Journal Article > ResearchFull Text
J Infect Dis. 2011 November 1; Volume 204 (Issue suppl_3); DOI:10.1093/infdis/jir312
Adjemian J, Farnon EC, Tschioko F, Wamala JF, Byaruhanga E, et al.
J Infect Dis. 2011 November 1; Volume 204 (Issue suppl_3); DOI:10.1093/infdis/jir312
Marburg hemorrhagic fever was detected among 4 miners in Ibanda District, Uganda, from June through September, 2007. Infection was likely acquired through exposure to bats or bat secretions in a mine in Kamwenge District, Uganda, and possibly human-to-human transmission between some patients. We describe the epidemiologic investigation and the health education response.
Journal Article > ResearchFull Text
Emerg Infect Dis. 2016 February 1; Volume 22 (Issue 2); 217-23.; DOI:10.3201/eid2202.151250
Crowe SJ, Maenner MJ, Kuah S, Erickson BR, Coffee M, et al.
Emerg Infect Dis. 2016 February 1; Volume 22 (Issue 2); 217-23.; DOI:10.3201/eid2202.151250
To determine whether 2 readily available indicators predicted survival among patients with Ebola virus disease in Sierra Leone, we evaluated information for 216 of the 227 patients in Bo District during a 4-month period. The indicators were time from symptom onset to healthcare facility admission and quantitative real-time reverse transcription PCR cycle threshold (Ct), a surrogate for viral load, in first Ebola virus-positive blood sample tested. Of these patients, 151 were alive when detected and had reported healthcare facility admission dates and Ct values available. Time from symptom onset to healthcare facility admission was not associated with survival, but viral load in the first Ebola virus-positive blood sample was inversely associated with survival: 52 (87%) of 60 patients with a Ct of >24 survived and 20 (22%) of 91 with a Ct of <24 survived. Ct values may be useful for clinicians making treatment decisions or managing patient or family expectations.
Journal Article > ResearchFull Text
Cell. 2015 June 18; Volume 161 (Issue 7); DOI:10.1016/j.cell.2015.06.007
Park DJ, Dudas G, Wohl S, Goba A, Whitmer SL, et al.
Cell. 2015 June 18; Volume 161 (Issue 7); DOI:10.1016/j.cell.2015.06.007
The 2013-2015 Ebola virus disease (EVD) epidemic is caused by the Makona variant of Ebola virus (EBOV). Early in the epidemic, genome sequencing provided insights into virus evolution and transmission and offered important information for outbreak response. Here, we analyze sequences from 232 patients sampled over 7 months in Sierra Leone, along with 86 previously released genomes from earlier in the epidemic. We confirm sustained human-to-human transmission within Sierra Leone and find no evidence for import or export of EBOV across national borders after its initial introduction. Using high-depth replicate sequencing, we observe both host-to-host transmission and recurrent emergence of intrahost genetic variants. We trace the increasing impact of purifying selection in suppressing the accumulation of nonsynonymous mutations over time. Finally, we note changes in the mucin-like domain of EBOV glycoprotein that merit further investigation. These findings clarify the movement of EBOV within the region and describe viral evolution during prolonged human-to-human transmission.