Abstract | BACKGROUND: METHODS: We performed a genetic case-control study of pneumococcal bacteremia in Kenyan children stratified across a period of falling malaria transmission between 1998 and 2010. RESULTS: Four hundred twenty-nine Kenyan children with pneumococcal bacteremia and 2677 control children were included in the study. Among control children, G6PD deficiency, secondary to the rs1050828 G>A mutation, was common, with 11.2% (n = 301 of 2677) being hemi- or homozygotes and 33.3% (n = 442 of 1329) of girls being heterozygotes. We found that G6PD deficiency increased the risk of pneumococcal bacteremia, but only during a period of high malaria transmission (P = 0.014; OR 2.33, 95% CI 1.19-4.57). We estimate that the population attributable fraction of G6PD deficiency on risk of pneumococcal bacteremia in areas under high malaria transmission is 0.129. CONCLUSIONS:
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Authors | James J Gilchrist, Sophie Uyoga, Matti Pirinen, Anna Rautanen, Salim Mwarumba, Patricia Njuguna, Neema Mturi, Kenyan Bacteraemia Study Group, Adrian V S Hill, J Anthony G Scott, Thomas N Williams |
Journal | BMC medicine
(BMC Med)
Vol. 18
Issue 1
Pg. 148
(06 15 2020)
ISSN: 1741-7015 [Electronic] England |
PMID | 32536341
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Glucosephosphate Dehydrogenase
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Topics |
- Bacteremia
(etiology)
- Case-Control Studies
- Child
- Child, Preschool
- Female
- Glucosephosphate Dehydrogenase
(adverse effects)
- Humans
- Infant
- Kenya
- Male
- Pneumococcal Infections
(etiology)
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