Pathomorphology of lungs lesions in new coronavirus infection Covid-19

Huang L, Zhang C, Liu S, Zhao P, Liu H, Zhu L, Tai Y, Bai C, Gao T, Song J, Xia P, Dong J, Zhao J, Wang FS. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med. 2020 Apr;8(4):420-422.

A 50-year-old man was admitted to a fever clinic on Jan 21, 2020, with symptoms of fever, chills, cough, fatigue and shortness of breath. He reported a travel history to Wuhan Jan 8–12, and that he had initial symptoms of mild chills and dry cough on Jan 14 (day 1 of illness) but did not see a doctor and kept working until Jan 21. Chest x-ray showed multiple patchy shadows in both lungs, and a throat swab sample was taken. On Jan 22 (day 9 of illness), the Beijing Centers for Disease Control (CDC) confirmed by reverse real-time PCR assay that the patient had COVID-19.

The right lung showed evident desquamation of pneumocytes and hyaline membrane formation, indicating acute respiratory distress syndrome (ARDS; figure 2A). The left lung tissue displayed pulmonary oedema with hyaline membrane formation, suggestive of early-phase ARDS (figure 2B). In both lungs- interstitial mononuclear infiltrates, dominated by lymphocytes. Multinucleated syncytial cells with atypical enlarged pneumocytes characterised by large nuclei, amphophilic granular cytoplasm, and prominent nucleoli were identified in the intra-alveolar spaces, showing viral cytopathic-like changes

The cut surfaces show tan-grey consolidation and/or patchy hemorrhagic areas.
(B)Grossly visible pulmonary emboli, and a peculiar patchy gross appearance of the lung parenchyma (both externally as well as on the cut sections), and thrombosis of the prostatic vein. Pleural adhesions were identified in one complete autopsy.

vaccine and therapeutic development.” Nature reviews. Microbiology vol. 7,3 (2009): 226-36. doi:10.1038/nrmicro2090

apoptosis;
B - Recruited macrophages releases cytokines causing capillary permeability increase and consequent neutrophils recruitment;
C - Neutrophils migrate and degranulate, culminating in permanent damage to cells, resulting in alveolar-capillary barrier disruption;
D - Interstitial and alveolar edema.

Batah, S. S., & Fabro, A. T. (2021). Pulmonary pathology of ARDS in COVID-19: A pathological review for clinicians. Respiratory medicine, 176, 106239. https://doi.org/10.1016/j.rmed.2020.106239

edema, neutrophil infiltration in the intra-alveolar space and mainly by hyaline membrane formed by fibrin polymerization contained in the plasma liquid, being recognized as DAD hallmark;
B - The second or proliferative phase: intense fibroblast/myofibroblast recruitment and proliferation, with subsequent extracellular matrix deposition. Over time and together with the fibrotic deposition, there is also the reepithelization by type I and II pneumocytes.

– green arrow); alveolar-capillary barrier injury with red blood cell extravasation (B – green arrows); intense inflammatory cells infiltration into the intra-alveolar space.
the proliferative phase: an exacerbated fibroblast/myofibroblast proliferation which can form acute fibrinous organizing pneumonia (C - dark blue circle) or organizing pneumonia (C – dark green circle) with subsequent extracellular matrix deposition=>parenchymal remodeling and pulmonary fibrosis; pneumocytes squamous metaplasia and proliferation of multinucleated giant cells.
Thrombotic events in pulmonary small arteries (D) may occur in this phase due to NET's influence.

× 200)

Interstitial inflammation in COVID-19. The inflammatory cells are predominantly lymphocytes (Hematoxylin & eosin, original magnification × 200)

Diffuse alveolar damage in COVID-19. with hyaline membranes. (Hematoxylin & eosin, original magnification × 200).

the bronchial mucosa (Hematoxylin & eosin, original magnification × 200). 

large arterial vessel with mononuclear and neutrophilic infiltration (arrow in upper inset).
The lower inset shows an immunohistochemical staining of caspase 3 on the same lung specimen; these staining patterns were consistent with apoptosis of endothelial cells and mononuclear cells observed in the haematoxylin-eosin-stained sections.

Varga, Zsuzsanna et al. “Endothelial cell infection and endotheliitis in COVID-19.” Lancet (London, England) vol. 395,10234 (2020): 1417-1418. doi:10.1016/S0140-6736(20)30937-5

Targeting potential drivers of COVID-19: Neutrophil extracellular traps. The Journal of experimental medicine, 217(6)

the lung

(A)Deposition of C4d within the interalveolar septa demonstrated by DAB staining.
C4d image appears green (B) while the SARS-CoV2 spike protein appears red (C). D -merged image shows a significant degree of C4d and SARS-CoV2 co-localization, as revealed by intense yellow staining.
E–H, A similar pattern was observed using an anti-C5b-9 reagent whose image appears green, with a significant degree of C5b-9 and SARS-CoV2 co-localization, as revealed by intense yellow staining.

COVID-19: is it "typical" ARDS? Crit Care. 2020 May 6;24(1):198.