Morphological characteristic of coronavirus infection of the first and second waves of the pandemic

Introduction. A peculiarity of the first two waves of the epidemic of a novel coronavirus infection was that during their development only diagnostic methods, treatment regimens and anti-epidemic measures were only being developed, there were no vaccines and no mass vaccination was carried out. In this regard, the pandemic of the novel coronavirus infection of the first two waves is characterized by spontaneous progression of the disease.
Aim of the research. Comparative study of morphological and clinical features of the novel coronavirus infection in the 1st and 2nd waves of the pandemic in 2020.
Materials and methods. The autopsy protocols of deceased patients at the City Clinical Hospital No. 1 (Novosibirsk) during the 1st (May — June 2020) (1st group) and 2nd (October — December 2020) (2nd group) waves of the epidemic were analyzed. The 1st group included 30 cases, that is 14 women (46.7%) and 16 men (53.3%), in the 2nd — 110 cases, of which 43 were women (39.1%) and 67 – men (60.9%). In all cases, the presence of SARS-CoV-2 RNA in nasopharyngeal swabs from the patients was confirmed by polymerase chain reaction.
Results. The novel coronavirus infection (coronavirus disease 2019 (COVID-19), ICD-10 code: U07.1) as the principal diagnosis in both the 1st and 2nd waves was recorded in more than 66% of observations. Among the comorbidities, the circulatory and endocrine disorders (primarily diabetes mellitus and obesity), kidneys and urinary tract diseases, mainly chronic pyelonephritis, prevailed. The COVID-19 pneumonia was predominantly bilateral polysegmental serоhemorrhagic in nature, however, in the 1st wave of the pandemic, the frequency of subtotal and seropurulent pneumonias was higher than in patients hospitalized during the 2nd wave. Diffuse alveolar damage in the 1st wave of the epidemic was characterized by the predominance of the early (exudative) phase of inflammation, in contrast to the 2nd wave, which was characterized by the predominance of the late (productive) phase in patients. Histologically, in patients of the 1st wave, the signs of exudative inflammation and hemorrhagic phenomena (with neutrophils and hyaline membranes in the alveoli, infarctions caused by thrombosis and pulmonary thromboembolism) prevailed. In the 2nd wave, signs of productive inflammation were more common in the lungs (predominance of macrophages in the alveoli, organizing pneumonia (pneumofibrosis), squamous cell metaplasia).
Conclusion. The differences in the course of the novel coronavirus infection in the 1st and 2nd waves of the 2020 epidemic concerned primarily the frequency and structure of comorbidities and the level of polymorbidity, which were higher in patients during the 2nd wave. The severity of lung damage in patients of the 2nd wave was less pronounced: subtotal bilateral pneumonias were less common, lower lobe seropurulent pneumonias were more common. Diffuse alveolar damage in the 1st wave of the epidemic was characterized by the predominance of the early (exudative) phase, in contrast to the 2nd wave, which was characterized by the predominance of the late, productive phase of inflammation.

1. Guo Y.R., Cao Q.D., Hong Z.S. et al. (2020). The origin, transmission and clinical therapies on coronavirus disease 2019 (COVID-19) outbreak — an update on the status. Mil. Med. Res., 7 (1), 11. doi: 10.1186/s40779-020-00240-0.

2. Bevova M.R., Netesov S.V., Aulchenko Yu.S. (2020). The new coronavirus COVID-19 infection. Molecular Genetics, Microbiology and Virology, 38, 2, 51–58. doi: 1017116/molgen20203802151.

3. Zhou P., Yang X.L., Wang X.G. et al. (2020). A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature, 579 (7798), 270–273. doi: 10.1038/s41586-020-2012-7.

4. Menter T., Haslbauer J.D., Nienhold R. et al. (2020). Postmortem examination of COVID-19 patients reveals diffuse alveolar damage with severe capillary congestion and variegated findings in lungs and other organs suggesting vascular dysfunction. Histopathology, 77 (2), 198–209. doi: 10.1111/his.14134.

5. Hoffmann M., Kleine-Weber H., Schroeder S. et al. (2020). SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell, 181 (2), 271–280.e8. doi: 10.1016/j.cell.2020.02.052.

6. Zairatiants O.V., Samsonova M.V., Mikhaleva L.M. et al. (2020). COVID-19 Pathological Anatomy: Atlas. Moscow, 140 p. (In Russ.)

7. Bösmüller H., Traxler S., Bitzer M. et al. (2020). The evolution of pulmonary pathology in fatal COVID-19 disease: an autopsy study with clinical correlation. Virchows Arch., 477 (3), 349–357. doi: 10.1007/s00428-020-02881-x.

8. Konopka K.E., Nguyen T., Jentzen J.M. et al. (2020). Diffuse alveolar damage (DAD) resulting from coronavirus disease 2019 infection is morphologically indistinguishable from other causes of DAD. Histopathology, 77 (4), 570–578. doi: 10.1111/his.14180.

9. Wichmann D., Sperhake J.P., Lütgehetmann M. et al. (2020). Autopsy findings and venous thromboembolism in patients with COVID-19: a prospective cohort study. Ann. Intern. Med., 173 (4), 268–277. doi: 10.7326/M20-2003.

10. Kogan E.A., Kukleva A.D., Berezovskiy Yu.S. et al. (2021). Clinical and morphological characteristics of SARS-CoV-2-related myocarditis proven by the presence of viral RNA and proteins in myocardial tissue. Archive of Pathology, 83, 4, 5–13. doi: 1017116/patol2021830415.

11. Lindner D., Fitzek A., Bräuninger H. et al. (2020). Association of cardiac infection with SARS-CoV-2 in confirmed COVID-19 autopsy cases. JAMA Cardiol., 5 (11), 1281–1285. doi: 10.1001/jamacardio.2020.3551.

12. Khryanin A.A., Sturov V.G., Nadeev A.P., Bocharova V.K. (2021). Dermatological manifestations in novel coronavirus infection COVID-19. Thrombosis, Hemostasis and Rheology, 2, 30–37. doi: 10/25555/THR.2021.2.0971.

13. Nadeev A.P., Alekseev A.Yu., Morozov D.V. et al. (2020). Clinical and anatomical case study of the first death from the novel coronavirus infection in the Novosibirsk Region. Journal of Siberian Medical Sciences, 4, 99–109.

14. Pomara C., Volti G.L., Cappello F. (2020). COVID-19 deaths: are we sure it is pneumonia? Please, autopsy, autopsy, autopsy! J. Clin. Med., 9 (5): 1259. doi: 10.3390/jcm9051259.

15. Edler C., Schröder A.S., Aepfelbacher M. et al. (2020). Dying with SARS-CoV-2 infection — an autopsy study of the first consecutive 80 cases in Hamburg, Germany. Int. J. Legal. Med., 134 (4), 1275–1284. doi: 10.1007/s00414-020-02317-w.

16. Remmelink M., De Mendonça R., D’Haene N. et al. (2020). Unspecific post-mortem findings despite multiorgan viral spread in COVID-19 patients. Crit. Care, 24 (1), 495. doi: 10.1186/s13054-020-03218-5.

17. Ojo A.S., Balogun S.A., Williams O.T., Ojo O.S. (2020). Pulmonary fibrosis in COVID-19 survivors: predictive factors and risk reduction strategies. Pulm. Med., 2020, 6175964. doi: 10.1155/2020/6175964.

18. Li H., Liu L., Zhang D. et al. (2020). SARS-CoV-2 and viral sepsis: observations and hypotheses. Lancet, 395 (10235), 1517–1520. doi: 10.1016/S0140-6736(20)30920-X.

19. Farkash E.A., Wilson A.M., Jentzen J.M.J. (2020). Ultrastructural evidence for direct renal infection with SARS-CoV-2. Am. Soc. Nephrol., 31 (8), 1683–1687. doi: 10.1681/ASN.2020040432.