Ouldali et al. has compared IVIG plus methylprednisolone vs IVIG alone as initial therapy in MIS-C through a retrospective cohort study of 106 patients with confirmed MIS-C [
13]. They showed that only 9% of children treated with IVIG and methylprednisolone did not respond to treatment vs 51% in the IVIG alone group. In this study, IVIG and methylprednisolone therapy compared to IVIG alone was also significantly associated with lower risk of use of second-line therapy, hemodynamic support, acute left ventricular dysfunction occurring after initial therapy, and duration of stay in the pediatric intensive care unit. Methylprednisolone was given to patients at a posology of 1.6 mg/kg to 2 mg/kg/d for 5 days or as a bolus of 15 to 30 mg/kg/d for 3 days. In our patient there was no signs of improvement after receiving IVIG. The child received only hydrocortisone, for the refractory shock to deal with an eventual acute adrenal failure. He didn’t receive methylprednisolone. And the outcome was rapidly fatal. High doses of methylprednisolone are useful to have a powerful anti-inflammatory effect, to fight the inflammatory storm. Jonat et al. [
19] have developed a protocol for the evaluation, management, and follow-up of patients with MIS-C. This protocol states that all patients fulfilling MIS-C criteria should receive IVIG plus corticosteroids. The recommended dose of steroids is variable depending of the severity of the clinical presentation. Severe cases should receive methylprednisolone 20–30 mg/kg/d for 1–3 days (maximum 1 g/d), followed by 2 mg/kg/d (maximum 60 mg/d). In these severe cases, steroids should be tapered slowly to avoid rebound illness. Refractory patients to pulse glucocorticoids should be treated by Anakinra [
19]. Other biologic immunomodulators may be considered in severe cases with no response to anakinra. Infliximab and tocilizumab, used in other hyper-inflammatory syndromes as biologic immunomodulators have been tried to modulate the dysregulated hyper-inflammation apparent in MIS-C with promised result in adults [
20,
21]. However, there is limited evidence to suggest these therapies in children.