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Terrie Taylor - Michigan State University. East Lansing, MI, UNITED STATES

Terrie Taylor

Internal Medicine Professor | Michigan State University

East Lansing, MI, UNITED STATES

Internationally recognized expert on malaria, tropical diseases and African health care.

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Biography

Terrie Taylor has studied and treated patients with malaria for more than 30 years.

An internationally recognized scientist and physician, Taylor spends six months a year in Malawi, conducting her research and caring for patients, the vast majority who are children, through the Blantyre Malaria Project, established by Taylor and her colleague Malcolm Molyneux.

Taylor was involved in bringing the first magnetic resonance imaging unit (MRI) to Malawi for use in her research and clinical efforts.

She can speak to all aspects of malaria and tropical medicine practices.

Industry Expertise (7)

Research

Writing and Editing

Education/Learning

Health and Wellness

Health Care - Facilities

Health Care - Providers

Health Care - Services

Areas of Expertise (4)

African Health Care

Tropical Medicine

Malaria Research

Malaria Treatment

Accomplishments (1)

Dr. Nathan Davis International Award in Medicine (professional)

2011-02-01

Awarded by AMA Foundation

Education (3)

Liverpool School of Tropical Medicine: M.A., Tropical Medicine 1986

Chicago College of Osteapathic Medicine: D.O. 1981

Swarthmore College: B.A., Biology 1977

Affiliations (4)

  • American Osteopathic Association
  • Michigan Association of Osteopathic Physicians and Surgeons
  • American Society of Tropical Medicine and Hygiene
  • American College of Osteopathic Internists

News (3)

MSU Doctors' Discovery of How Malaria Kills Children Will Lead to Life-Saving Treatments

MSU Today  online

2015-03-15

In a groundbreaking study published in the New England Journal of Medicine, Michigan State University’s Terrie Taylor and her team discovered what causes death in children with cerebral malaria, the deadliest form of the disease...

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Brain Swelling Tied to Deaths From Malaria

The New York Times  print

2015-03-18

“What’s killing these kids is that they stop breathing, because the respiratory center in the brain stem is compressed by the swelling,” said Dr. Terrie E. Taylor, the senior author of the study and a professor at the Michigan State University College of Osteopathic Medicine. She spends about half the year working in Malawi...

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Terrie Taylor: One head cannot hold up a roof

MSU Today : 360 Perspective  

2014-02-12

University Distinguished Professor Terrie Taylor is an Internationally recognized expert on malaria. Taylor’s battle against malaria, which she refers to as the “Voldemort of parasites,” has been waged for the last 28 years. She has spent six months of each of these years in the African nation of Malawi conducting malaria research and treating patients, the vast majority of whom are children...

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Journal Articles (5)

Decreased rate of plasma arginine appearance in murine malaria may explain hypoargininemia in children with cerebral malaria


The Journal of Infectious Diseases

2016 Plasmodium infection depletes arginine, the substrate for nitric oxide synthesis, and impairs endothelium-dependent vasodilation. Increased conversion of arginine to ornithine by parasites or host arginase is a proposed mechanism of arginine depletion.

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Brain swelling and death in children with cerebral malaria


The New England Journal of Medicine

2015 Case fatality rates among African children with cerebral malaria remain in the range of 15 to 25%. The key pathogenetic processes and causes of death are unknown, but a combination of clinical observations and pathological findings suggests that increased brain volume leading to raised intracranial pressure may play a role. Magnetic resonance imaging (MRI) became available in Malawi in 2009, and we used it to investigate the role of brain swelling in the pathogenesis of fatal cerebral malaria in African children.

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Plasmodium falciparum transmission stages accumulate in the human bone marrow


Science Translational Medicine

2014 Transmission of Plasmodium falciparum malaria parasites requires formation and development of gametocytes, yet all but the most mature of these sexual parasite forms are absent from the blood circulation. We performed a systematic organ survey in pediatric cases of fatal malaria to characterize the spatial dynamics of gametocyte development in the human host. Histological studies revealed a niche in the extravascular space of the human bone marrow where gametocytes formed in erythroid precursor cells and underwent development before reentering the circulation. Accumulation of gametocytes in the hematopoietic system of human bone marrow did not rely on cytoadherence to the vasculature as does sequestration of asexual-stage parasites. This suggests a different mechanism for the sequestration of gametocytes that could potentially be exploited to block malaria transmission.

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Loss of endothelial protein C receptors links coagulation and inflammation to parasite sequestration in cerebral malaria in African children


Blood

2013 Cerebral malaria (CM) is a major cause of mortality in African children and the mechanisms underlying its development, namely how malaria-infected erythrocytes (IEs) cause disease and why the brain is preferentially affected, remain unclear. Brain microhemorrhages in CM suggest a clotting disorder, but whether this phenomenon is important in pathogenesis is debated. We hypothesized that localized cerebral microvascular thrombosis in CM is caused by a decreased expression of the anticoagulant and protective receptors thrombomodulin (TM) and endothelial protein C receptor (EPCR) and that low constitutive expression of these regulatory molecules in the brain make it particularly vulnerable. Autopsies from Malawian children with CM showed cerebral fibrin clots and loss of EPCR, colocalized with sequestered IEs. Using a novel assay to examine endothelial phenotype ex vivo using subcutaneous microvessels, we demonstrated that loss of EPCR and TM at sites of IE cytoadherence is detectible in nonfatal CM. In contrast, although clotting factor activation was seen in the blood of CM patients, this was compensated and did not disseminate. Because of the pleiotropic nature of EPCR and TM, these data implicate disruption of the endothelial protective properties at vulnerable sites and particularly in the brain, linking coagulation and inflammation with IE sequestration.

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Plasma concentrations of parasite histidine-rich protein 2 distinguish between retinopathy-positive and retinopathy-negative cerebral malaria in Malawian children


The Journal of Infectious Diseases

2012 Brain histology and ophthalmoscopy suggest that approximately 25% of children with World Health Organization-defined cerebral malaria (CM) have a nonmalarial cause of death. Misclassification complicates clinical care, confounds studies of association, and may obfuscate successes in malaria control. Retinopathy predicts intracerebral parasite sequestration with >90% sensitivity and specificity, but detecting retinopathy requires well-trained personnel and expensive equipment.

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