Author: Gupta, Neha; Richter, Robert; Robert, Stephen; Kong, Michele
Title: Viral Sepsis in Children Document date: 2018_9_18
ID: 050vjj6k_19
Snippet: Secondary bacterial infections are commonly associated with respiratory viral infections (85) . In the winter of 1995-96, an outbreak of Streptococcus pneumoniae pneumonia developed in otherwise healthy children who had a preceding influenza A viral illness (86) . During the 2009-10 influenza A pandemic, one third of critically ill children afflicted with influenza were diagnosed with concurrent bacterial infections (87) . In this study, the lead.....
Document: Secondary bacterial infections are commonly associated with respiratory viral infections (85) . In the winter of 1995-96, an outbreak of Streptococcus pneumoniae pneumonia developed in otherwise healthy children who had a preceding influenza A viral illness (86) . During the 2009-10 influenza A pandemic, one third of critically ill children afflicted with influenza were diagnosed with concurrent bacterial infections (87) . In this study, the leading three bacterial coinfections were Staphylococcus aureus, Pseudomonas spp., and Haemophilus influenza (87) . In children hospitalized for RSV, Haemophilus influenzae and Streptococcus pneumoniae were the most common organisms isolated in those who developed bacteremia (88) . These secondary bacterial infections may exacerbate innate immune dysfunction (89) and convey substantially increased risk of worse outcomes (90, 91) . However, to date, the mechanisms underlying bacterial synergism and increased susceptibility to secondary bacterial infection in the setting of a preceding respiratory viral infection remain unclear. In general, this phenomenon appears to involve impairment of respiratory epithelial and innate immune system defenses. Viral destruction of the airway epithelium affects mucociliary clearance, allowing bacterial attachment to mucins and eventual colonization of the respiratory tract (92, 93) . Additionally, viral-induced upregulation of IFN-γ and TNFα may lead to a dysregulated host T-cell response, decreased neutrophil chemotaxis, and impaired macrophage phagocytosis that increases the host susceptibility to secondary bacterial pathogens (94) . Upregulation of the surface platelet-activating factor receptor on epithelial cells and leukocytes by proinflammatory cytokines may also increase adhesion and invasion of certain virulent pneumococcal strains (95) .
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