SummaryBackgroundRespiratory syncytial virus (RSV) infection is an important cause of pneumonia mortality in young children. However, clinical data for fatal RSV infection are scarce. We aimed to identify clinical and socioeconomic characteristics of children aged younger than 5 years with RSV-related mortality using individual patient data.MethodsIn this retrospective case series, we developed an online questionnaire to obtain individual patient data for clinical and socioeconomic characteristics of children aged younger than 5 years who died with community-acquired RSV infection between Jan 1, 1995, and Oct 31, 2015, through leading research groups for child pneumonia identified through a comprehensive literature search and existing research networks. For the literature search, we searched PubMed for articles published up to Feb 3, 2015, using the key terms “RSV”, “respiratory syncytial virus”, or “respiratory syncytial viral” combined with “mortality”, “fatality”, “death”, “died”, “deaths”, or “CFR” for articles published in English. We invited researchers and clinicians identified to participate between Nov 1, 2014, and Oct 31, 2015. We calculated descriptive statistics for all variables.FindingsWe studied 358 children with RSV-related in-hospital death from 23 countries across the world, with data contributed from 31 research groups. 117 (33%) children were from low-income or lower middle-income countries, 77 (22%) were from upper middle-income countries, and 164 (46%) were from high-income countries. 190 (53%) were male. Data for comorbidities were missing for some children in low-income and middle-income countries. Available data showed that comorbidities were present in at least 33 (28%) children from low-income or lower middle-income countries, 36 (47%) from upper middle-income countries, and 114 (70%) from high-income countries. Median age for RSV-related deaths was 5·0 months (IQR 2·3–11·0) in low-income or lower middle-income countries, 4·0 years (2·0–10·0) in upper middle-income countries, and 7·0 years (3·6–16·8) in high-income countries.InterpretationThis study is the first large case series of children who died with community-acquired RSV infection. A substantial proportion of children with RSV-related death had comorbidities. Our results show that perinatal immunisation strategies for children aged younger than 6 months could have a substantial impact on RSV-related child mortality in low-income and middle-income countries.FundingBill & Melinda Gates Foundation.
Very low birth weight (VLBW) infants with suspected late-onset infection requiring sepsis screening were enrolled in a prospective study to evaluate the diagnostic utilities of a comprehensive panel of key chemokines and cytokines, both individually and in combination, to identify diagnostic markers for early recognition of bacterial sepsis and necrotizing enterocolitis (NEC). Plasma chemokines interleukin (IL)-8, interferon-␥-inducible protein 10 (IP-10), monokine induced by interferon-␥ (MIG), monocyte chemoattractant protein 1 (MCP-1), growth-related oncogene-␣ (GRO-␣), and regulated upon activation of normal T cell expressed and secreted (RAN-TES) and cytokines IL-1, IL-6, IL-10, IL-12p70, and tumor necrosis factor ␣ (TNF-␣) were measured at the onset of sepsis (0 h) and 24 h later. Of 155 suspected infection episodes, 44 were classified as infected. Concentrations of all studied inflammatory mediators (except IL-1 and RANTES) were significantly higher in the infected than in the noninfected group at 0 h, but the levels decreased precipitously by 24 h. IP-10 with a plasma cutoff concentration Ն1250 pg/mL could identify all septicemic and NEC cases and had the highest overall sensitivity (93%) and specificity (89%) at 0 h. We conclude that preterm infants have the ability to induce a robust chemokine and cytokine response during sepsis, and IP-10 is a sensitive early marker of infection. and NEC are important risk factors that predispose to increased morbidity and mortality in preterm VLBW infants (1-4). A recent multicenter survey suggested that 21% of VLBW infants who survived Ͼ72 h of age had at least one episode of septicemia (1). Preterm infants who developed NEC had threefold increased risk of mortality (4). As the immunologic defense of preterm infants is considered to be immature and/or deficient (5), this category of patients is particularly vulnerable to developing severe and opportunistic infections in the immediate postnatal period (1,3,4). However, early warning signs and symptoms of systemic infection and NEC are often nonspecific and inconspicuous and can easily be confused with noninfective causes such as apnea of prematurity, gastrointestinal dysmotility, and acute exacerbation of bronchopulmonary dysplasia (6 -8). Thus, early identification of infants with bacterial sepsis and NEC has been recognized to be a major diagnostic challenge (7,8).Exposure to microorganisms and their derived products triggers a rapid and coordinated sequence of host reactions resulting in recruitment of leukocytes into areas of inflammation or sites of microbial invasion (9 -12). The regulation and trafficking of leukocytes into specific body tissues are principally controlled by chemoattractant cytokines or chemokines (10). The activation of leukocytes coupled with interaction of pro-and anti-inflammatory cytokines can influence the orchestration of the anti-infectious process and the magnitude of tissue damage and ultimately can determine the outcome of infection (13-16). Up-regulation (or down-regula...
Background:The progression to disseminated intravascular coagulation (DIC) in infected very low birth weight (VLBW; <1500 g) infants is difficult to predict with precision at the onset of sepsis. We investigated the immunologic profiles of preterm infants with sepsis, using chemokine and cytokine measurements to predict the development of sepsis-induced DIC at the onset of infection.
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