Influenza Myocarditis and Myositis: Case Presentation and Review of the Literature

Kumar, Kanwal; Guirgis, Mina; Zieroth, Shelley; Lo, Evelyn; Menkis, Alan H.; Arora, Rakesh C.; Freed, Darren H.

doi:10.1016/j.cjca.2011.03.005

Cited by 66 publications

(48 citation statements)

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“…Abrupt onset of CPA suggests a cardiogenic origin such as fatal arrhythmia from undetected myocarditis ( 29 , 30 ). Myocarditis associated with pandemic (H1N1) 2009 has been reported ( 31 , 32 ). Gdynia et al reported an unexpected death of a young adult caused by pandemic (H1N1) 2009–associated myocarditis ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

Deaths Associated with Pandemic (H1N1) 2009 among Children, Japan, 2009–2010

Okumura

Nakagawa²,

Kawashima³

et al. 2011

Emerg. Infect. Dis.

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To clarify the cause of deaths associated with pandemic (H1N1) 2009 among children in Japan, we retrospectively studied 41 patients <20 years of age who had died of pandemic (H1N1) 2009 through March 31, 2010. Data were collected through interviews with attending physicians and chart reviews. Median age of patients was 59 months; one third had a preexisting condition. Cause of death was categorized as unexpected cardiopulmonary arrest for 15 patients, encephalopathy for 15, and respiratory failure for 6. Preexisting respiratory or neurologic disorders were more frequent in patients with respiratory failure and less frequent in patients with unexpected cardiopulmonary arrest. The leading causes of death among children with pandemic (H1N1) 2009 in Japan were encephalopathy and unexpected cardiopulmonary arrest. Deaths associated with respiratory failure were infrequent and occurred primarily among children with preexisting conditions. Vaccine use and public education are necessary for reducing influenza-associated illness and death.

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Section: Discussionmentioning

confidence: 99%

Deaths Associated with Pandemic (H1N1) 2009 among Children, Japan, 2009–2010

Okumura

Nakagawa²,

Kawashima³

et al. 2011

Emerg. Infect. Dis.

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“…Although the hypothesis of a “cytokine storm” contributing to the development of IAM is sometimes put forward, levels of proinflammatory cytokines were rarely measured in IAM patients. The data available for one patient with IAM, acute renal failure and myocarditis, show moderate levels of serum proinflammatory cytokines, as observed in most patients with influenza A infection [27]. Rare histological observations from muscle biopsies reveal signs of muscle regeneration together with fiber necrosis, the latter being either moderate and patchy, or more extensive [11,28-36].…”

Section: Introductionmentioning

confidence: 99%

Productive Infection of Human Skeletal Muscle Cells by Pandemic and Seasonal Influenza A(H1N1) Viruses

et al. 2013

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Besides the classical respiratory and systemic symptoms, unusual complications of influenza A infection in humans involve the skeletal muscles. Numerous cases of acute myopathy and/or rhabdomyolysis have been reported, particularly following the outbreak of pandemic influenza A(H1N1) in 2009. The pathogenesis of these influenza-associated myopathies (IAM) remains unkown, although the direct infection of muscle cells is suspected. Here, we studied the susceptibility of cultured human primary muscle cells to a 2009 pandemic and a 2008 seasonal influenza A(H1N1) isolate. Using cells from different donors, we found that differentiated muscle cells (i. e. myotubes) were highly susceptible to infection by both influenza A(H1N1) isolates, whereas undifferentiated cells (i. e. myoblasts) were partially resistant. The receptors for influenza viruses, α2-6 and α2-3 linked sialic acids, were detected on the surface of myotubes and myoblasts. Time line of viral nucleoprotein (NP) expression and nuclear export showed that the first steps of the viral replication cycle could take place in muscle cells. Infected myotubes and myoblasts exhibited budding virions and nuclear inclusions as observed by transmission electron microscopy and correlative light and electron microscopy. Myotubes, but not myoblasts, yielded infectious virus progeny that could further infect naive muscle cells after proteolytic treatment. Infection led to a cytopathic effect with the lysis of muscle cells, as characterized by the release of lactate dehydrogenase. The secretion of proinflammatory cytokines by muscle cells was not affected following infection. Our results are compatible with the hypothesis of a direct muscle infection causing rhabdomyolysis in IAM patients.

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“…Cardiac and striated muscle coinvolvement in autoimmune myositis has been described, suggesting a common muscular epitope(s) 12,13 . Viral Influenza-A myocarditis has also been associated with concomitant myositis in 10% of cases 14 . In fact, the clinical presentation of our case is compatible with early-onset myositis, which evolved later to affect the myocardium.…”

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confidence: 99%