Gross and Histopathology of COVID-19 With First Histology Report of Olfactory Bulb Changes

Multi-Organ Histopathological Changes in a Mouse Hepatitis Virus Model of COVID-19

“…The most common clinical presentation of severe COVID-19 is acute respiratory failure consistent with the acute respiratory distress syndrome (ARDS). Studies have shown diffuse alveolar damage with hyaline membrane formation, pneumocyte activation, microvascular thrombi, lymphocytic inflammation, proteinaceous edema, vascular remodeling via intussusceptive angiogenesis in the presence of microvascular thrombi, fibrosis, chronic inflammation, loose fibrous plugs associated with organizing pneumonia, endothelial injury with vacuolization of the cytoplasm and detachment of cells in small and medium-sized pulmonary arteries, deposition of fibrin and erythrocytes in the alveolar spaces and septa, hemorrhage, and hemosiderin deposition accompanied by complement complex deposition (especially near the alveolar capillaries), as well as alveolar type II (AT2) cell hyperplasia, fibrin exudates, vascular congestion, and mononuclear and multinucleated giant cell alveolar inflammation (with a noted absence of neutrophilic inflammation) in humans with COVID-19 [ 64 , 78 , 79 , 80 , 81 , 82 ].…”

“…Histopathologically, inflammatory cell cuffs around small blood vessels and degenerative neurons, inflammatory cell infiltration and focal hemorrhages were observed in humans with COVID-19 [ 80 ]. These findings correlate well with our observations in MHV-1 infected mice, strongly suggesting the usefulness of the mice model to study mechanisms occurring in SARS-CoV-2 infection in humans.…”

“…The same study found high levels of the blood enzyme troponin, an indicator of heart damage, in 76% of patients tested, even though heart function appeared to be generally preserved. Furthermore, current evidence demonstrates myocardial inflammation with or without direct cardiomyocyte damage in humans with SARS-CoV-2 infection [ 77 , 78 , 79 , 80 , 94 , 95 , 96 , 97 ]. Myocarditis results from direct heart invasion by the virus itself or more commonly by inflammation caused by cytokine storm, resulting in an enlarged and weakened heart, leading to low blood pressure and fluid deposition in the lungs.…”

“…Kidney histopathology examined in an autopsy series of 42 patients who died with COVID-19 showed varying degrees of acute tubular necrosis, collapsing focal segmental glomerulosclerosis [ 85 , 86 , 87 , 88 , 89 , 90 , 91 , 102 , 103 , 104 , 105 , 106 , 107 , 108 ], interstitial infiltration by lymphocytes, tubular epithelial cell necrosis, fibrinoid necrosis of blood vessels, and microthrombi in small vessels. There were also erythrocyte casts in some of the tubules (erythrocyturia), as well as ballooned glomeruli with mild mesangial expansion akin to diabetic nephropathy class IIa [ 80 , 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 ]. We also found similar events when mice were inoculated with MHV-1.…”

Zebrafish as a Translational Model: An Experimental Alternative to Study the Mechanisms Involved in Anosmia and Possible Neurodegenerative Aspects of COVID-19?

“…The SARS-CoV-2 infection has been associated with brain damage in the olfactory bulb and its neuroanatomically connected areas. Stoyanov and colleagues (2020) described severe neurodegeneration and inflammatory cell infiltration in the olfactory bulb of two COVID-19 patients (Stoyanov et al, 2020). In a post-mortem case series conducted in Germany, neuropathological analysis of glial activation patterns revealed a high degree of astrogliosis and microgliosis in the olfactory bulb, with low levels of cytotoxic-T cell infiltration (Matschke et al, 2020).…”