Welcome to the ESPID 2021 Meeting Calendar
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Introduction (ID 2337)
Novel Approaches in Digital Tools to Diagnose Pneumonia in Children (ID 229)
Ultrasound to Diagnose Lung Infections in Adults and Children (ID 230)
AN ANALYSIS OF IN-VIVO HOST AND PATHOGEN TRANSCRIPTOMIC SIGNATURES ASSOCIATED WITH SEVERE OUTCOMES IN PEDIATRIC INFLUENZA-STAPHYLOCOCCUS AUREUS PNEUMONIA (ID 655)
Abstract
Background
S.aureus pneumonia complicating influenza infection is an important cause of PICU related child-mortality. Delineating pathogen-related and host immune predictors of severe outcomes will aid in prioritising targeted interventions and indentifying at-risk children.
Methods
mRNA was extracted from endotracheal aspirates from 34 previously healthy children requiring intubation for influenza infection. Ten each had confirmed respiratory coinfection with MRSA and MSSA, and 14 children with influenza alone served as controls. mRNA expression of 200 S.aureus and 600 human immune genes were analysed to identify relevant gene signatures and pathways associated with survival and death/prolonged multiple organ dysfunction syndrome (pMODS).
Results
More host genes were differentially expressed in the MRSA group than in the MSSA group. Down-regulation of host genes such as CXCL10 and CXCL11 were associated with death/pMODS (Figure1). Forty-four significant genes in the MRSA group and 17 genes in the MSSA group satisfied criteria for biological plausibility and were involved in programmed cell death, complement, cytokine signalling and expression of C-type lecithin receptors. Among those infected with S.aureus in the died/pMODS group [n=10] 65 significant genes met biological criteria while 16 genes met similar criteria in the group who survived [n=10]. Interferon-alpha, -beta and -gamma as well as interleukin signalling – IL-1, -36, -38, -10, -4, -13, -21 were the most significant pathways down-regulated in the died/pMODS group. Upregulation of interleukin signalling – IL-6, -10, -27, -4,-13 were the most significant pathways in the survivors. The mecA gene was the only significantly differentially expressed pathogen gene between MRSA and MSSA groups.
Conclusions
Early in the course of severe influenza-S.aureus pneumonia, airway host gene expression profiles delineate adverse outcomes, unlike pathogen genes. Innate immune pathways, involving CXCL10 and CXCL11, drive host responses that may impact outcome.
Clinical Trial Registration
Clinical trial registration: N/A
MYCOPLASMA PNEUMONIAE CARRIAGE EVADES INDUCTION OF PROTECTIVE MUCOSAL ANTIBODIES (ID 322)
Abstract
Background
Mycoplasma pneumoniae is the most common bacterial cause of pneumonia in children hospitalized for community-acquired pneumonia. Prevention of infection by vaccines may be an important strategy in the presence of emerging macrolide resistant M. pneumoniae. However, knowledge of immune responses to M. pneumoniae is limited, complicating vaccine design. We therefore studied the antibody response during M. pneumoniae infection and asymptomatic carriage.
Methods
We measured mucosal and systemic antibody levels to M. pneumoniae in nasal lavage and serum samples from M. pneumoniae pneumonia patients, non-M. pneumoniae pneumonia patients, asymptomatic M. pneumoniae carriers and non-carriers in two independent cohorts. We used an in vitro assay to measure the ability of antibodies to block adhesion of M. pneumoniae to respiratory epithelium.
Results
In a nested case-control study (n=80) of M. pneumoniae carriers and matched controls we observed that carriage by M. pneumoniae does not lead to a rise in either mucosal or systemic M. pneumoniae-specific antibodies, even after months of persistent carriage. We replicated this finding in a second cohort (n=69) and also found that during M. pneumoniae community-acquired pneumonia, mucosal levels of M. pneumoniae-specific IgA and IgG did increase significantly. In vitro adhesion assays revealed that high levels of M. pneumoniae-specific antibodies in nasal secretions of pediatric patients prevented the adhesion of M. pneumoniae to respiratory epithelial cells.
Conclusions
In conclusion, our study demonstrates that M. pneumoniae-specific mucosal antibodies protect against bacterial adhesion to respiratory epithelial cells and are induced only during M. pneumoniae infection and not during asymptomatic carriage. This is strikingly different from carriage with bacteria such as Streptococcus pneumoniae where mucosal antibodies are induced by bacterial carriage.
Clinical Trial Registration
Medical Ethics Review Board of the Erasmus MC NL20418.078.08
“PREDICTING MORTALITY AMONG CHILDREN ADMITTED WITH PNEUMONIA TO A DISTRICT HOSPITAL IN MANHIÇA, MOZAMBIQUE” (ID 1516)
Abstract
Background
Pneumonia is the single largest infectious cause of death in children worldwide. In low- and middle-income countries the in-hospital management of child pneumonia remains a challenge in part due to lack of specificity in the diagnosis. The goal of this study is to identify how to better predict mortality in children under 5 years of age with suspected pneumonia in Manhiça’s District Hospital (Mozambique), a malaria endemic setting.
Methods
In this study we analised the records of 835 children admitted from September 2006 to September 2007 with suspected pneumonia. Primary outcome was mortality during hospital admission and up to 21 days post-discharge. The pre-defined list of candidate predictors of mortality included both clinical variables and complementary test results on admission. We developed 2 models using automated stepwise regression with backward elimination. We calculated Area Under the Curve (AUC) for both models as well as for the Lambaréné Organ Disfunction score (LOD score).
Results
We reported 102 deaths. We identified 11 predictors for the comprehensive model including: age, sex, WAZ, history of seizures, deep breathing, nasal flaring, prostration, hyperpyrexia, wheezing, HIV status and parasitaemia. In the absence of complementary test variables (pragmatic model), cyanosis was found to be a predictor, and deep breathing and hyperpyrexia were dropped from the model. Pragmatic and comprehensive models presented AUC of 0.9 and 0.92 respectively and the LOD score AUC was 0.81 in the same sample.
Conclusions
Both models demonstrated an outstanding discrimination performance in the same sample, but further analysis needs to be carried out before this model can be used in a clinical setting. The LOD score still constitutes a very good predictive score for mortality in this group, similar to what has been previously reported.