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31 results on '"Kabyemela, Edward"'

1. Immunization with PfGBP130 generates antibodies that inhibit RBC invasion by P. falciparum parasites

Author

Johnson, Yannick, primary, Shakri, Ahmad Rushdi, additional, Pond-Tor, Sunthorn, additional, Jnawali, Anup, additional, Najrana, Tanbir, additional, Wu, Haiwei, additional, Badhai, Jhasketan, additional, Alameh, Mohamad-Gabriel, additional, Weissman, Drew, additional, Kabyemela, Edward, additional, Duffy, Patrick, additional, Fried, Michal, additional, Kurtis, Jonathan, additional, and Raj, Dipak Kumar, additional

Published
2024
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3. Anti-PfGARP activates programmed cell death of parasites and reduces severe malaria

Author

Raj, Dipak K., Das Mohapatra, Alok, Jnawali, Anup, Zuromski, Jenna, Jha, Ambrish, Cham-Kpu, Gerald, Sherman, Brett, Rudlaff, Rachel M., Nixon, Christina E., Hilton, Nicholas, Oleinikov, Andrew V., Chesnokov, Olga, Merritt, Jordan, Pond-Tor, Sunthorn, Burns, Lauren, Jolly, Grant, Ben Mamoun, Choukri, Kabyemela, Edward, Muehlenbachs, Atis, Lambert, Lynn, Orr-Gonzalez, Sachy, Gnädig, Nina F., Fidock, David A., Park, Sangshin, Dvorin, Jeffrey D., Pardi, Norbert, Weissman, Drew, Mui, Barbara L., Tam, Ying K., Friedman, Jennifer F., Fried, Michal, Duffy, Patrick E., and Kurtis, Jonathan D.

Published
2020
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4. Parasite burden and severity of malaria in Tanzanian children.

Author

Gonçalves, Bronner, Huang, Chiung-Yu, Morrison, Robert, Holte, Sarah, Kabyemela, Edward, Prevots, D, Fried, Michal, and Duffy, Patrick

Subjects
Child, Preschool, Disease Resistance, Female, Humans, Infant, Infant, Newborn, Longitudinal Studies, Malaria, Falciparum, Male, Parasite Load, Parasitemia, Parity, Placenta, Placenta Diseases, Plasmodium falciparum, Pregnancy, Proportional Hazards Models, Risk Factors, Severity of Illness Index, Sickle Cell Trait, Tanzania
Abstract

BACKGROUND: Severe Plasmodium falciparum malaria is a major cause of death in children. The contribution of the parasite burden to the pathogenesis of severe malaria has been controversial. METHODS: We documented P. falciparum infection and disease in Tanzanian children followed from birth for an average of 2 years and for as long as 4 years. RESULTS: Of the 882 children in our study, 102 had severe malaria, but only 3 had more than two episodes. More than half of first episodes of severe malaria occurred after a second infection. Although parasite levels were higher on average when children had severe rather than mild disease, most children (67 of 102) had high-density infection (>2500 parasites per 200 white cells) with only mild symptoms before severe malaria, after severe malaria, or both. The incidence of severe malaria decreased considerably after infancy, whereas the incidence of high-density infection was similar among all age groups. Infections before and after episodes of severe malaria were associated with similar parasite densities. Nonuse of bed nets, placental malaria at the time of a womans second or subsequent delivery, high-transmission season, and absence of the sickle cell trait increased severe-malaria risk and parasite density during infections. CONCLUSIONS: Resistance to severe malaria was not acquired after one or two mild infections. Although the parasite burden was higher on average during episodes of severe malaria, a high parasite burden was often insufficient to cause severe malaria even in children who later were susceptible. The diverging rates of severe disease and high-density infection after infancy, as well as the similar parasite burdens before and after severe malaria, indicate that naturally acquired resistance to severe malaria is not explained by improved control of parasite density. (Funded by the National Institute of Allergy and Infectious Diseases and others.).

Published
2014

9. Independent lineages of highly sulfadoxine-resistant Plasmodium falciparum haplotypes, Eastern Africa

Author

Taylor, Steve M., Antonia, Alejandro L., Harrington, Whitney E., Goheen, Morgan M., Mwapasa, Victor, Chaluluka, Ebbie, Fried, Michal, Kabyemela, Edward, Madanitsa, Mwayi, Khairallah, Carole, Kalilani-Phiri, Linda, Tshefu, Antoinette K., Rogerson, Stephen J., ter Kuile, Feiko O., Duffy, Patrick E., and Meshnick, Steven R.

Subjects
World Health Organization, International economic relations, Analysis, Antimalarials -- Analysis, Drug resistance -- Analysis, Plasmodium falciparum -- Analysis, Malaria -- Analysis
Abstract

Antimalarial drug resistance threatens to undermine efforts to control Plasmodium falciparum malaria. In sub-Saharan Africa, P. falciparum resistance to sulfadoxine/pyrimethamine (SP) is widespread, as shown by clinical treatment failures and [...]

Published
2014
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13. Elevated ferritin and malaria: cause or effect?

Author

Lowe, David, Pasvol, Geoffrey, Kabyemela, Edward, Fried, Michal, Kurtis, Jonathan, and Duffy, Patrick

Subjects
Malaria -- Risk factors, Malaria -- Demographic aspects, Ferritin -- Physiological aspects, Health
Published
2009

15. Maternal peripheral blood level of IL-10 as a marker for inflammatory placental malaria

Author

Mutabingwa Theonest K, Kurtis Jonathan D, Fried Michal, Muehlenbachs Atis, Kabyemela Edward R, and Duffy Patrick E

Subjects
Arctic medicine. Tropical medicine, RC955-962, Infectious and parasitic diseases, RC109-216
Abstract

Abstract Background Placental malaria (PM) is an important cause of maternal and foetal mortality in tropical areas, and severe sequelae and mortality are related to inflammation in the placenta. Diagnosis is difficult because PM is often asymptomatic, peripheral blood smear examination detects parasitemia as few as half of PM cases, and no peripheral markers have been validated for placental inflammation. Methods In a cohort of Tanzanian parturients, PM was determined by placental blood smears and placental inflammation was assessed by histology and TNF mRNA levels. Maternal peripheral blood levels of several immune mediators previously implicated in PM pathogenesis, as well as ferritin and leptin were measured. The relationship between the levels of these soluble factors to PM and placental inflammation was examined. Results Peripheral levels of TNF, TNF-RI, TNF-RII, IL-1, IL-10, and ferritin were elevated during PM, whereas levels of IFN-γ, IL-4, IL-5 and IL-6 were unchanged and levels of leptin were decreased. In receiver operating characteristic curve analysis, IL-10 had the greatest area under the curve, and would provide a sensitivity of 60% with a false positive rate of 10%. At a cut off level of 15 pg/mL, IL-10 would detect PM with a sensitivity of 79.5% and a specificity of 84.3%. IL-10 levels correlated with placental inflammatory cells and placental TNF mRNA levels in first time mothers. Conclusion These data suggest that IL-10 may have utility as a biomarker for inflammatory PM in research studies, but that additional biomarkers may be required to improve clinical diagnosis and management of malaria during pregnancy.

Published
2008
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17. Maternally-derived Antibodies to Schizont Egress Antigen-1 and Protection of Infants From Severe Malaria

Author

Kurtis, Jonathan D, primary, Raj, Dipak K, additional, Michelow, Ian C, additional, Park, Sangshin, additional, Nixon, Christina E, additional, McDonald, Emily A, additional, Nixon, Christian P, additional, Pond-Tor, Sunthorn, additional, Jha, Ambrish, additional, Taliano, Ross J, additional, Kabyemela, Edward R, additional, Friedman, Jennifer F, additional, Duffy, Patrick E, additional, and Fried, Michal, additional

Published
2018
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21. Fetal origins of malarial disease: cord blood cytokines as risk markers for pediatric severe malarial anemia

Author

Brickley, Elizabeth B, Wood, Angela M, Kabyemela, Edward, Morrison, Robert, Kurtis, Jonathan D, Fried, Michal, and Duffy, Patrick E

Abstract

BACKGROUND: Severe malarial anemia (SMA) remains a major cause of pediatric illness and mortality in Sub-Saharan Africa. Here we test the hypothesis that prenatal exposures, reflected by soluble inflammatory mediators in cord blood, can condition an individual's susceptibility to SMA. METHODS: In a Tanzanian birth cohort (n = 743), we measured cord blood concentrations of tumor necrosis factor (TNF), TNF receptors I and II (TNF-RI and TNF-RII), interleukin (IL)-1β, IL-4, IL-5, IL-6, IL-10, and interferon gamma (IFN-γ). After adjusting for conventional covariates, we calculated the hazard ratios (HR) for time to first SMA event with log(e) cytokine concentrations dichotomized at the median, by quartile, and per standard deviation (SD) increase. RESULTS: Low levels of TNF, TNF-RI, IL-1β, and IL-5 and high levels of TNF-RII were associated statistically significantly and respectively with approximately 3-fold, 2-fold, 8-fold, 4-fold, and 3-fold increased risks of SMA (Hb < 50 g/L). TNF, TNF-RI, and IL-1β concentrations were inversely and log-linearly associated with SMA risk; the HR (95% confidence interval [CI]) per 1-SD increase were respectively 0.81 (.65, 1.02), 0.76 (.62, .92), and 0.50 (.40, .62). CONCLUSIONS: These data suggest that proinflammatory cytokine levels at birth are inversely associated with SMA risk and support the hypothesis that pediatric malarial disease has fetal origins.

Published
2014

24. Independent Lineages of Highly Sulfadoxine-ResistantPlasmodium falciparumHaplotypes, Eastern Africa

Author

Taylor, Steve M., primary, Antonia, Alejandro L., additional, Harrington, Whitney E., additional, Goheen, Morgan M., additional, Mwapasa, Victor, additional, Chaluluka, Ebbie, additional, Fried, Michal, additional, Kabyemela, Edward, additional, Madanitsa, Mwayi, additional, Khairallah, Carole, additional, Kalilani-Phiri, Linda, additional, Tshefu, Antoinette K., additional, Rogerson, Stephen J., additional, ter Kuile, Feiko O., additional, Duffy, Patrick E., additional, and Meshnick, Steven R., additional

Published
2014
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