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Setting: All community health workers (CHWs) in rural Kenema District, Sierra Leone. Objective: CHW programmes provide basic health services to fill gaps in human health resources. We compared trends in the reporting and management of childhood malaria, diarrhoea and pneumonia by CHWs before, during and after the Ebola outbreak (2014-2016). Design: Retrospective cross-sectional study using programme data. Results: CHW reporting increased from 59% pre-outbreak to 95% during the outbreak (P < 0.001), and was sustained at 98% post-outbreak. CHWs stopped using rapid diagnostic tests for malaria mid-outbreak, and their use had not resumed post-outbreak. The average monthly number of presumptive treatments for malaria increased from 2931 pre-outbreak to 5013 during and 5331 post-outbreak (P < 0.001). The average number of monthly treatments for diarrhoea and pneumonia decreased from respectively 1063 and 511 pre-outbreak to 547 and 352 during the outbreak (P = 0.01 and P = 0.04). Post-outbreak pneumonia treatments increased (mean 1126 compared to pre-outbreak, P = 0.003), and treatments for diarrhoea returned to pre-outbreak levels (P = 0.2). Conclusion: The CHW programme demonstrated vulnerability, but also resilience, during and in the early period after the Ebola outbreak. Investment in CHWs is required to strengthen the health care system, as they can cover pre-existing gaps in facility-based health care and those created by outbreaks.

Setting: All public health facilities in Bonthe District, rural Sierra Leone. Objective: To compare, in the periods before and during the Ebola virus disease outbreak, 1) the submission and completeness of monthly human immunodeficiency virus (HIV) reports, and 2) the uptake of HIV testing and care for pregnant women and the general population. Design: A cross-sectional study using routine programme data. Results: Of the 627 HIV reports expected in each period, 406 (65%) were submitted in the pre-Ebola period and 376 (60%) during the Ebola outbreak (P = 0.08), of which respectively 318 (78%) and 335 (89%) had complete information (P < 0.001). In the pre-Ebola period, 5012 pregnant women underwent testing for HIV, of whom 25 were HIV-positive, compared to 4254 during the Ebola period, of whom 21 were HIV-positive (P < 0.001). Of those who were HIV-positive, respectively 14 (56%) and 21 (100%) received antiretroviral prophylaxis or antiretroviral therapy (ART) (P < 0.001). In the general population, 5770 persons underwent HIV testing pre-Ebola vs. 3095 in the Ebola period (P < 0.001); of those who tested positive for HIV, respectively 62% (33/53) and 81% (33/41) were started on ART (P = 0.06). Conclusion: There was suboptimal reporting on HIV/acquired immune-deficiency disease syndrome activities before and during the Ebola virus disease outbreak. HIV testing decreased during the Ebola outbreak, while the uptake of prevention of mother-to-child transmission and ART increased. Pre-emptive actions are needed to maintain the levels of HIV testing in any future outbreak.

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”.