Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 291
Filtrar
1.
Adv Clin Chem ; 104: 299-340, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34462057

RESUMO

Cryoglobulins consist of serum immunoglobulins that precipitate below 37°C and resolubilize upon warming. The clinical triad of cryoglobulinemia usually includes purpura, weakness, and arthralgia. Cryoglobulinemic syndrome, clinically defined as a systemic vasculitis, is associated with chronic infection with hepatitis C virus (HCV) and autoimmune disorders and can evolve into B-cell malignancies. While the current literature about HCV-associated cryoglobulinemia is not very limited, little is known about the immunologic and serologic profiles of affected patients. Therefore, comprehension of the pathogenetic mechanisms underlying cryoprecipitation could be very helpful. Due to the persistence of viral antigenic stimulation, biomarkers to use after the worsening progression of HCV infection to lymphoproliferative and/or autoimmune diseases are widely needed. Laboratory methods used to detect and characterize low concentrations of cryoprecipitates and immunotyping patterns could improve patient management. The most critical factor affecting cryoglobulin testing is that the pre-analytical phase is not fully completed at 37°C.


Assuntos
Biomarcadores/sangue , COVID-19/complicações , Crioglobulinemia/sangue , Crioglobulinas/análise , Hepatite C/fisiopatologia , Animais , Autoanticorpos/sangue , Precipitação Química , Crioglobulinemia/terapia , Crioglobulinas/química , Hepatite C/sangue , Humanos , Vasculite/virologia
2.
Viruses ; 13(4)2021 04 08.
Artigo em Inglês | MEDLINE | ID: mdl-33918079

RESUMO

Vascular changes represent a characteristic feature of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection leading to a breakdown of the vascular barrier and subsequent edema formation. The aim of this study was to provide a detailed characterization of the vascular alterations during SARS-CoV-2 infection and to evaluate the impaired vascular integrity. Groups of ten golden Syrian hamsters were infected intranasally with SARS-CoV-2 or phosphate-buffered saline (mock infection). Necropsies were performed at 1, 3, 6, and 14 days post-infection (dpi). Lung samples were investigated using hematoxylin and eosin, alcian blue, immunohistochemistry targeting aquaporin 1, CD3, CD204, CD31, laminin, myeloperoxidase, SARS-CoV-2 nucleoprotein, and transmission electron microscopy. SARS-CoV-2 infected animals showed endothelial hypertrophy, endothelialitis, and vasculitis. Inflammation mainly consisted of macrophages and lower numbers of T-lymphocytes and neutrophils/heterophils infiltrating the vascular walls as well as the perivascular region at 3 and 6 dpi. Affected vessels showed edema formation in association with loss of aquaporin 1 on endothelial cells. In addition, an ultrastructural investigation revealed disruption of the endothelium. Summarized, the presented findings indicate that loss of aquaporin 1 entails the loss of intercellular junctions resulting in paracellular leakage of edema as a key pathogenic mechanism in SARS-CoV-2 triggered pulmonary lesions.


Assuntos
Aquaporina 1/metabolismo , COVID-19/patologia , Células Endoteliais/metabolismo , Células Endoteliais/ultraestrutura , Inflamação/patologia , Animais , Vasos Sanguíneos/ultraestrutura , Modelos Animais de Doenças , Imuno-Histoquímica , Pulmão/irrigação sanguínea , Pulmão/ultraestrutura , Pulmão/virologia , Mesocricetus , SARS-CoV-2 , Vasculite/patologia , Vasculite/virologia
3.
Rinsho Shinkeigaku ; 61(4): 239-242, 2021 Apr 21.
Artigo em Japonês | MEDLINE | ID: mdl-33762495

RESUMO

A 78-year-old woman was diagnosed with herpes zoster in the first branch of the trigeminal nerve and was treated with amenamevir. Subsequently, she was hospitalized for postherpetic neuralgia. Fever and unconsciousness were observed, and a diagnosis of varicella-zoster virus meningoencephalitis and vasculitis was made. In addition to the antithrombotic therapy, she was treated with intravenous acyclovir and steroid pulse therapy; however, her unconsciousness persisted. Amenamevir was not transferrable to the spinal fluid and resulted in an incomplete treatment of herpes zoster in the cerebral nerve region, suggesting that this case may be related to the severe course of the disease.


Assuntos
Aciclovir/administração & dosagem , Antivirais/uso terapêutico , Herpes Zoster/complicações , Herpes Zoster/tratamento farmacológico , Meningoencefalite/tratamento farmacológico , Meningoencefalite/etiologia , Oxidiazóis/uso terapêutico , Nervo Trigêmeo , Vasculite/tratamento farmacológico , Vasculite/etiologia , Idoso , Antivirais/administração & dosagem , Antivirais/efeitos adversos , Antivirais/líquido cefalorraquidiano , Feminino , Humanos , Infusões Intravenosas , Imageamento por Ressonância Magnética , Meningoencefalite/diagnóstico , Meningoencefalite/virologia , Metilprednisolona/administração & dosagem , Oxidiazóis/efeitos adversos , Oxidiazóis/líquido cefalorraquidiano , Pulsoterapia , Índice de Gravidade de Doença , Vasculite/diagnóstico , Vasculite/virologia
4.
Atherosclerosis ; 322: 39-50, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33706082

RESUMO

BACKGROUND AND AIMS: The new coronavirus disease (COVID-19) is a systemic disease. Mounting evidence depict signs and symptoms involving multiple organs, most of which supported by pathological data. A plausible link to these manifestations is vascular and endothelial dysfunction/damage. However, much of the current knowledge relies on opinion and incipient evidence. We aim to objectively appraise current evidence on the association between COVID-19 and vascular disease, specifically endotheliitis and vasculitis. METHODS: Two researchers independently entered the search terms COVID-19 OR SARS-CoV-2 AND vasculitis, endotheliitis OR endothelium in the following online platforms: MedRxiv and LitCovid (PubMed). The search period was set from November 1, 2019 to August 28, 2020. Manuscripts with unavailable full texts, not in English, mainly on pre-clinical data, presenting only study designs or not directly related to the topics of this review were excluded. Retrospective and prospective studies, especially longitudinal ones, were given priority to the purpose of this review. Since there was paucity of prospective controlled evidence, case reports/series were also considered. RESULTS: A total of 318 manuscripts were initially found. Sixty-seven (21%) were excluded: 59 (18.5%) met exclusion criteria and 8 (2.5%) were duplicates. One hundred and forty-two manuscripts (44,6%) did not provide original data and were also excluded: 35 (11%) were comments, 108 (33.9%) reviews; 1 (0.3%) position paper. One hundred and seven (33.6%) studies were considered for the present scoping review: 81 (25,5%) case reports/series; 18 (5.7%) prospective; 8 (2.5%) retrospective. Viral inclusions in endothelial cells, mononuclear cell infiltrates in the intima of small vessels and markers of endothelial cell apoptosis were demonstrated. Specificities of COVID-19 may lead to diverse vascular manifestations in different levels of the vascular bed. CONCLUSIONS: Evidence indicates that COVID-19 targets vasculature and endothelium. However, high quality data is still lacking and studies with prospective designs and appropriately matched controls are needed.


Assuntos
COVID-19/complicações , Endotélio Vascular/patologia , Inflamação/virologia , Vasculite/virologia , Células Endoteliais/virologia , Humanos , Estudos Prospectivos , Estudos Retrospectivos
6.
Br J Haematol ; 193(1): 43-51, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33538335
7.
Int J Dermatol ; 60(5): 547-553, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-33533036

RESUMO

INTRODUCTION: Since COVID-19 has become a pandemic, extensive literature has been produced. The commonest symptoms of COVID-19 disease are fever, cough, anosmia, and lymphocytopenia. However, other apparently less common clinical symptoms have been described, including skin lesions. We conducted a systematic review to evaluate skin involvement in COVID-19. METHODS: The authors performed a systematic review of literature, in accordance with the Preferred Reporting Items for Systematic and Meta-Analysis (PRISMA). The search was reiterated until May 06, 2020. RESULTS: Overall, 1593 patients (M/F ratio: 1 : 9) with suspect of COVID-19 were examined. The mean age was 37.8 (range 0-91) years. Among the analyzed patients, 84 (5.3%) were pediatrics (<18 years). Chilblains are very common among skin lesions and represent almost half of all skin lesions reported (46%); in 75% of patients with cutaneous manifestation, the latter presented before other typical clinical manifestation of COVID-19. Vasculitis or thrombosis was identified in almost 70% of patients who suffered from skin manifestations. CONCLUSION: The present study highlights the importance of skin involvement in COVID-19. Limbs should be examined to eventually foresee the onset of further typical symptoms. Chilblains can be considered typical features. Studies with higher scientific evidence are required.


Assuntos
COVID-19/complicações , Dermatopatias/virologia , Pérnio/epidemiologia , Pérnio/virologia , Humanos , Pandemias , Dermatopatias/epidemiologia , Trombose/epidemiologia , Trombose/virologia , Vasculite/epidemiologia , Vasculite/virologia
8.
J Thromb Haemost ; 19(2): 574-581, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33217134

RESUMO

OBJECTIVE: Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can lead to severe pneumonia, but also thrombotic complications and non-pulmonary organ failure. Recent studies suggest intravascular neutrophil activation and subsequent immune cell-triggered immunothrombosis as a central pathomechanism linking the heterogenous clinical picture of coronavirus disease 2019 (COVID-19). We sought to study whether immunothrombosis is a pathognomonic factor in COVID-19 or a general feature of (viral) pneumonia, as well as to better understand its upstream regulation. APPROACH AND RESULTS: By comparing histopathological specimens of SARS-CoV-2 with influenza-affected lungs, we show that vascular neutrophil recruitment, NETosis, and subsequent immunothrombosis are typical features of severe COVID-19, but less prominent in influenza pneumonia. Activated neutrophils were typically found in physical association with monocytes. To explore this further, we combined clinical data of COVID-19 cases with comprehensive immune cell phenotyping and bronchoalveolar lavage fluid scRNA-seq data. We show that a HLADRlow CD9low monocyte population expands in severe COVID-19, which releases neutrophil chemokines in the lungs, and might in turn explain neutrophil expansion and pulmonary recruitment in the late stages of severe COVID-19. CONCLUSIONS: Our data underline an innate immune cell axis causing vascular inflammation and immunothrombosis in severe SARS-CoV-2 infection.


Assuntos
COVID-19/imunologia , Imunidade Inata , Influenza Humana/imunologia , Pulmão/imunologia , Neutrófilos/imunologia , Trombose/imunologia , Vasculite/imunologia , COVID-19/diagnóstico , COVID-19/virologia , Diagnóstico Diferencial , Interações Hospedeiro-Patógeno , Humanos , Influenza Humana/diagnóstico , Influenza Humana/virologia , Pulmão/patologia , Pulmão/virologia , Neutrófilos/virologia , Valor Preditivo dos Testes , SARS-CoV-2/imunologia , SARS-CoV-2/patogenicidade , Trombose/virologia , Vasculite/virologia
9.
Inflamm Res ; 69(12): 1181-1189, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32918567

RESUMO

BACKGROUND: COVID-19-associated coagulopathy (CAC) characterized by the elevated D-dimer without remarkable changes of other global coagulation markers is associated with various thrombotic complications and disease severity. The purpose of this review is to elucidate the pathophysiology of this unique coagulopathy. METHODS: The authors performed online search of published medical literature through PubMed using the MeSH (Medical Subject Headings) term "COVID-19," "SARS-CoV-2," "coronavirus," "coagulopathy," and "thrombus." Then, selected 51 articles that closely relevant to coagulopathy in COVID-19. RESULTS: The primary targets of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are the pneumocytes, immune cells, and vascular endothelial cells. The alveolar damage and the pulmonary microvascular thrombosis are the major causes of acute lung injury in COVID-19. The endotheliopathy that occurs is due to direct SARS-CoV-2 infection and activation of other pathways that include the immune system and thromboinflammatory responses leading to what is termed CAC. As a result, both microvascular and macrovascular thrombotic events occur in arterial, capillary, venule, and large vein vascular beds to produce multiorgan dysfunction and thrombotic complications. In addition to the endothelial damage, SARS-CoV-2 also can cause vasculitis and presents as a systemic inflammatory vascular disease. Clinical management of COVID-19 includes anticoagulation but novel therapies for endotheliopathy, hypercoagulability, and vasculitis are needed. CONCLUSION: The endotheliopathy due to direct endothelial infection with SARS-COV-2 and the indirect damage caused by inflammation play the predominant role in the development of CAC. The intensive control of thromboinflammation is necessary to improve the outcome of this highly detrimental contagious disease.


Assuntos
Betacoronavirus , Transtornos da Coagulação Sanguínea/virologia , Infecções por Coronavirus/complicações , Endotélio Vascular/fisiopatologia , Pneumonia Viral/complicações , Vasculite/virologia , Transtornos da Coagulação Sanguínea/tratamento farmacológico , COVID-19 , Infecções por Coronavirus/fisiopatologia , Células Endoteliais , Produtos de Degradação da Fibrina e do Fibrinogênio/análise , Humanos , Pulmão/irrigação sanguínea , Microvasos , Pandemias , Pneumonia Viral/fisiopatologia , PubMed , Embolia Pulmonar , SARS-CoV-2 , Trombose/virologia
10.
Intern Med ; 59(23): 3075-3078, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-32759579

RESUMO

We herein report a 33-year-old woman who was an asymptomatic hepatitis B virus (HBV) carrier and presented with distal muscle weakness in the legs and asymmetrical paresthesia in the distal extremities. A nerve biopsy specimen revealed fibrinoid necrosis associated with inflammatory infiltration in the perineural space, and deposition of hepatitis B core antigen and C4d complement was detected in the vascular endothelial cells as well as around the vessels. She was diagnosed with HBV-related vasculitic neuropathy and treated with intravenous immunoglobulin (IVIG). Her symptoms completely subsided after eight weeks. Vasculitic neuropathy rarely develops in the chronic inactive stages of HBV infection. This is the first report of an HBV-inactive carrier with vasculitic neuropathy successfully treated with IVIG.


Assuntos
Portador Sadio , Hepatite B/complicações , Doenças do Sistema Nervoso Periférico/etiologia , Vasculite/etiologia , Adulto , Células Endoteliais/patologia , Feminino , Vírus da Hepatite B , Humanos , Imunoglobulinas Intravenosas/uso terapêutico , Doenças do Sistema Nervoso Periférico/virologia , Vasculite/virologia
11.
Am J Case Rep ; 21: e925779, 2020 Aug 13.
Artigo em Inglês | MEDLINE | ID: mdl-32790652

RESUMO

BACKGROUND Coronavirus disease 2019 (COVID-19) infection commonly presents as fever, cough, and shortness of breath in adults. Children are thought to have milder respiratory symptoms and to recover more quickly. We describe a new presentation of COVID-19 infection in children consisting of multisystem inflammation with decreased left ventricular function and evidence of lung disease. CASE REPORT Three children presented with fever, conjunctivitis, dry and cracked lips, rash, and/or cervical lymphadenopathy for at least 5 days. Two of these children required mechanical ventilation, and 1 of the 2 needed extracorporeal membrane oxygenation (ECMO) to support cardiorespiratory function. All of these children had moderate to severe hyponatremia and lymphopenia, which is usually seen in COVID-19. They were treated with intravenous immunoglobulin and high-dose aspirin. All of the children recovered. CONCLUSIONS Early recognition of children with multisystem inflammation is important because they are at increased risk for deterioration. Treatment with intravenous immunoglobulin and aspirin was used because this regimen has been shown to be beneficial in vasculitis of Kawasaki disease. The development of shock due to cardiac involvement may require ECMO.


Assuntos
Betacoronavirus , Infecções por Coronavirus/diagnóstico , Pneumonia Viral/diagnóstico , Síndrome de Resposta Inflamatória Sistêmica/virologia , Antipiréticos/uso terapêutico , Aspirina/uso terapêutico , COVID-19 , Criança , Pré-Escolar , Conjuntivite/terapia , Conjuntivite/virologia , Infecções por Coronavirus/terapia , Exantema/terapia , Exantema/virologia , Oxigenação por Membrana Extracorpórea , Feminino , Febre/terapia , Febre/virologia , Insuficiência Cardíaca/terapia , Insuficiência Cardíaca/virologia , Humanos , Hiponatremia/terapia , Hiponatremia/virologia , Imunoglobulinas Intravenosas , Linfadenopatia/terapia , Linfadenopatia/virologia , Linfopenia/terapia , Linfopenia/virologia , Masculino , Pandemias , Pneumonia Viral/terapia , Respiração Artificial , SARS-CoV-2 , Síndrome de Resposta Inflamatória Sistêmica/diagnóstico , Síndrome de Resposta Inflamatória Sistêmica/terapia , Vasculite/terapia , Vasculite/virologia
13.
J Thromb Thrombolysis ; 50(3): 499-511, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32700024

RESUMO

The COVID-19 pandemic now totaling 13,000,000 cases and over 571,000 deaths has continued to teach the medical, scientific and lay communities about viral infectious disease in the modern era. Among the many lessons learned for the medical community is the potential for transmissibility and host infectivity of the SARS-CoV-2 virus. Moreover, it has become clear that the virus can affect any organ including the circulatory system, directly via either tissue tropism or indirectly stemming from inflammatory responses in the form of innate immunity, leukocyte debris such as cell-free DNA and histones and RNA viral particles. The following review considers COVID-19-associated vasculitis and vasculopathy as a defining feature of a virus-induced systemic disease with acute, subacute and potential chronic health implications.


Assuntos
Betacoronavirus/patogenicidade , Vasos Sanguíneos/virologia , Infecções por Coronavirus/virologia , Pneumonia Viral/virologia , Vasculite/virologia , Animais , Betacoronavirus/imunologia , Coagulação Sanguínea , Vasos Sanguíneos/imunologia , Vasos Sanguíneos/patologia , Vasos Sanguíneos/fisiopatologia , COVID-19 , Infecções por Coronavirus/diagnóstico , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/fisiopatologia , Interações Hospedeiro-Patógeno , Humanos , Mediadores da Inflamação/sangue , Pandemias , Pneumonia Viral/diagnóstico , Pneumonia Viral/imunologia , Pneumonia Viral/fisiopatologia , Prognóstico , Fatores de Risco , SARS-CoV-2 , Vasculite/diagnóstico , Vasculite/imunologia , Vasculite/fisiopatologia
14.
Clin Immunol ; 217: 108493, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32526273

Assuntos
Complexo Antígeno-Anticorpo/biossíntese , Betacoronavirus/patogenicidade , Infecções por Coronavirus/imunologia , Síndrome da Liberação de Citocina/imunologia , Doenças do Complexo Imune/imunologia , Pneumonia Viral/imunologia , Síndrome Respiratória Aguda Grave/imunologia , Vasculite/imunologia , Anticorpos Antivirais/biossíntese , Complexo Antígeno-Anticorpo/efeitos dos fármacos , Betacoronavirus/imunologia , Vasos Sanguíneos/efeitos dos fármacos , Vasos Sanguíneos/imunologia , Vasos Sanguíneos/patologia , Vasos Sanguíneos/virologia , COVID-19 , Complemento C3/antagonistas & inibidores , Complemento C3/biossíntese , Inativadores do Complemento/uso terapêutico , Infecções por Coronavirus/complicações , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/virologia , Síndrome da Liberação de Citocina/complicações , Síndrome da Liberação de Citocina/tratamento farmacológico , Síndrome da Liberação de Citocina/virologia , Humanos , Doenças do Complexo Imune/complicações , Doenças do Complexo Imune/tratamento farmacológico , Doenças do Complexo Imune/virologia , Imunidade Humoral/efeitos dos fármacos , Proteína Antagonista do Receptor de Interleucina 1/uso terapêutico , Interleucina-6/antagonistas & inibidores , Interleucina-6/biossíntese , Pandemias , Pneumonia Viral/complicações , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/virologia , Receptores de Interleucina-1/antagonistas & inibidores , Receptores de Interleucina-1/biossíntese , SARS-CoV-2 , Síndrome Respiratória Aguda Grave/complicações , Síndrome Respiratória Aguda Grave/tratamento farmacológico , Síndrome Respiratória Aguda Grave/virologia , Índice de Gravidade de Doença , Vasculite/complicações , Vasculite/tratamento farmacológico , Vasculite/virologia
16.
Clin Immunol ; 217: 108487, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32479986

RESUMO

Coronavirus Disease 2019 (COVID-19) is an ongoing public health emergency and new knowledge about its immunopathogenic mechanisms is deemed necessary in the attempt to reduce the death burden, globally. For the first time in worldwide literature, we provide scientific evidence that in COVID-19 vasculitis a life-threatening escalation from type 2 T-helper immune response (humoral immunity) to type 3 hypersensitivity (immune complex disease) takes place. The subsequent deposition of immune complexes inside the vascular walls is supposed to induce a severe inflammatory state and a cytokine release syndrome, whose interleukin-6 is the key myokine, from the smooth muscle cells of blood vessels.


Assuntos
Betacoronavirus/patogenicidade , Infecções por Coronavirus/imunologia , Síndrome da Liberação de Citocina/imunologia , Doenças do Complexo Imune/imunologia , Pneumonia Viral/imunologia , Síndrome Respiratória Aguda Grave/imunologia , Células Th2/imunologia , Vasculite/imunologia , Idoso , Anticorpos Antivirais/biossíntese , Complexo Antígeno-Anticorpo/biossíntese , Betacoronavirus/imunologia , Vasos Sanguíneos/imunologia , Vasos Sanguíneos/patologia , Vasos Sanguíneos/virologia , COVID-19 , Complemento C3/biossíntese , Infecções por Coronavirus/complicações , Infecções por Coronavirus/virologia , Síndrome da Liberação de Citocina/complicações , Síndrome da Liberação de Citocina/virologia , Progressão da Doença , Células Endoteliais/imunologia , Células Endoteliais/patologia , Células Endoteliais/virologia , Humanos , Doenças do Complexo Imune/complicações , Doenças do Complexo Imune/virologia , Imunidade Humoral , Imunoglobulina G/biossíntese , Imunoglobulina M/biossíntese , Interleucina-6/biossíntese , Masculino , Pandemias , Pneumonia Viral/complicações , Pneumonia Viral/virologia , SARS-CoV-2 , Síndrome Respiratória Aguda Grave/complicações , Síndrome Respiratória Aguda Grave/virologia , Células Th2/patologia , Células Th2/virologia , Vasculite/complicações , Vasculite/virologia
17.
Br J Dermatol ; 183(4): 729-737, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32562567

RESUMO

BACKGROUND: Chilblains ('COVID toes') are being seen with increasing frequency in children and young adults during the COVID-19 pandemic. Detailed histopathological descriptions of COVID-19 chilblains have not been reported, and causality of SARS-CoV-2 has not yet been established. OBJECTIVES: To describe the histopathological features of COVID-19 chilblains and to explore the presence of SARS-CoV-2 in the tissue. METHODS: We examined skin biopsies from seven paediatric patients presenting with chilblains during the COVID-19 pandemic. Immunohistochemistry for SARS-CoV-2 was performed in all cases and electron microscopy in one. RESULTS: Histopathology showed variable degrees of lymphocytic vasculitis ranging from endothelial swelling and endotheliitis to fibrinoid necrosis and thrombosis. Purpura, superficial and deep perivascular lymphocytic inflammation with perieccrine accentuation, oedema, and mild vacuolar interface damage were also seen. SARS-CoV-2 immunohistochemistry was positive in endothelial cells and epithelial cells of eccrine glands. Coronavirus particles were found in the cytoplasm of endothelial cells on electron microscopy. CONCLUSIONS: Although the clinical and histopathological features were similar to other forms of chilblains, the presence of viral particles in the endothelium and the histological evidence of vascular damage support a causal relation of the lesions with SARS-CoV-2. Endothelial damage induced by the virus could be the key mechanism in the pathogenesis of COVID-19 chilblains and perhaps also in a group of patients severely affected by COVID-19 presenting with features of microangiopathic damage. What is already known about this topic? Despite the high number of cases of chilblains seen during the COVID-19 pandemic, a definite causative role for SARS-CoV-2 has not yet been proven. Different pathogenetic hypotheses have been proposed, including coagulation anomalies, interferon release and external factors. What does this study add? The demonstration of SARS-CoV-2 in endothelial cells of skin biopsies by immunohistochemistry and electron microscopy confirms that these lesions are part of the spectrum of COVID-19. Virus-induced vascular damage and secondary ischaemia could explain the pathophysiology of COVID-19 chilblains. Our findings support the hypothesis that widespread endothelial infection by SARS-CoV-2 could have a pathogenetic role in the severe forms of COVID-19. Linked Comment: Wetter. Br J Dermatol 2020; 183:611.


Assuntos
Pérnio/virologia , Infecções por Coronavirus/complicações , Endotélio Vascular/patologia , Pneumonia Viral/complicações , Dermatopatias/virologia , Vasculite/virologia , Betacoronavirus/isolamento & purificação , Betacoronavirus/patogenicidade , Biópsia , COVID-19 , Pérnio/patologia , Criança , Infecções por Coronavirus/patologia , Infecções por Coronavirus/virologia , Células Endoteliais/patologia , Células Endoteliais/ultraestrutura , Células Endoteliais/virologia , Endotélio Vascular/virologia , Humanos , Imuno-Histoquímica , Microscopia Eletrônica , Pandemias , Pneumonia Viral/patologia , Pneumonia Viral/virologia , SARS-CoV-2 , Pele/irrigação sanguínea , Pele/patologia , Pele/virologia , Dermatopatias/patologia , Vasculite/patologia
20.
Vet Pathol ; 57(3): 388-396, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32314676

RESUMO

Lumpy skin disease is a high-consequence disease in cattle caused by infection with the poxvirus lumpy skin disease virus (LSDV). The virus is endemic in most countries in Africa and an emerging threat to cattle populations in Europe and Asia. As LSDV spreads into new regions, it is important that signs of disease are recognized promptly by animal caregivers. This study describes the gross, microscopic, and ultrastructural changes that occur over time in cattle experimentally challenged with LSDV. Four calves were inoculated with wildtype LSDV and monitored for 19 to 21 days. At 7 days after inoculation, 2 of the 4 cattle developed multifocal cutaneous nodules characteristic of LSD. Some lesions displayed a targetoid appearance. Histologically, intercellular and intracellular edema was present in the epidermis of some nodules. Occasional intracytoplasmic inclusion bodies were identified in keratinocytes. More severe and consistent changes were present in the dermis, with marked histiocytic inflammation and necrotizing fibrinoid vasculitis of dermal vessels, particularly the deep dermal plexus. Chronic lesions consisted of full-thickness necrosis of the dermis and epidermis. Lesions in other body organs were not a major feature of LSD in this study, highlighting the strong cutaneous tropism of this virus. Immunohistochemistry and electron microscopy identified LSDV-infected histiocytes and fibroblasts in the skin nodules of affected cattle. This study highlights the noteworthy lesions of LSDV and how they develop over time.


Assuntos
Doença Nodular Cutânea , Vírus da Doença Nodular Cutânea/isolamento & purificação , Animais , Ásia/epidemiologia , Bovinos , Doenças dos Bovinos/virologia , Doenças Transmissíveis Emergentes/veterinária , Doenças Transmissíveis Emergentes/virologia , Dermatite/patologia , Dermatite/veterinária , Dermatite/virologia , Doenças Endêmicas/veterinária , Europa (Continente)/epidemiologia , Doença Nodular Cutânea/epidemiologia , Doença Nodular Cutânea/patologia , Doença Nodular Cutânea/transmissão , Doença Nodular Cutânea/virologia , Vírus da Doença Nodular Cutânea/patogenicidade , Vírus da Doença Nodular Cutânea/ultraestrutura , Pele/patologia , Pele/virologia , Vasculite/patologia , Vasculite/veterinária , Vasculite/virologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...