Development of a Pediatric Ebola Predictive Score, Sierra Leone1.

We compared children who were positive for Ebola virus disease (EVD) with those who were negative to derive a pediatric EVD predictor (PEP) score. We collected data on all children <13 years of age admitted to 11 Ebola holding units in Sierra Leone during August 2014-March 2015 and performed multivariable logistic regression. Among 1,054 children, 309 (29%) were EVD positive and 697 (66%) EVD negative, with 48 (5%) missing. Contact history, conjunctivitis, and age were the strongest positive predictors for EVD. The PEP score had an area under receiver operating characteristics curve of 0.80. A PEP score of 7/10 was 92% specific and 44% sensitive; 3/10 was 30% specific, 94% sensitive. The PEP score could correctly classify 79%-90% of children and could be used to facilitate triage into risk categories, depending on the sensitivity or specificity required.

Ebola Virus Disease in Children, Sierra Leone, 2014-2015.

Little is known about potentially modifiable factors in Ebola virus disease in children. We undertook a retrospective cohort study of children <13 years old admitted to 11 Ebola holding units in the Western Area, Sierra Leone, during 2014-2015 to identify factors affecting outcome. Primary outcome was death or discharge after transfer to Ebola treatment centers. All 309 Ebola virus-positive children 2 days-12 years old were included; outcomes were available for 282 (91%). Case-fatality was 57%, and 55% of deaths occurred in Ebola holding units. Blood test results showed hypoglycemia and hepatic/renal dysfunction. Death occurred swiftly (median 3 days after admission) and was associated with younger age and diarrhea. Despite triangulation of information from multiple sources, data availability was limited, and we identified no modifiable factors substantially affecting death. In future Ebola virus disease epidemics, robust, rapid data collection is vital to determine effectiveness of interventions for children.

Reductions in inpatient mortality following interventions to improve emergency hospital care in Freetown, Sierra Leone.

BACKGROUND: The demand for high quality hospital care for children in low resource countries is not being met. This paper describes a number of strategies to improve emergency care at a children's hospital and evaluates the impact of these on inpatient mortality. In addition, the cost-effectiveness of improving emergency care is estimated. METHODS AND FINDINGS: A team of local and international staff developed a plan to improve emergency care for children arriving at The Ola During Children's Hospital, Freetown, Sierra Leone. Following focus group discussions, five priority areas were identified to improve emergency care; staff training, hospital layout, staff allocation, medical equipment, and medical record keeping. A team of international volunteers worked with local staff for six months to design and implement improvements in these five priority areas. The improvements were evaluated collectively rather than individually. Before the intervention, the inpatient mortality rate was 12.4%. After the intervention this improved to 5.9%. The relative risk of dying was 47% (95% CI 0.369-0.607) lower after the intervention. The estimated number of lives saved in the first two months after the intervention was 103. The total cost of the intervention was USD 29 714, the estimated cost per death averted was USD 148. There are two main limitation of the study. Firstly, the brevity of the study and secondly, the assumed homogeneity of the clinical cases that presented to the hospital before and after the intervention. CONCLUSIONS: This study demonstarted a signficant reductuion in inpatient mortality rate after an intervention to improve emergency hospital care If the findings of this paper could be reproduced in a larger more rigorous study, improving the quality of care in hospitals would be a very cost effective strategy to save children's lives in low resource settings.

G6PD deficiency assessment in Freetown, Sierra Leone, reveals further insight into the molecular heterogeneity of G6PD A-.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency in Africa is of high prevalence, although precise data are lacking in many individual nations. We investigated 129 unrelated subjects (71 male subjects, 58 female subjects) visiting a teaching hospital in Freetown, Sierra Leone, to collect baseline data on the distribution of G6PD deficiency among respective ethnic groups in the country. We confirmed eight G6PD-deficient male subjects by two formazan-based blood tests (11.3% of the male subjects examined), and also detected the common 376A > G mutation in 11 male subjects and eight female subjects by sequencing exons 3-5 of the G6PD gene. Selected samples were further sequenced for exons 2-13 and introns 5, 7, 8, and 11. Among the deficient male subjects, six were G6PD A- carrying the double mutations (202G > A and 376A > G), all of whom were in the Temne and Mende ethnic groups. Others included A- Betica, and a novel variant having double mutations in exon 5 (311G > A and 376A > G forming 104 Arg > His and 126 Asn > Asp, respectively), which we designate as G6PD Sierra Leone. Subsequent haplotype analysis linked this novel variant to the G6PD A- "family".