Fulminant myocarditis associated with the H1N1 influenza virus: case report and literature review.

A case of fulminant myocarditis associated with the H1N1 influenza virus. This case report describes the patient's clinical course and emphasizes the importance of bedside echocardiography as an aid in the early diagnosis and management of children with severe myocardial dysfunction. It also discusses aspects relevant to the treatment and prognosis of fulminant myocarditis. The patient was a female, 4 years and 8 months old, previously healthy and with a history of flu symptoms in the past two weeks. The patient was admitted to the emergency room with signs of hemodynamic instability, requiring ventilatory support and vasoactive drugs. The laboratory tests, chest X-ray and echocardiogram suggested the presence of myocarditis. The test for H1N1 in nasopharyngeal secretions was positive. The patient evolved to refractory cardiogenic shock despite the clinical measures applied and died 48 hours after admission to the intensive care unit. The H1N1 influenza virus is an etiological agent associated with acute myocarditis, but there are few reported cases of fulminant myocarditis caused by the H1N1 virus. The identification of signs and symptoms suggestive of fulminant progression should be immediate, and bedside echocardiography is a useful tool for the early detection of myocardial dysfunction and for therapeutic guidance. The use of immunosuppressive therapy and antiviral therapy in acute myocarditis of viral etiology is controversial; hence,the treatment is based on hemodynamic and ventilatory support. The use of hemodynamic support by extracorporeal membrane oxygenation emerges as a promising treatment.

Miocardite fulminante associada ao vírus influenza H1N1: relato de caso e revisão de literatura / Fulminant myocarditis associated with the H1N1 influenza virus: case report and literature review

Caso de miocardite fulminante associada ao vírus influenza H1N1, em que foi descrita a evolução clínica do paciente e enfatizada a importância do ecocardiograma à beira do leito como auxílio no diagnóstico precoce e manejo de crianças com disfunção miocárdica grave, além de terem sido discutidos aspectos relevantes relacionados à terapêutica e ao prognóstico da miocardite fulminante. Trata-se de paciente do sexo feminino, 4 anos e 8 meses, previamente hígida, com história de quadro gripal há 2 semanas. Admitida no pronto-socorro com sinais de instabilidade hemodinâmica, necessitando de suporte ventilatório e drogas vasoativas. Exames laboratoriais, radiografia de tórax e ecocardiograma sugestivos de miocardite. Pesquisa positiva para H1N1 em secreção de nasofaringe. Evoluiu com choque cardiogênico refratário a despeito das medidas clínicas, indo a óbito em 48 horas após admissão na unidade de terapia intensiva. O vírus influenza H1N1 é agente etiológico associado a quadros de miocardite aguda, porém poucos são os casos relatados de miocardite fulminante pelo vírus H1N1. A identificação de sinais e sintomas sugestivos de evolução fulminante deve ser imediata e o ecocardiograma à beira do leito é uma ferramenta útil para detecção precoce de disfunção miocárdica e orientação terapêutica. O uso de terapia imunossupressora, em casos de miocardite fulminante de etiologia viral, é controverso, bem como o de terapia antiviral, de tal forma que o tratamento baseia-se em suporte hemodinâmico e ventilatório. O uso de suporte hemodinâmico, por meio de oxigenação por membrana extracorpórea, aparece como terapia promissora.

A case of fulminant myocarditis associated with the H1N1 influenza virus. This case report describes the patient's clinical course and emphasizes the importance of bedside echocardiography as an aid in the early diagnosis and management of children with severe myocardial dysfunction. It also discusses aspects relevant to the treatment and prognosis of fulminant myocarditis. The patient was a female, 4 years and 8 months old, previously healthy and with a history of flu symptoms in the past two weeks. The patient was admitted to the emergency room with signs of hemodynamic instability, requiring ventilatory support and vasoactive drugs. The laboratory tests, chest X-ray and echocardiogram suggested the presence of myocarditis. The test for H1N1 in nasopharyngeal secretions was positive. The patient evolved to refractory cardiogenic shock despite the clinical measures applied and died 48 hours after admission to the intensive care unit. The H1N1 influenza virus is an etiological agent associated with acute myocarditis, but there are few reported cases of fulminant myocarditis caused by the H1N1 virus. The identification of signs and symptoms suggestive of fulminant progression should be immediate, and bedside echocardiography is a useful tool for the early detection of myocardial dysfunction and for therapeutic guidance. The use of immunosuppressive therapy and antiviral therapy in acute myocarditis of viral etiology is controversial; hence, the treatment is based on hemodynamic and ventilatory support. The use of hemodynamic support by extracorporeal membrane oxygenation emerges as a promising treatment.

Leishmania amazonensis infection impairs dendritic cell migration from the inflammatory site to the draining lymph node.

BACKGROUND: In vitro studies show that Leishmania infection decreases the adhesion of inflammatory phagocytes to connective tissue by a mechanism dependent on the modulation of integrin function. However, we know little about the influence of this reduction in leukocyte adhesion on parasite dissemination from the infection site. METHODS: In this work, we used a model of chronic peritonitis induced by thioglycollate to study the effect of L. amazonensis infection on the ability of inflammatory phagocyte populations to migrate from an inflammatory site to the draining lymph node. Uninfected or Leishmania-infected thioglycollate-elicited peritoneal exudate cells were transferred from C57BL/6 to BALB/c mice or from Ly5.1+ to Ly5.1- mice. The transferred cells were injected into the peritoneal cavity and tracked to the draining lymph node. RESULTS: Migrating cells corresponded to approximately 1% of the injected leukocytes. The proportion of migrating CD11b+CD11c+ (myeloid dendritic cell) was lower after incubation with Leishmania (1.3 to 2.6 times lower in the experiments using C57BL/6 to BALB/c animals and 2.7 to 3.4 times lower in the experiments using Ly5.1+ to Ly5.1- animals) than after leukocyte incubation with medium alone (P < 0.01). There was no consistent decrease in the migration of CD11b+F4/80+ (macrophage) or SSChi GR-1+ (neutrophil) populations. CONCLUSIONS: Coincubation with Leishmania changes the migratory pattern of dendritic cells in vivo. Such changes in dendritic cell migration may be associated with immunological events that maintain inflammation at the sites of infection.