Lungs Infected With Sars‐Cov 2.......Immunohistochemistry for the receptor of the SARS‐COV 2, ACE2, and its priming activatorTMPRSS2 revealed that both proteins co‐localize in airway cells. In particular, the ACE2 protein was expressed in both endothelial cells and alveolar type I and II pneumocytes in the areas of histological diffuse alveolar damage (DAD). Pneumocytes but not endothelial cells also expressed TMPRSS2. There are no distinctive histological features of SARS‐COV 2 infection with respect to SARS‐COV 1 and other DAD with different aetiology.

Pathological Post Mortem Findings in Lungs Infected With Sars‐Cov 2:

Abstract

Italy was the first European nation to be massively infected by SARS‐COV 2. Up to the end of May 2020 more than thirty‐three thousand deaths had been recorded in Italy with a large prevalence among males, those over 75 years of age, and in association with co‐morbidities. We describe the lung pathological and immunohistochemical post‐mortem findings at the autopsy of 9 patients who died of SARS‐COV 2 associated disease. We found in the lung tissues of all patients histological changes consistent with diffuse alveolar damage in various evolution phases ranging from acute exudative to acute proliferative to fibrotic phase. Alveolar damage was associated a prominent involvement of the vascular component in both the interstitial capillaries and in the mid‐size vessels, with capillary fibrin micro‐thrombi, as well as organized thrombi even in medium sized arteries, in most cases not related to sources of embolism. Eosinophilic infiltrate was also seen, probably reactive to pharmacological treatment. Viral RNA of SARS‐COV 2 was detected from the lung tissues of all the nine patients. Immunohistochemistry for the receptor of the SARS‐COV 2, ACE2, and its priming activatorTMPRSS2 revealed that both proteins co‐localize in airway cells. In particular, the ACE2 protein was expressed in both endothelial cells and alveolar type I and II pneumocytes in the areas of histological diffuse alveolar damage (DAD). Pneumocytes but not endothelial cells also expressed TMPRSS2. There are no distinctive histological features of SARS‐COV 2 infection with respect to SARS‐COV 1 and other DAD with different aetiology. The identification of the cause of death in course of SARS‐COV 2 infection is more likely multi‐factorial.

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