ABSTRACT
Background: COVID19 and its etiological agent SARS-COV2 may cause a wide spectrum of clinical disease ranging from asymptomatic infection to severe disease and death. Clinical severity of disease has been linked to the variable immune responses to the virus. Identification of markers that distinguish clinically mild from severe disease may be of benefit in predicting disease severity. Design: Analysis of T cells (CD3), three subsets of macrophages (CD11b, CD163, and CD206), PDL1 and viral load in nasopharyngeal swabs of 20 people that were reverse transcriptase polymerase chain reaction positive with mild disease and 20 reverse transcriptase polymerase chain reaction negative controls versus the same variables in 20 lungs from people who died with COVID-19 versus normal aged matched controls was performed. The fatal COVID-19 lung data were stratified into the lung sections with high viral load versus lung sections, often from the same person, where viral involvement was not evident by in situ hybridization. Results: There was a 20X fold increase in the percentage of CD3+ cells in the viral positive nasopharyngeal swabs versus the controls whereas no change was noted in the CD3 count in the lungs of fatal COVID-19 with high viral load. The percentage of cells positive for the macrophage marker CD163 and for PDL1 were equivalent in the mild versus fatal disease samples. There was a significant increase in the number of cells expressing CD11b and CD206 in the fatal lungs with virus compared to the normal lungs;however, these increases were significantly higher in the nasopharyngeal swabs with mild infection. In the fatal COVID-19 lungs without detectable virus, the PDL1, CD11b and CD206 counts were very low, indicating that even in fatal disease the virus was inducing this immune response. Surprisingly, viral load was equivalent in mild versus fatal disease. Conclusions: It is concluded that markedly increased counts of CD3 T cells as well as CD11b and CD206 macrophages can differentiate mild versus fatal COVID-19 which may provide a way to predict clinical outcome by analyzing viral nasopharyngeal swabs for the T cell and macrophage response.
ABSTRACT
Introduction Bilateral cavitary lung lesions with calcification in a patient with chronic COVID requiring transplantation are described. Case Report 46-year-old woman presented for lung transplant with respiratory failure due to COVID-19 pneumonia following remdesivir, decadron, tocilizumab and baricitinib therapy. Cavitary upper lobe lung lesions were noted on imaging with negative cultures. She was started on VV ECMO as a bridge to bilateral lung transplant. Explanted lungs were consolidated and fibrotic with bilateral upper lobe calcification surrounding cavitary lesions. Varied microscopic pathology included NSIP pattern of inflammation, and foci of airway centered inflammation with giant cells suggesting chronic hypersensitivity reaction. The calcification was reminiscent of dendriform/metastatic calcification, and involved areas of necrotic/mummified parenchyma. Summary Cavitation as a late stage complication of COVID19 has been described in rare cases and is considered atypical. The constellation of findings in our case, including cavitary lesions with associated dendriform like calcifications are unique and maybe attributable to COVID19 itself +/- exacerbation of underlying chronic lung disease +/- intercurrent infection, or COVID19 related cavitation with superimposed secondary changes due to ECMO treatment. Bilateral lung transplantation has a reasonable short-term prognosis for patients with end stage respiratory failure secondary to COVID19;examination of these native lungs may expand our concept of COVID19 related chronic lung injury patterns.