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1.
J Vet Diagn Invest ; 35(3): 317-321, 2023 May.
Article in English | MEDLINE | ID: covidwho-20241750

ABSTRACT

Four turkeys from a commercial flock with acutely elevated mortality levels were submitted for postmortem examination and diagnostic workup. No clinical signs had been observed before death. On gross examination, hemorrhage and necrosis were present throughout the intestinal tracts, and the spleens were markedly enlarged and speckled. Microscopically, numerous, large basophilic-to-amphophilic intranuclear inclusion bodies were observed in mononuclear cells of the spleen and the lamina propria of the small intestine. In addition, there were lesions of diffuse villus blunting and necrosis of the small intestine, with large numbers of rod-shaped bacteria adhered to the epithelium and in the intestinal lumen. Hemorrhagic enteritis virus (HEV) infection was confirmed via PCR on the spleen. Clostridium perfringens was demonstrated in the small intestine by anaerobic culture and immunohistochemistry. The C. perfringens isolate was type F by PCR and, to our knowledge, necrotic enteritis in turkeys has not been described in association with C. perfringens type F infection.


Subject(s)
Clostridium Infections , Enteritis , Poultry Diseases , Animals , Enteritis/microbiology , Enteritis/veterinary , Poultry Diseases/microbiology , Intestines/microbiology , Clostridium perfringens , Necrosis/veterinary , Necrosis/pathology , Turkeys , Clostridium Infections/microbiology , Clostridium Infections/veterinary , Chickens
2.
J Med Virol ; 95(2): e28566, 2023 02.
Article in English | MEDLINE | ID: covidwho-2234665

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) caused by infection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) manifests diverse clinical pathologies involving multiple organs. While the respiratory tract is the primary SARS-CoV-2 target, acute kidney injury is common in COVID-19 patients, displaying as acute tubular necrosis (ATN) resulting from focal epithelial necrosis and eosinophilia, glomerulosclerosis, and autolysis of renal tubular cells. However, whether any renal cells are infected by SARS-CoV-2 and the mechanism involved in the COVID-19 kidney pathology remain unclear. METHODS: Kidney tissues obtained at autopsy from four severe COVID-19 patients and one healthy subject were examined by hematoxylin and eosin staining. Indirect immunofluorescent antibody assay was performed to detect SARS-CoV-2 spike protein S1 and nonstructural protein 8 (NSP8) together with markers of different kidney cell types and immune cells to identify the infected cells. RESULTS: Renal parenchyma showed tissue injury comprised of ATN and glomerulosclerosis. Positive staining of S1 protein was observed in renal parenchymal and tubular epithelial cells. Evidence of viral infection was also observed in innate monocytes/macrophages and NK cells. Positive staining of NSP8, which is essential for viral RNA synthesis and replication, was confirmed in renal parenchymal cells, indicating the presence of active viral replication in the kidney. CONCLUSIONS: In fatal COVID-19 kidneys, there are SARS-CoV-2 infection, minimally infiltrated innate immune cells, and evidence of viral replication, which could contribute to tissue damage in the form of ATN and glomerulosclerosis.


Subject(s)
Acute Kidney Injury , COVID-19 , Humans , COVID-19/pathology , SARS-CoV-2 , Kidney/pathology , Acute Kidney Injury/pathology , Necrosis/pathology
3.
Medicina (Kaunas) ; 59(1)2023 Jan 12.
Article in English | MEDLINE | ID: covidwho-2200508

ABSTRACT

Acute esophageal necrosis is a rare condition, characterized by a distinctive endoscopic/necropsic image-circumferential black area of the esophagus. This paper presents a case of a 78-year-old patient with recent history of a severe form of COVID-19 (2 months previously), with multiple comorbidities, which presents sudden death in hospital. Anatomic-pathological autopsy showed extensive esophageal necrosis, pulmonary thromboses, and coronarian and aortic atherosclerosis. The histopathological examination revealed necrosis of the esophageal mucosa and phlegmonous inflammation extended to the mediastinum, chronic pneumonia with pulmonary fibrosis, viral myocarditis, papillary muscle necrosis, and pericoronary neuritis. Thromboses and necroses were identified also in the liver, pancreas, and adrenal glands. Post-COVID-19 thromboses can manifest late, affecting various vascular territories, including esophageal ones. Their clinical picture may be diminished or absent in elderly and/or diabetic patients.


Subject(s)
COVID-19 , Humans , Aged , Autopsy , COVID-19/complications , COVID-19/pathology , Esophagus , Necrosis/pathology , Comorbidity
4.
Forensic Sci Med Pathol ; 18(4): 516-529, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-2007252

ABSTRACT

Clinical features of COVID-19 range from mild respiratory symptoms to fatal outcomes. Autopsy findings are important for understanding COVID-19-related pathophysiology and clinical manifestations. This systematic study aims to evaluate autopsy findings in paediatric cases. We searched PubMed, EMBASE, and Cochrane Database Reviews. We included studies that reported autopsy findings in children with COVID-19. A total of 11 studies (24 subjects) were included. The mean age of patients was 5.9 ± 5.7 years. Grossly, there was pericardial and pleural effusion, hepatosplenomegaly, cardiomegaly, heavy soft lung, enlarged kidney, and enlarged brain. The autopsy findings of the lungs were diffuse alveolar damage (78.3%), fibrin thrombi (43.5%), haemorrhage (30.4%), pneumonia (26%), congestion and oedema (26%), angiomatoid pattern (17.4%), and alveolar megakaryocytes (17.4%). The heart showed interstitial oedema (80%), myocardial foci of band necrosis (60%), fibrin microthrombi (60%), interstitial and perivascular inflammation (40%), and pancarditis (30%). The liver showed centrilobular congestion (60%), micro/macrovesicular steatosis (30%), and arterial/venous thrombi (20%). The kidney showed acute tubular necrosis (75%), congestion (62.5%), fibrin thrombi in glomerular capillaries (37.5%), and nephrocalcinosis, mesangial cell hyperplasia, tubular hyaline/granular casts (25% each). The spleen showed splenitis (71.4%), haemorrhage (71.4%), lymphoid hypoplasia (57.1%), and haemophagocytosis (28.6%). The brain revealed oedema (87.5%), congestion (75%), reactive microglia (62.5%), neuronal ischaemic necrosis (62.5%), meningoencephalitis (37.5%), and fibrin thrombi (25%). SARS-CoV-2 and CD68 were positive by immunohistochemistry in 85.7% and 33.3% cases, respectively. Autopsy findings of COVID-19 in children are variable in all important organs. It may help in better understanding the pathogenesis of SARS-CoV-2.


Subject(s)
COVID-19 , Thrombosis , Humans , Child , Infant , Child, Preschool , SARS-CoV-2 , Autopsy , Lung/pathology , Thrombosis/pathology , Fibrin , Necrosis/pathology
5.
J Clin Neuromuscul Dis ; 24(1): 38-48, 2022 Sep 01.
Article in English | MEDLINE | ID: covidwho-2005014

ABSTRACT

ABSTRACT: We cover intensive care unit-acquired neuromuscular disorders associated with coronavirus disease 2019. Outcomes may be worse than expected in these patients, and there is some evidence that coronavirus disease 2019 causes myopathy directly. Corticosteroid regimens in Duchenne muscular dystrophy are addressed including outcomes in pulmonary and cardiac function. A recent article notes a continued diagnostic delay in Duchenne muscular dystrophy. An interesting report of a Canary Islands cohort of patients with oculopharyngeal muscular dystrophy is discussed. Features and clinical pearls related to a series of patients with limb-girdle muscle dystrophy R12 (anoctaminopathy) and a misdiagnosis of idiopathic inflammatory myopathy are provided. The last section on autoimmune myopathy includes articles on clinical and pathologic features associated with myositis-specific antibodies and dermatomyositis, the epidemiology of immune-mediated necrotizing myopathies (IMNMs) in Olmsted County, Minnesota, and features of a German cohort of hydroxy-3-methylglutaryl coenzyme A reductase-associated IMNM. A recent article proposes the benefit of early intravenous immunoglobulin use for adults with IMNM. We also highlight a report of 2 unusual cases of antisignal recognition particle myopathy presenting with asymmetric distal weakness.


Subject(s)
Autoimmune Diseases , COVID-19 , Muscular Diseases , Muscular Dystrophy, Duchenne , Myositis , Autoantibodies , COVID-19/complications , Delayed Diagnosis , Humans , Muscle, Skeletal/pathology , Muscular Diseases/pathology , Myositis/diagnosis , Necrosis/pathology
6.
Cardiovasc Pathol ; 60: 107447, 2022.
Article in English | MEDLINE | ID: covidwho-1894842

ABSTRACT

SARS-Cov-2 infection is not limited to the respiratory tract and can involve other organs including the heart, blood vessels, kidneys, liver, gastrointestinal tract, placenta, and skin. Covid-19 patients with cardiac involvement usually have higher morbidity and mortality compared to those without cardiac involvement. The frequency and the specificity of the myocardial pathological changes in patients who die after documented infection with SARS-Cov-2 is uncertain. Macrophages can be found in the normal heart (interstitium, around the endothelial cells and in the epicardial adipose tissue), and they are considered part of the major immune cell population in the heart. In this case-control autopsy study, we compare the gross and microscopic cardiac findings, and the available clinical characteristics between a group of 10 Covid-19 decedents and a control group of 20 patients who died with non-SARS-Cov-2 severe bronchopneumonia and/or diffuse alveolar damage. The objectives of this semi-quantitative study are to study single myocyte necrosis and its relation to the strain on the heart caused by lung injury as a causative mechanism, and to study the density of myocardial and epicardial macrophages in Covid-19 hearts in comparison to the control group, and in Covid-19 hearts with single myocyte necrosis in comparison to Covid-19 hearts without single myocyte necrosis. Lymphocytic myocarditis was not identified in any of the hearts from the Covid-19 or the control group. Single myocyte necrosis is more frequent in the Covid-19 group compared to the control group, suggesting that it is unrelated to the strain on the heart caused by underlying lung injury. The density of the macrophages in the epicardium and myocardium in the hearts of the Covid-19 group is higher compared to those in the control group. The density of epicardial macrophages is higher in the Covid-19 hearts with single myocyte necrosis than in those without. These observations contribute to our increasing appreciation of the role of macrophages in the pathophysiologic response to infection by SARS-CoV-2.


Subject(s)
Acute Lung Injury , COVID-19 , Acute Lung Injury/pathology , COVID-19/complications , Endothelial Cells , Humans , Macrophages , Muscle Cells , Myocardium/pathology , Necrosis/pathology , SARS-CoV-2
7.
Clin Dermatol ; 40(4): 397-401, 2022.
Article in English | MEDLINE | ID: covidwho-1788026

ABSTRACT

A wide range of extrapulmonary manifestations in patients with COVID-19 has been reported during the ongoing pandemic, thus making the clinical spectrum of this new disease very heterogeneous. While COVID-19-associated vasculitis and vasculopathy have been described, cutaneous leukocytoclastic vasculitis (cLcV) due to SARS-CoV-2 has rarely been reported, and if it has, with relatively mild courses. We present the case of a 93-year-old man who, after having survived classic COVID-19 infection, developed a fulminant cLcV leading to extensive skin necrosis and tissue damage that resulted in his death. Considering the negative workup for other triggers of vasculitis, we find that cLcV is a secondary manifestation of COVID-19, even though SARS-CoV-2 polymerase chain reaction in the skin biopsy was not present in the tissue. We hypothesize this by providing a pathophysiologic rationale (eg, SARS-CoV-2-induced endotheliitis, complement activation, and interleukin 6 dominant intra- and perivascular inflammation).


Subject(s)
COVID-19 , Skin Diseases, Vascular , Vasculitis, Leukocytoclastic, Cutaneous , Vasculitis , Aged, 80 and over , COVID-19/complications , Humans , Interleukin-6/adverse effects , Male , Necrosis/pathology , SARS-CoV-2 , Skin/pathology , Skin Diseases, Vascular/pathology , Vasculitis/complications , Vasculitis, Leukocytoclastic, Cutaneous/etiology
8.
Int J Environ Res Public Health ; 19(7)2022 03 24.
Article in English | MEDLINE | ID: covidwho-1780025

ABSTRACT

The aim of this study is to verify the role of laminar necrosis (LN) in the diagnosis of hypoxic damage of the placenta. This is a retrospective case-control study in which 50 cases with laminar necrosis were compared with 100 gestational age-matched controls without laminar necrosis in a 1:2 ratio. The parameters analyzed were: the presence of other placental lesions, obstetric characteristics and neonatal outcome. For each of the 50 cases, the area affected by the lesion was detected, and the lesions were classified into three groups based on the morphology and time of onset of the lesion in order to understand whether these characteristics of the lesion had a clinical-pathology. The results showed that including the search for LN among placental lesions generally examined is useful to guide the pathologist in the diagnosis of placental dysfunction of hypoxic origin.


Subject(s)
Placenta Diseases , Placenta , Case-Control Studies , Female , Humans , Hypoxia , Infant, Newborn , Necrosis/pathology , Pregnancy , Pregnancy Outcome , Retrospective Studies
9.
Cells ; 10(10)2021 10 15.
Article in English | MEDLINE | ID: covidwho-1470800

ABSTRACT

Pulmonary epithelial cells are widely considered to be the first line of defence in the lung and are responsible for coordinating the innate immune response to injury and subsequent repair. Consequently, epithelial cells communicate with multiple cell types including immune cells and fibroblasts to promote acute inflammation and normal wound healing in response to damage. However, aberrant epithelial cell death and damage are hallmarks of pulmonary disease, with necrotic cell death and cellular senescence contributing to disease pathogenesis in numerous respiratory diseases such as idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and coronavirus disease (COVID)-19. In this review, we summarise the literature that demonstrates that epithelial damage plays a pivotal role in the dysregulation of the immune response leading to tissue destruction and abnormal remodelling in several chronic diseases. Specifically, we highlight the role of epithelial-derived damage-associated molecular patterns (DAMPs) and senescence in shaping the immune response and assess their contribution to inflammatory and fibrotic signalling pathways in the lung.


Subject(s)
COVID-19/immunology , Epithelium/immunology , Idiopathic Pulmonary Fibrosis/immunology , Lung/immunology , Alarmins , Animals , Cellular Senescence , Coculture Techniques , Epithelial Cells/cytology , Epithelial Cells/metabolism , Fibroblasts/cytology , Fibroblasts/metabolism , Fibrosis/metabolism , Humans , Idiopathic Pulmonary Fibrosis/metabolism , Immunity , Inflammation/metabolism , Ligands , Necroptosis , Necrosis/pathology , Pulmonary Disease, Chronic Obstructive , SARS-CoV-2 , Signal Transduction
10.
J Matern Fetal Neonatal Med ; 35(25): 8412-8418, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-1429081

ABSTRACT

OBJECTIVE: SARS-CoV-2 is known to impact multiple organ systems, with growing data to suggest the potential for placental infection and resultant pathology. Understanding how maternal COVID-19 disease can affect placental histopathology has been limited by small study cohorts with mild disease, review by multiple pathologists, and potential confounding by maternal-fetal comorbidities that can also influence placental findings. This study aims to identify pathologic placental findings associated with COVID-19 disease and severity, as well as to distinguish them from changes related to coexisting maternal-fetal comorbidities. METHODS: This is an observational study of 61 pregnant women with confirmed SARS-CoV-2 infection who delivered and had a placental histological evaluation at NYU Langone Health between March 19, 2020 and June 30, 2020. Primary outcomes were the prevalence of placental histopathologic features and their association with maternal-fetal comorbidities and severity of COVID-19 related hypoxia. Analysis was performed using Fisher's exact test and t-test with p < 0.05 considered significant. RESULTS: Sixty-one placentas were included in the study cohort, 71% from pregnancies complicated by at least one maternal-fetal comorbidity. Twenty-five percent of placentas were small for gestational age and 77% exhibited at least one feature of maternal vascular malperfusion. None of the histopathologic features in the examined placentas were associated with the presence of any specific maternal-fetal comorbidity. Thirteen percent of the cohort required maternal respiratory support for COVID-19 related hypoxia. Villous trophoblast necrosis was associated with maternal supplemental oxygen requirement (67 vs. 33%, p = 0.04) and intubation (67 vs. 33%, p = 0.01). CONCLUSION: In pregnancies complicated by COVID-19 disease, there was a high prevalence of placental histopathologic changes identified, particularly features of maternal vascular malperfusion, which could not be attributed solely to the presence of maternal-fetal comorbidities. The significantly increased prevalence of villous trophoblast necrosis in women needing respiratory support suggests a connection to the severity of COVID-19 illness.


Subject(s)
COVID-19 , Pregnancy Complications, Infectious , Female , Pregnancy , Humans , SARS-CoV-2 , COVID-19/complications , Placenta/pathology , Pregnancy Complications, Infectious/epidemiology , Pregnancy Complications, Infectious/pathology , Comorbidity , Hypoxia/epidemiology , Necrosis/epidemiology , Necrosis/pathology
11.
Molecules ; 25(21)2020 Nov 02.
Article in English | MEDLINE | ID: covidwho-1389462

ABSTRACT

Zebrafish has been a reliable model system for studying human viral pathologies. SARS-CoV-2 viral infection has become a global chaos, affecting millions of people. There is an urgent need to contain the pandemic and develop reliable therapies. We report the use of a humanized zebrafish model, xeno-transplanted with human lung epithelial cells, A549, for studying the protective effects of a tri-herbal medicine Coronil. At human relevant doses of 12 and 58 µg/kg, Coronil inhibited SARS-CoV-2 spike protein, induced humanized zebrafish mortality, and rescued from behavioral fever. Morphological and cellular abnormalities along with granulocyte and macrophage accumulation in the swim bladder were restored to normal. Skin hemorrhage, renal cell degeneration, and necrosis were also significantly attenuated by Coronil treatment. Ultra-high-performance liquid chromatography (UHPLC) analysis identified ursolic acid, betulinic acid, withanone, withaferine A, withanoside IV-V, cordifolioside A, magnoflorine, rosmarinic acid, and palmatine as phyto-metabolites present in Coronil. In A549 cells, Coronil attenuated the IL-1ß induced IL-6 and TNF-α cytokine secretions, and decreased TNF-α induced NF-κB/AP-1 transcriptional activity. Taken together, we show the disease modifying immunomodulatory properties of Coronil, at human equivalent doses, in rescuing the pathological features induced by the SARS-CoV-2 spike protein, suggesting its potential use in SARS-CoV-2 infectivity.


Subject(s)
Antiviral Agents/therapeutic use , Coronavirus Infections/drug therapy , Plant Extracts/therapeutic use , Pneumonia, Viral/drug therapy , Spike Glycoprotein, Coronavirus/antagonists & inhibitors , Air Sacs/drug effects , Air Sacs/virology , Animals , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , COVID-19 , Chromatography, High Pressure Liquid/methods , Coronavirus Infections/pathology , Coronavirus Infections/physiopathology , Disease Models, Animal , Fever/drug therapy , Fever/etiology , Hemorrhage/prevention & control , Humans , Interleukin-6/metabolism , Kidney/drug effects , Necrosis/pathology , Necrosis/prevention & control , Pandemics , Phytotherapy , Pneumonia, Viral/pathology , Pneumonia, Viral/physiopathology , Respiratory Mucosa/transplantation , Transcriptional Activation/drug effects , Tumor Necrosis Factor-alpha/metabolism , Zebrafish , COVID-19 Drug Treatment
12.
Front Immunol ; 12: 676828, 2021.
Article in English | MEDLINE | ID: covidwho-1320577

ABSTRACT

In coronavirus disease 2019 (COVID-19), ulcerative lesions have been episodically reported in various segments of the gastrointestinal (GI) tract, including the oral cavity, oropharynx, esophagus, stomach and bowel. In this report, we describe an autopsy case of a COVID-19 patient who showed two undiagnosed ulcers at the level of the anterior and posterior walls of the hypopharynx. Molecular testing of viruses involved in pharyngeal ulcers demonstrated the presence of severe acute respiratory syndrome - coronavirus type 2 (SARS-CoV-2) RNA, together with herpes simplex virus 1 DNA. Histopathologic analysis demonstrated full-thickness lympho-monocytic infiltration (mainly composed of CD68-positive cells), with hemorrhagic foci and necrosis of both the mucosal layer and deep skeletal muscle fibers. Fibrin and platelet microthrombi were also found. Cytological signs of HSV-1 induced damage were not found. Cells expressing SARS-CoV-2 spike subunit 1 were immunohistochemically identified in the inflammatory infiltrations. Immunohistochemistry for HSV1 showed general negativity for inflammatory infiltration, although in the presence of some positive cells. Thus, histopathological, immunohistochemical and molecular findings supported a direct role by SARS-CoV-2 in producing local ulcerative damage, although a possible contributory role by HSV-1 reactivation cannot be excluded. From a clinical perspective, this autopsy report of two undiagnosed lesions put the question if ulcers along the GI tract could be more common (but frequently neglected) in COVID-19 patients.


Subject(s)
COVID-19/complications , Hypopharynx/pathology , SARS-CoV-2/isolation & purification , Ulcer/pathology , Aged , Antigens, CD/metabolism , Antigens, Differentiation, Myelomonocytic/metabolism , Autopsy , Blood Platelets/metabolism , Blood Platelets/pathology , COVID-19/mortality , COVID-19/pathology , COVID-19/physiopathology , Gastrointestinal Tract/pathology , Herpesvirus 1, Human/genetics , Herpesvirus 1, Human/isolation & purification , Humans , Hypopharynx/virology , Immunohistochemistry , Inflammation/immunology , Inflammation/metabolism , Inflammation/virology , Lymphocytes/metabolism , Monocytes/metabolism , Mucous Membrane/pathology , Muscle, Skeletal/pathology , Necrosis/pathology , SARS-CoV-2/genetics , Spike Glycoprotein, Coronavirus/metabolism , Thrombosis/pathology , Ulcer/virology
13.
Pediatr Nephrol ; 36(4): 1019-1023, 2021 04.
Article in English | MEDLINE | ID: covidwho-1047246

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) is thought to cause kidney injury via a variety of mechanisms. The most common reported kidney injury following COVID-19 infection is acute tubular injury (ATI); however, the procoagulant state induced by the virus may also damage the kidneys. CASE-DIAGNOSIS/TREATMENT: Herein, we report two cases of acute necrotizing glomerulonephritis (GN) with fibrinoid necrosis in the context of COVID-19 infection. The one with more chronic features in the kidney biopsy progressed to permanent kidney failure but the second one had an excellent response to glucocorticoid pulse therapy with subsequent normal kidney function at 2-month follow-up. CONCLUSIONS: Both reported cases had an acute presentation of kidney injury with positive nasopharyngeal PCR test for COVID-19. Based on the data review by the researchers, this is the first report of acute necrotizing GN associated with COVID-19 infection.


Subject(s)
Acute Kidney Injury/etiology , COVID-19/complications , Glomerulonephritis/etiology , Kidney Glomerulus/pathology , SARS-CoV-2/pathogenicity , Acute Kidney Injury/pathology , Acute Kidney Injury/therapy , Adolescent , Biopsy , Blood Coagulation , COVID-19/blood , COVID-19/diagnosis , COVID-19/virology , Glomerulonephritis/pathology , Glomerulonephritis/therapy , Glucocorticoids/administration & dosage , Humans , Kidney Glomerulus/blood supply , Male , Necrosis/immunology , Necrosis/pathology , Platelet Count , Pulse Therapy, Drug , Renal Dialysis , SARS-CoV-2/isolation & purification , Treatment Outcome
14.
Viruses ; 12(11)2020 11 15.
Article in English | MEDLINE | ID: covidwho-927534

ABSTRACT

The mechanism(s) by which neonates testing positive for coronavirus disease 2019 (COVID-19) acquire their infection has been largely unknown. Transmission of the etiological agent, SARS-CoV-2, from mother to infant has been suspected but has been difficult to confirm. This communication summarizes the spectrum of pathology findings from pregnant women with COVID-19 based upon the infection status of their infants and addresses the potential interpretation of these results in terms of the effects of SARS-CoV-2 on the placenta and the pathophysiology of maternal-fetal infection. Placentas from pregnant women with COVID-19 and uninfected neonates show significant variability in the spectrum of pathology findings. In contrast, placentas from infected maternal-neonatal dyads are characterized by the finding of mononuclear cell inflammation of the intervillous space, termed chronic histiocytic intervillositis, together with syncytiotrophoblast necrosis. These placentas show prominent positivity of syncytiotrophoblast by SARS-CoV-2, fulfilling the published criteria for transplacental viral transmission as confirmed in fetal cells through identification of viral antigens by immunohistochemistry or viral nucleic acid using RNA in situ hybridization. The co-occurrence of chronic histiocytic intervillositis and trophoblast necrosis appears to be a risk factor for placental infection with SARS-CoV-2 as well as for maternal-fetal viral transmission, and suggests a potential mechanism by which the coronavirus can breach the maternal-fetal interface.


Subject(s)
COVID-19/transmission , Chorionic Villi/pathology , Necrosis/pathology , Pregnancy Complications, Infectious/pathology , SARS-CoV-2/pathogenicity , Trophoblasts/pathology , COVID-19/mortality , COVID-19/pathology , COVID-19/virology , Chorionic Villi/virology , Female , Fetal Mortality , Fetus , Humans , Infectious Disease Transmission, Vertical/statistics & numerical data , Necrosis/mortality , Necrosis/virology , Pregnancy , Pregnancy Complications, Infectious/mortality , Pregnancy Complications, Infectious/virology , RNA, Viral/biosynthesis , Risk Factors , Severity of Illness Index , Survival Analysis , Trophoblasts/virology , Virus Replication
15.
Rev Med Virol ; 31(3): e2176, 2021 05.
Article in English | MEDLINE | ID: covidwho-815924

ABSTRACT

The novel coronavirus (SARS-CoV-2) has turned into a life-threatening pandemic disease (Covid-19). About 5% of patients with Covid-19 have severe symptoms including septic shock, acute respiratory distress syndrome, and the failure of several organs, while most of them have mild symptoms. Frequently, the kidneys are involved through direct or indirect mechanisms. Kidney involvement mainly manifests itself as proteinuria and acute kidney injury (AKI). The SARS-CoV-2-induced kidney damage is expected to be multifactorial; directly it can infect the kidney podocytes and proximal tubular cells and based on an angiotensin-converting enzyme 2 (ACE2) pathway it can lead to acute tubular necrosis, protein leakage in Bowman's capsule, collapsing glomerulopathy and mitochondrial impairment. The SARS-CoV-2-driven dysregulation of the immune responses including cytokine storm, macrophage activation syndrome, and lymphopenia can be other causes of the AKI. Organ interactions, endothelial dysfunction, hypercoagulability, rhabdomyolysis, and sepsis are other potential mechanisms of AKI. Moreover, lower oxygen delivery to kidney may cause an ischaemic injury. Understanding the fundamental molecular pathways and pathophysiology of kidney injury and AKI in Covid-19 is necessary to develop management strategies and design effective therapies.


Subject(s)
Acute Kidney Injury/pathology , COVID-19/physiopathology , Cytokine Release Syndrome/pathology , Disseminated Intravascular Coagulation/pathology , Lymphopenia/pathology , Necrosis/pathology , Proteinuria/pathology , Sepsis/pathology , Acute Kidney Injury/immunology , Acute Kidney Injury/virology , Angiotensin-Converting Enzyme 2/genetics , Angiotensin-Converting Enzyme 2/immunology , COVID-19/immunology , COVID-19/virology , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/virology , Cytokines/genetics , Cytokines/immunology , Disseminated Intravascular Coagulation/immunology , Disseminated Intravascular Coagulation/virology , Host-Pathogen Interactions/genetics , Host-Pathogen Interactions/immunology , Humans , Kidney Tubules, Proximal/immunology , Kidney Tubules, Proximal/physiopathology , Lymphopenia/immunology , Lymphopenia/virology , Necrosis/immunology , Necrosis/virology , Podocytes/immunology , Podocytes/pathology , Proteinuria/immunology , Proteinuria/virology , SARS-CoV-2/immunology , SARS-CoV-2/pathogenicity , Sepsis/immunology , Sepsis/virology , Serine Endopeptidases/genetics , Serine Endopeptidases/immunology , Spike Glycoprotein, Coronavirus/genetics , Spike Glycoprotein, Coronavirus/immunology
16.
Cells ; 9(6)2020 06 02.
Article in English | MEDLINE | ID: covidwho-459483

ABSTRACT

The COVID-19 pandemic is progressing worldwide with an alarming death toll. There is an urgent need for novel therapeutic strategies to combat potentially fatal complications. Distinctive clinical features of severe COVID-19 include acute respiratory distress syndrome, neutrophilia, and cytokine storm, along with severe inflammatory response syndrome or sepsis. Here, we propose the putative role of enhanced neutrophil infiltration and the release of neutrophil extracellular traps, complement activation and vascular thrombosis during necroinflammation in COVID-19. Furthermore, we discuss how neutrophilic inflammation contributes to the higher mortality of COVID-19 in patients with underlying co-morbidities such as diabetes and cardiovascular diseases. This perspective highlights neutrophils as a putative target for the immunopathologic complications of severely ill COVID-19 patients. Development of the novel therapeutic strategies targeting neutrophils may help reduce the overall disease fatality rate of COVID-19.


Subject(s)
Coronavirus Infections/immunology , Coronavirus Infections/pathology , Extracellular Traps/immunology , Neutrophils/immunology , Pneumonia, Viral/immunology , Pneumonia, Viral/pathology , Angiotensin-Converting Enzyme 2 , Animals , Betacoronavirus/physiology , COVID-19 , Cardiovascular Diseases/complications , Coronavirus Infections/complications , Coronavirus Infections/drug therapy , Diabetes Complications/virology , Humans , Inflammation/immunology , Inflammation/pathology , Necrosis/immunology , Necrosis/pathology , Neutrophils/metabolism , Pandemics , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/complications , Pneumonia, Viral/drug therapy , SARS-CoV-2
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