Clinical management of severe acute respiratory infection (SARI) when COVID-19 disease is suspected: Interim guidance recent multivariable analysis confirmed older age, higher Sequential Organ Failure Assessment (SOFA) score and d-dimer > 1 µg/L on admission were associated with higher mortality. This study also observed a median duration of viral RNA detection of 20.0 days (IQR 17.0-24.0) in survivors, but COVID-19 virus was detectable until death in non-survivors. The longest observed duration of viral shedding in survivors was 37 days (3,4).Building on evidence-informed guidelines developed by a multidisciplinary panel of health care providers with experience in the clinical management of patients with COVID-19 and other viral infections, including SARS and MERS, as well as sepsis and ARDS, this guidance should serve as a foundation for optimized supportive care to ensure the best possible chance for survival and to allow for reliable comparison of investigational therapeutic interventions as part of randomized controlled trials (5,6).There are few data on the clinical presentation of COVID-19 in specific populations, such as children and pregnant women. In children with COVID-19 the symptoms are usually less severe than adults and present mainly with cough and fever, and coinfection has been observed (7, 8). Relatively few cases have been reported of infants confirmed with COVID-19; those experienced mild illness (9). There is currently no known difference between the clinical manifestations of COVID-19 pregnant and non-pregnant women or adults of reproductive age. Pregnant and recently pregnant women with suspected or confirmed COVID-19 should be treated with supportive and management therapies, as described below, taking into account the immunologic and physiologic adaptations during and after pregnancy. * See Global Surveillance for human infection with coronavirus disease (COVID-19) for latest case definitions.

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Aims Immunocompromised patients have been excluded from studies of SARS-CoV-2 messenger RNA vaccines. The immune response to vaccines against other infectious agents has been shown to be blunted in such patients. We aimed to analyse the humoral and cellular response to prime-boost vaccination with the BNT162b2 vaccine (Pfizer-BioNTech) in cardiothoracic transplant recipients. Methods and results A total of 50 transplant patients [1–3 years post heart (42), lung (7), or heart–lung (1) transplant, mean age 55 ± 10 years] and a control group of 50 healthy staff members were included. Blood samples were analysed 21 days after the prime and the boosting dose, respectively, to quantify anti-SARS-CoV-2 spike protein (S) immunoglobulin titres (tested by Abbott, Euroimmun and RocheElecsys Immunoassays, each) and the functional inhibitory capacity of neutralizing antibodies (Genscript). To test for a specific T-cell response, heparinized whole blood was stimulated with SARS-CoV-2 specific peptides, covering domains of the viral spike, nucleocapsid and membrane protein, and the interferon-γ release was measured (QuantiFERON Monitor ELISA, Qiagen). The vast majority of transplant patients (90%) showed neither a detectable humoral nor a T-cell response three weeks after the completed two-dose BNT162b2 vaccination; these results are in sharp contrast to the robust immunogenicity seen in the control group: 98% exhibited seroconversion after the prime dose already, with a further significant increase of IgG titres after the booster dose (average > tenfold increase), a more than 90% inhibition capability of neutralizing antibodies as well as evidence of a T-cell responsiveness. Conclusions The findings of poor immune responses to a two-dose BNT162b2 vaccination in cardiothoracic transplant patients have a significant impact for organ transplant recipients specifically and possibly for immunocompromised patients in general. It urges for a review of future vaccine strategies in these patients.

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