Friends,

As we await the Resurrection, I have been doing as much research on SARS-CoV-2 as I can. As many of you know, I am working on a vaccine, which, thus far, has failed. Every single mouse shows no immunity. But I am pushing onward.

Both LSU and Tulane, treating one of the first epicenters of the disease in these United States, have a vital role at dispensing good research on this novel disease. As such, I have vigilantly watched for pre-published studies coming from these institutions. One of the first is Pulmonary and Cardiac Pathology in Covid-19: The First Autopsy Series from New Orleans

Here's what I have learned:

1. Autopsies were done on four morbidly obese, hypertensive African Americans, three with insulin-controlled diabetes. They were 44-76 years old.

2. The course of their disease included 3 days of fever around 101 and mild cough. On day 4, they developed respiratory distress and were hospitalized. Soon after, they were intubated and put in the ICU. Chest x-rays showed bilateral ground-glass opacities.

3. All four patients were put on broad spectrum antibiotics, including vancomycin, azithromycin, and aefepime. One patient received a steroid.

4. Lab findings showed high ferritin, fibrinogen, prothrombin time, glucose, AST, and creatinine. D-dimers in two were very high. CBC showed low lymphocytes and high neutrophils. All tested positive for Covid-19.

5. Autopsy of the lungs revealed no emboli. Bronchi had pink froth in three patients; in the other there was white mucous. All had serosanguinous pleural effusions. Lung parenchyma showed evidence of ARDS: edema and firmness. Dark hemorrhage were present in the peripheral parenchyma in three patients.

6. One patient who was on immunosuppressive methotrexate had advanced pneumonia with focal consolidation. The other three showed no gross evidence for an inflammatory process nor did these three have any neutrophilic infiltrate, which if present would suggest a bacterial suprainfection.

7. Slides of the lungs showed extensive damage to the alveoli. The alveoli were filled with CD4+ and CD8+ lymphocytes. Inside the alveoli were type 2 pneumocytes showing enlarged cells, enlarged nuclei, and eosinophilic nucleoli, consistent with damage from virus. CD61+ megakaryocytes, possibly with receptors for the virus, were present in alveolar capillaries. Fibrin and platelets were also found in these capillaries, which may have increased the inflammatory process there.

8. Three hearts were examined, each was enlarged (likely present before infection). Coronary arteries were not blocked by clots nor plaque formation. Slides of the heart revealed there was no obvious significant viral myocarditis. There was, however, scattered necrosis of individual heart muscle cells.

9. Death was caused by diffuse alveolar damage and CD4+ collection around small vessels, significant bleeding in the lungs, and possibly an overly aggressive cytokine and platelet response to the infection

10. Therapy, the authors suggest, should target the virus itself and the thrombotic effects the virus has on the lungs. Possibly a third branch of treatment could focus on the cytokine storm, which likely caused the CD4+ and CD8+ invasion of the alveoli.

If any of you have additional studies you would share, please share them here.

Yours,
TulaneLSU

This post was edited on 4/11/20 at 9:20 pm