Subject(s)
Humans , Pneumonia, Viral/epidemiology , Disease Outbreaks/prevention & control , Coronavirus Infections/prevention & control , Coronavirus Infections/epidemiology , Epidemics , Pandemics/prevention & control , Pneumonia, Viral/prevention & control , Brazil/epidemiology , Public Health Surveillance , BetacoronavirusABSTRACT
We conducted the genome sequencing and analysis of the first confirmed COVID-19 infections in Brazil. Rapid sequencing coupled with phylogenetic analyses in the context of travel history corroborate multiple independent importations from Italy and local spread during the initial stage of COVID-19 transmission in Brazil. (AU)
Subject(s)
Brazil , Public Health Surveillance , SARS-CoV-2 , COVID-19 , COVID-19/transmissionABSTRACT
A leptospirose é uma zoonose de alta morbidade em humanos e um importante problema de saúde pública. Causada por bactérias do gênero Leptospira, a doença apresenta diversas formas clínicas e é especialmente importante em países em desenvolvimento. Síndrome pulmonar hemorrágica é a maior causa de óbito em pacientes com formas severas da doença. Os mecanismos patogênicos relacionados à síndrome pulmonar hemorrágica na leptospirose humana são desconhecidos. Com o objetivo de avaliar estes mecanismos patogênicos, 30 necrópsias (tecido pulmonar) de pacientes com síndrome pulmonar hemorrágica na leptospirose e 7 controles foram avaliados. Para determinar a participação os mecanismos patogênicos envolvidos, experimentos de histologia e imunohistoquímica (IgM, IgG, IgA, and C3) foram realizados em amostras de tecidos pulmonares, bem como dosagem sérica de auto-anticorpos específicos (anticardiolipina e anti-membrana basal) de amostras pareadas de soros de pacientes com leptospirose com e sem síndrome hemorrágica pulmonar e de indivíduos doadores de banco de sangue. Nos achados patológicos, os pacientes com síndrome hemorrágica pulmonar na leptospirose diferem dos controles com hemorragia pulmonar em alguns aspectos: moderada ou intensa presença de macrófagos na luz alveolar (97% versus 29%, respectivamente; p < 0.01); presença de membrana hialina na superficie alveolar (100% versus 0% respectivamente; p < 0.01); intensa necrose e regeneração de pneumócitos II (100% versus 0%, respectivamente; p < 0.01); e presença de plasmócitos no septo aveolar (80% versus 29%; p < 0.02). Nenhuma diferença estatisticamente significativa foi observada em relação ao número de outras células no septo alveolar. Leptospiras intactas foram raramente observadas. A detecção de antígeno de leptospira não foi correlacionada com a intensidade de hemorragia pulmonar. Em nenhum dos tecidos pulmonares estudados foi evidenciado alterações microscópicas sugestivas de coagulação intravascular...
Leptospirosis is a zoonotic disease that is a cause of high morbidity and mortality in humans and is an important public health problem. Caused by bacteria of Leptospira genus, this disease presents diverse clinical manifestations and is especially important in developing countries. Leptospirosis pulmonary hemorrhage syndrome is the major cause of death in patients with the severe form of leptospirosis. The pathogenic mechanisms of this syndrome are unknown. With the purpose of identifying these pathogenic mechanisms, 30 necropsies (pulmonary samples) from patients with leptospirosis pulmonary hemorrhage syndrome and seven controls were evaluated. . To determine whether the immune system is involved, histology and immunohistochemistry (IgM, IgG, IgA, and C3) experiments were performed on lung tissue samples, as well sera measurements of autoantibodies (against the basal membrane and anti-cardiolipin) were performed in leptospirosis patients with and without pulmonary hemorrhage syndrome (in paired samples) and in healthy donors from a blood bank. We found that patients with leptospirosis pulmonary hemorrhage syndrome differed from control pulmonary hemorrhage patients in several features: the presence of moderate to high levels of macrophages in the alveolar space (77% versus 29%, respectively; p = 0.02), the presence of the focal hyaline membrane on alveolar surface (100% versus 0%; p < 0.01), extensive necrosis and regeneration of pneumocyte II cells (100% versus 0%; p < 0.01) and the presence of plasma cells in the alveolar septum (77% versus 29%, respectively; p =0.02). No statistically significant differences were observed in the number of others cells in the alveolar septae. Intact leptospires were rarely detected. Leptospiral antigen was not correlated with the intensity of the lesions. None of the patients showed microscopic evidence for disseminated intravascular coagulation. Immunoglobulin deposits were detected on the alveolar surface...