Studies on Influenza in the Pandemic of 1957-1958. Ii. Pulmonary Complications of Influenza*†

Louria, Donald B.; Blumenfeld, Herbert L.; Ellis, John Tracy; Kilbourne, Edwin D.; Rogers, David E.

doi:10.1172/jci103791

Cited by 444 publications

(265 citation statements)

References 20 publications

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“…In seasonal epidemics, influenza bacterial coinfection is associated with increases in hospital admissions,4, 5 more severe symptoms,6 and increases in mortality 7. Viral damage to the epithelial lining of the respiratory tract is believed to facilitate establishment of bacterial infections 8, 9, 10. However, other factors, such as changes in airway function, up‐regulation and exposure of receptors, dampening of the immune response, or enhancement of inflammation may also play a role 11…”

Section: Introductionmentioning

confidence: 99%

The frequency of influenza and bacterial coinfection: a systematic review and meta‐analysis

Klein

Monteforte

Gupta

et al. 2016

Influenza Resp Viruses

455

355

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AimCoinfecting bacterial pathogens are a major cause of morbidity and mortality in influenza. However, there remains a paucity of literature on the magnitude of coinfection in influenza patients.MethodA systematic search of MeSH, Cochrane Library, Web of Science, SCOPUS, EMBASE, and PubMed was performed. Studies of humans in which all individuals had laboratory confirmed influenza, and all individuals were tested for an array of common bacterial species, met inclusion criteria.ResultsTwenty‐seven studies including 3215 participants met all inclusion criteria. Common etiologies were defined from a subset of eight articles. There was high heterogeneity in the results (I 2 = 95%), with reported coinfection rates ranging from 2% to 65%. Although only a subset of papers were responsible for observed heterogeneity, subanalyses and meta‐regression analysis found no study characteristic that was significantly associated with coinfection. The most common coinfecting species were Streptococcus pneumoniae and Staphylococcus aureus, which accounted for 35% (95% CI, 14%–56%) and 28% (95% CI, 16%–40%) of infections, respectively; a wide range of other pathogens caused the remaining infections. An assessment of bias suggested that lack of small‐study publications may have biased the results.ConclusionsThe frequency of coinfection in the published studies included in this review suggests that although providers should consider possible bacterial coinfection in all patients hospitalized with influenza, they should not assume all patients are coinfected and be sure to properly treat underlying viral processes. Further, high heterogeneity suggests additional large‐scale studies are needed to better understand the etiology of influenza bacterial coinfection.

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Section: Introductionmentioning

confidence: 99%

The frequency of influenza and bacterial coinfection: a systematic review and meta‐analysis

Klein

Monteforte

Gupta

et al. 2016

Influenza Resp Viruses

455

355

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show abstract

“…Most deaths occur due to pulmonary complications, such as primary viral pneumonia (3) or a superimposed bacterial pneumonia (4). In both, respiratory deterioration is marked by acute lung injury (3,5), a potentially fatal syndrome of pulmonary edema that occurs due to the increased permeability of the lung microvasculature (6,7). Therapeutic options are limited.…”

mentioning

confidence: 99%

Influenza Virus Infection Induces Platelet-Endothelial Adhesion Which Contributes to Lung Injury

Sugiyama

Gamage

Zyla

et al. 2016

J Virol

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Lung injury after influenza infection is characterized by increased permeability of the lung microvasculature, culminating in acute respiratory failure. Platelets interact with activated endothelial cells and have been implicated in the pathogenesis of some forms of acute lung injury. Autopsy studies have revealed pulmonary microthrombi after influenza infection, and epidemiological studies suggest that influenza vaccination is protective against pulmonary thromboembolism; however, the effect of influenza infection on platelet-endothelial interactions is unclear. We demonstrate that endothelial infection with both laboratory and clinical strains of influenza virus increased the adhesion of human platelets to primary human lung microvascular endothelial cells. Platelets adhered to infected cells as well as to neighboring cells, suggesting a paracrine effect. Influenza infection caused the upregulation of von Willebrand factor and ICAM-1, but blocking these receptors did not prevent platelet-endothelial adhesion. Instead, platelet adhesion was inhibited by both RGDS peptide and a blocking antibody to platelet integrin ␣ 5 ␤ 1 , implicating endothelial fibronectin. Concordantly, lung histology from infected mice revealed viral dose-dependent colocalization of viral nucleoprotein and the endothelial marker PECAM-1, while platelet adhesion and fibronectin deposition also were observed in the lungs of influenza-infected mice. Inhibition of platelets using acetylsalicylic acid significantly improved survival, a finding confirmed using a second antiplatelet agent. Thus, influenza infection induces platelet-lung endothelial adhesion via fibronectin, contributing to mortality from acute lung injury. The inhibition of platelets may constitute a practical adjunctive strategy to the treatment of severe infections with influenza. Here, we show that this infection causes platelets to adhere to the lung endothelium. Importantly, blocking platelets using two distinct antiplatelet drugs improved survival in a mouse model of severe influenza infection. Thus, platelet inhibition may constitute a novel therapeutic strategy to improve the host response to severe infections with influenza.

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“…La descripción clásica de Louria para neumonía después de la pandemia H2N2 de 1957, señala cuatro categorías: neumonía sin compromiso radiológico, infección viral seguida de neumonía bacteriana, neumonía viral rápidamente progresiva y la concomitancia de neumonía bacteriana y viral 12 .…”

Section: Discussionunclassified

Impacto clínico de la influenza A H1N1 pandémica en el hospital de Puerto Montt, Chile

et al. 2011

Rev. méd. Chile

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Studies on Influenza in the Pandemic of 1957-1958. Ii. Pulmonary Complications of Influenza*†

Cited by 444 publications

References 20 publications

The frequency of influenza and bacterial coinfection: a systematic review and meta‐analysis

The frequency of influenza and bacterial coinfection: a systematic review and meta‐analysis

Influenza Virus Infection Induces Platelet-Endothelial Adhesion Which Contributes to Lung Injury

Impacto clínico de la influenza A H1N1 pandémica en el hospital de Puerto Montt, Chile

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