Journal Article > ResearchFull Text
J Infect Dis. 2016 May 25; Volume 215 (Issue 1); 64–69.; DOI:10.1093/infdis/jiw206
Muehlenbachs A, de la Rosa Vazquez O, Bausch DG, Schafer IJ, Paddock C, et al.
J Infect Dis. 2016 May 25; Volume 215 (Issue 1); 64–69.; DOI:10.1093/infdis/jiw206
Here we describe clinicopathologic features of EVD in pregnancy. One woman infected with Sudan virus in Gulu, Uganda in 2000 had a stillbirth and survived, and another woman with Bundibugyo virus had a livebirth with maternal and infant death in Isiro, the Democratic Republic of the Congo in 2012. Ebolavirus antigen was seen in the syncytiotrophoblast and placental maternal mononuclear cells by immunohistochemistry, and no antigen was seen in fetal placental stromal cells or fetal organs. In the Gulu case, ebolavirus antigen localized to malaria pigment-laden macrophages. These data suggest trophoblast infection may be a mechanism of transplacental ebolavirus transmission.
Journal Article > ResearchFull Text
Clin Infect Dis. 2016 August 15; Volume 63 (Issue 8); 1026-1033.; DOI:10.1093/cid/ciw452
Rosenke K, Adjemian J, Munster VJ, Marzi A, Falzarano D, et al.
Clin Infect Dis. 2016 August 15; Volume 63 (Issue 8); 1026-1033.; DOI:10.1093/cid/ciw452
BACKGROUND
The ongoing Ebola outbreak in West Africa has resulted in 28 646 suspected, probable, and confirmed Ebola virus infections. Nevertheless, malaria remains a large public health burden in the region affected by the outbreak. A joint Centers for Disease Control and Prevention/National Institutes of Health diagnostic laboratory was established in Monrovia, Liberia, in August 2014, to provide laboratory diagnostics for Ebola virus.
METHODS
All blood samples from suspected Ebola virus-infected patients admitted to the Médecins Sans Frontières ELWA3 Ebola treatment unit in Monrovia were tested by quantitative real-time polymerase chain reaction for the presence of Ebola virus and Plasmodium species RNA. Clinical outcome in laboratory-confirmed Ebola virus-infected patients was analyzed as a function of age, sex, Ebola viremia, and Plasmodium species parasitemia.
RESULTS
The case fatality rate of 1182 patients with laboratory-confirmed Ebola virus infections was 52%. The probability of surviving decreased with increasing age and decreased with increasing Ebola viral load. Ebola virus-infected patients were 20% more likely to survive when Plasmodium species parasitemia was detected, even after controlling for Ebola viral load and age; those with the highest levels of parasitemia had a survival rate of 83%. This effect was independent of treatment with antimalarials, as this was provided to all patients. Moreover, treatment with antimalarials did not affect survival in the Ebola virus mouse model.
CONCLUSIONS
Plasmodium species parasitemia is associated with an increase in the probability of surviving Ebola virus infection. More research is needed to understand the molecular mechanism underlying this remarkable phenomenon and translate it into treatment options for Ebola virus infection.
The ongoing Ebola outbreak in West Africa has resulted in 28 646 suspected, probable, and confirmed Ebola virus infections. Nevertheless, malaria remains a large public health burden in the region affected by the outbreak. A joint Centers for Disease Control and Prevention/National Institutes of Health diagnostic laboratory was established in Monrovia, Liberia, in August 2014, to provide laboratory diagnostics for Ebola virus.
METHODS
All blood samples from suspected Ebola virus-infected patients admitted to the Médecins Sans Frontières ELWA3 Ebola treatment unit in Monrovia were tested by quantitative real-time polymerase chain reaction for the presence of Ebola virus and Plasmodium species RNA. Clinical outcome in laboratory-confirmed Ebola virus-infected patients was analyzed as a function of age, sex, Ebola viremia, and Plasmodium species parasitemia.
RESULTS
The case fatality rate of 1182 patients with laboratory-confirmed Ebola virus infections was 52%. The probability of surviving decreased with increasing age and decreased with increasing Ebola viral load. Ebola virus-infected patients were 20% more likely to survive when Plasmodium species parasitemia was detected, even after controlling for Ebola viral load and age; those with the highest levels of parasitemia had a survival rate of 83%. This effect was independent of treatment with antimalarials, as this was provided to all patients. Moreover, treatment with antimalarials did not affect survival in the Ebola virus mouse model.
CONCLUSIONS
Plasmodium species parasitemia is associated with an increase in the probability of surviving Ebola virus infection. More research is needed to understand the molecular mechanism underlying this remarkable phenomenon and translate it into treatment options for Ebola virus infection.
Journal Article > CommentaryFull Text
Nat Microbiol. 2016 February 24; Volume 1 (Issue 3); 16007.; DOI:10.1038/nmicrobiol.2016.7
Sprecher A, Feldman H, Hensley L, Kobinger GP, Nichol ST, et al.
Nat Microbiol. 2016 February 24; Volume 1 (Issue 3); 16007.; DOI:10.1038/nmicrobiol.2016.7
Concern over Ebola becoming endemic in West Africa has appeared in the medical and lay media. Routes of transmission, rates of viral evolution, suitability of humans as hosts and rarity of spillover events make this very unlikely. Without evidence that endemic Ebola is likely, ending epidemics should remain the focus.
Journal Article > ResearchFull Text
Emerg Infect Dis. 2016 February 1; Volume 22 (Issue 2); 323-326.; DOI:10.3201/eid2202.151656
de Wit E, Falzarano D, Onyango C, Rosenke K, Marzi A, et al.
Emerg Infect Dis. 2016 February 1; Volume 22 (Issue 2); 323-326.; DOI:10.3201/eid2202.151656
Malaria is a major public health concern in the countries affected by the Ebola virus disease epidemic in West Africa. We determined the feasibility of using molecular malaria diagnostics during an Ebola virus disease outbreak and report the incidence of Plasmodium spp. parasitemia in persons with suspected Ebola virus infection.
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.