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652 Presentations
PROGRESSION FROM VTEC ENTERITIS TO HAEMOLYTIC URAEMIC SYNDROME (HUS) AMONG PAEDIATRIC CASES IN THE REPUBLIC OF IRELAND: A RETROSPECTIVE CASE/CASE STUDY (ID 147)
Abstract
Background
Ireland currently has the highest VTEC notification rate in Europe, progressing to haemolytic uraemic syndrome (HUS) in approximately 5-10% of cases and most frequently among paediatric cases. To date the effect of “place” as it relates to VTEC serotype, source, pathway and receptor have received little attention.
Methods
All confirmed cases of paediatric (≤ 5 years ) VTEC enteritis notified from January 1st 2013 to December 31st 2017 were geo-coded to one of ~19,000 Census Small Areas, and binary coded (Y/N) for HUS progression. Several national datasets were geo-referenced to the case dataset including socioeconomic profile, hydrogeological setting, landuse, and infrastructure , with penalised classification models employed to account for statistical “rarity”. Chi-square Automatic Interaction Detector (CHAID) trees were used to identifyattribute “breakpoints” .
Results
Overall, 63 cases of paediatric HUS (63/1,102; 5.7%) were analysed, with a classification accuracy of approximately 96% (60% of HUS cases accurately classified). Case age (breakpoint ≤3 years), case type (hospital inpatient), and VTEC serotype (O157, O26) were significantly predictive. Socioeconomic components (female unemployment rate ≤13%, rented accommodation >20%) and groundwater vulnerability classification (breakpoint: high/extreme) were also predictive. Local spatial attributes (deprivation, groundwater) were more significant than regional variables.
Conclusions
Developed models could be used as an “early-warning” system for HUS progression among paediatric VTEC cases. While VTEC progression appears to be both case- and therapy-related (i.e., severity), there is also a level of spatiotemporality. The association with groundwater vulnerability indicates a waterborne mode of transmission, with elevated groundwater vulnerability in parallel with higher rates of progression potentially due to higher VTEC contamination rates (i.e., dose). Higher levels of affluence associated with HUS progression may potentially serve as a proxy for exposure i.e. international travel, dietary variation and/or healthcare access.
NEONATAL BCG VACCINATION REDUCES THE RISK OF ECZEMA IN PREDISPOSED INFANTS – RESULTS FROM THE MIS BAIR RANDOMISED CONTROLLED TRIAL (ID 148)
Abstract
Background
Bacille Calmette-Guérin (BCG) vaccine could play a role in counteracting the rising prevalence of atopic diseases through its beneficial off-target effects. One aim of the MIS BAIR trial was to determine whether neonatal BCG vaccination reduces the incidence of eczema in the first year of life.
Methods
In this randomised controlled trial, the incidence and severity of eczema in the first 12 months of life was determined with 3-monthly questionnaires using the UK diagnostic tool and POEM score, respectively. Eczema was also assessed at a 12-month clinic visit using SCORAD.
Results
1272 infants were randomised to receive BCG-Denmark (median 1.5 days of life; IQR 0.9 to 2.5) or no BCG. The incidence of eczema in the first 12 months of life was lower in the BCG group (32.2%) compared with controls (36.6%) (risk difference (RD) -4.3%,95%CI -9.9% to 1.3%; multiple imputation model), resulting in a number needed to treat (NNT) of 23. Compared with controls, infants in the BCG group were less likely to have active eczema lesions at the 12-month visit (15.7% vs.19.2%;RD -3.5%,95%CI -8.0% to 1.0%), to use topical steroids (35.7% vs.39.0%;RD -3.3%,95%CI -9.2 to 2.7), and to have severe eczema scores (7.3% vs.10.2%;RD -3.0%,95%CI -8.8% to 2.7%), especially in the 3-month questionnaire (4.9% vs.15.9%;RD -11.0%,95%CI -23.7% to 1.6%). In high-risk infants (two atopic parents, n=344), the incidence of eczema was lower in the BCG group (35.3%) compared with controls (46.8%) (RD -11.5%,95%CI -21.9% to -1.2%) with a NNT of 8.7 (95%CI 4.6 to 83.3).
Conclusions
A single dose of BCG-Denmark soon after birth reduced the incidence of eczema, especially in infants with two atopic parents. There is insufficient evidence to recommend neonatal BCG vaccination for the general prevention of eczema.
Clinical Trial Registration
ClinicalTrial.gov: NCT01906853.
POPULATION PHARMACOKINETICS OF INTRAVENOUS COLISTIN ADMINISTERED IN CRITICALLY ILL PEDIATRIC PATIENTS AT HIGHER THAN RECOMMENDED DOSES (ID 161)
Abstract
Background
A limited amount of pharmacokinetic (PK) data suggest that currently recommended pediatric dosages of colistimethate sodium (CMS) by the Food and Drug Administration and European Medicines Agency [75,000-150,000 IU/kg/day, equivalent to ~2.5-5 mg/kg/day of colistin base activity (CBA)] may lead to suboptimal exposure, resulting in plasma colistin concentrations frequently <2 mg/L.
Methods
We conducted a population PK study in critically ill patients 1 month-14 years old, who received CMS for infections caused by carbapenem-resistant Gram-negative bacteria. CMS was dosed at 200,000 IU/kg/day (6.6 mg CBA/kg/day), 300,000 IU/kg/day (9.9 mg CBA/kg/day) or 350,000 IU/kg/day (11.6 mg CBA/kg/day), according to patient age and severity of infection. Plasma colistin concentrations were determined using ultra-performance liquid chromatography combined with electrospray ionization tandem mass spectrometry. Patients were closely monitored for adverse events.
Results
A total of 17 patients, 3 months-13.75 years (median 3.3 years) old, were studied. Colistin PK was described by a one-compartment disposition model including creatinine clearance, body weight and the presence or absence of systemic inflammatory response syndrome (SIRS) as covariates. The average colistin plasma steady-state concentration (Css,avg) ranged from 1.11-8.47 mg/L (median 2.92 mg/L). Ten patients had Css,avg ≥2 mg/L. The presence of SIRS was associated with decreased apparent clearance of colistin (47.8% of that without SIRS). The relationship between the mg/day of CBA to achieve each 1 mg/L of plasma colistin Css,avg and creatinine clearance (mL/min) was described by linear regression with different slopes for patients with and without SIRS. Nephrotoxicity, probably colistin-unrelated, was observed in one patient.
Conclusions
Administration of CMS at the above doses improved exposure and was well tolerated. Apparent clearance of colistin was influenced by creatinine clearance and the presence or absence of SIRS.
Clinical Trial Registration
This study does not report the results of a controlled trial.
PARASITES UNDER THE RADAR: ASYMPTOMATIC INFECTION WITH PLASMODIUM FALCIPARUM ELICITS NO TRANSCRIPTOMIC HOST-RESPONSE (ID 174)
Abstract
Background
Naturally acquired immunity to malaria, which follows many previous infections, eventually allows individuals in endemic countries to tolerate infection without symptoms. However, asymptomatic infections do act as an undetected reservoir sustaining malaria transmission. Therefore, understanding the mechanisms enabling the asymptomatic state, and identifying biomarkers of asymptomatic infection could contribute to malaria elimination. This study analysed whole blood transcriptomes of Ghanaian children without malaria, with asymptomatic Plasmodium falciparum infection, and with symptomatic P. falciparum malaria to investigate the host response.
Methods
Children (n=37) were recruited in Obom, a high transmission peri-urban region in Ghana, frequency-matched for age and sex between groups. Illumina RNA-sequencing was undertaken from Paxgene whole blood samples. Differential gene expression analysis was conducted using DESeq2, with adjustment for variation in major leukocyte populations measured by flow-cytometry analysis (false discovery rate ≤ 5%).
Results
Comparison of symptomatic (n=9) vs uninfected (n=7) children revealed 735 differentially expressed genes, enriched in immune response pathways. In contrast, comparison of asymptomatic (n=21) vs uninfected (n=7) children showed no differentially expressed genes. We replicated these results by reanalysis of a published microarray dataset (Gene Expression Omnibus database ID: GSE1124).
Conclusions
These findings suggest that the asymptomatic state in P. falciparum infection is not the result of a suppressive response acting on-, or orchestrated by circulating blood cells. Parasites instead appear to be “under the radar”, not triggering any immune response at all. This suggests that host-response biomarkers of asymptomatic infection will not be successful and alternative mechanisms enabling and maintaining the asymptomatic state, including epigenetic modifications, should be investigated.
Clinical Trial Registration
My trial/study does not report the results of a controlled trial.