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INFORMATION FOR

Mahalia S. Desruisseaux, MD

Associate Professor of Medicine (Infectious Diseases); Affiliated Faculty, Yale Institute for Global Health

Contact Information

Mahalia S. Desruisseaux, MD

Mailing Address

  • Infectious Diseases

    PO Box 208022

    New Haven, CT 06520-8022

    United States

Research Summary

The focus of the Desruisseaux laboratory is on the brain microvascular and neural cell responses to parasitic infections that lead to debilitating neurological sequelae and mortality, and on the mechanisms that underlie these responses.

Extensive Research Description

The Desruisseaux laboratory works on cerebral malaria, a disease in which > 25% of survivors suffer from persistent neurological and cognitive deficits, despite successful anti-parasitic treatment. The goal of the laboratory is to identify the factors that cause these adverse long-term neurological sequelae.

The Desruisseaux lab has been particularly interested in the aberrant regulation of cerebral vascular tone, inflammation, blood-brain barrier disturbances, and eventually neuronal and glial degeneration after plasmodial infection, using a mouse model of experimental cerebral malaria. Our focus is on alterations in the synthesis and activation of vasomodulatory compounds during parasitic disease, and the effects of these alterations on cerebral perfusion, inflammation and blood-brain barrier disruption, and ultimately on gliopathy, neuronal damage and long-term neurological deficits. We identified endothelin-1, a potent vasoactive peptide with mitogenic and pro-inflammatory properties, as a key contributor to endothelial remodeling, neuroinflammation, long-term neurological damage and mortality during cerebral malaria. We also demonstrated that tau protein, a protein important in the formation of neurofibrillary tangles in neurodegenerative diseases, is abnormally regulated in our experimental model, demonstrating that long term sequelae are the result of potentially reversible vascular, biochemical and physiological changes in brains of infected mice.

In collaboration with investigators at the University of Malawi College of Medicine in Blantyre Malawi and at Indiana University, our laboratory will study the mechanisms of the disease process in pediatric patients from malaria endemic regions to test the translatability of our findings in the experimental model and to potentially derive novel therapeutic targets.


Coauthors

Research Interests

Blood-Brain Barrier; Neuroglia; Neurons; Chagas Disease; Endothelins; Malaria, Cerebral; Neurocognitive Disorders; Central Nervous System Parasitic Infections; Endothelial Cells

Public Health Interests

Global Health; Infectious Diseases; Malaria; Neglected Tropical Diseases

Selected Publications

  • 87. Infectious Disease Diversity, Equity, and Antiracism (ID2EA): A Dedicated Curriculum for Infectious Disease ProfessionalsGleeson S, Bathgate M, Frederick J, Desruisseaux M, Meyer J, Virata M, Zapata H, Shenoi S, Radin J, Golden M, Trubin P, Shaw A, Friedland G, Aoun-Barakat L. 87. Infectious Disease Diversity, Equity, and Antiracism (ID2EA): A Dedicated Curriculum for Infectious Disease Professionals Open Forum Infectious Diseases 2021, 8: s55-s55. PMCID: PMC8644171, DOI: 10.1093/ofid/ofab466.087.
  • Use of Convalescent Plasma Therapy in Severe Coronavirus Disease 2019: The Yale-New Haven Health System ExperienceBrowning S, Gormally M, Briggs N, Li M, Zakko A, Laurent-Rolle M, Ladines-Lim J, Morrison A, Kandel P, Khan M, McLeod G, Buller G, Owusu K, Treggiari M, Hendrickson J, Tormey C, Desruisseaux M. Use of Convalescent Plasma Therapy in Severe Coronavirus Disease 2019: The Yale-New Haven Health System Experience Blood 2020, 136: 39-40. PMCID: PMC8330251, DOI: 10.1182/blood-2020-137352.
  • Captain Herbert B. Tanowitz, M.D., F.I.D.S.A., F.A.C.P., F.R.S.T.M.H., 1941–2018Desruisseaux M, Engman D. Captain Herbert B. Tanowitz, M.D., F.I.D.S.A., F.A.C.P., F.R.S.T.M.H., 1941–2018 American Journal Of Pathology 2019, 189: 2-3. DOI: 10.1016/j.ajpath.2018.10.003.
  • Chapter 14 Trypanosoma cruzi and Chagas Disease: Innate Immunity, ROS, and Cardiovascular SystemTanowitz H, Wen J, Machado F, Desruisseaux M, Robello C, Garg N. Chapter 14 Trypanosoma cruzi and Chagas Disease: Innate Immunity, ROS, and Cardiovascular System 2016, 183-193. DOI: 10.1016/b978-0-12-801078-5.00014-5.
  • The Brain Microvasculature in Cerebral MalariaDorovini-Zis K, Stins M, Desruisseaux M, Martins Y, van der Heyde H. The Brain Microvasculature in Cerebral Malaria 2015, 68-117. DOI: 10.1201/b19299-5.
  • 228Building Bridges: Improving Antibiotic Prescribing in the Emergency DepartmentMadaline T, Feldmesser M, Chung P, Daily J, Desruisseaux M, Hochman S, Keller M, Leviton I, Murphy K, Sharma A, Pearlman S, Katz N, White D, Pirofski L, Ostrowsky B. 228Building Bridges: Improving Antibiotic Prescribing in the Emergency Department Open Forum Infectious Diseases 2014, 1: s99-s99. DOI: 10.1093/ofid/ofu052.94.
  • Endothelin-1 treatment induces experimental cerebral malaria during Plasmodium berghei NK65 infectionMartins Y, Tanowitz H, Weiss L, Desruisseaux M. Endothelin-1 treatment induces experimental cerebral malaria during Plasmodium berghei NK65 infection Life Sciences 2013, 93: e27. DOI: 10.1016/j.lfs.2013.12.107.
  • The role of endothelin-1 in the vascular pathobiology of cerebral malariaFreeman B, Dai M, Desruisseaux M. The role of endothelin-1 in the vascular pathobiology of cerebral malaria Life Sciences 2013, 93: e7. DOI: 10.1016/j.lfs.2013.12.045.
  • Gene expression alterations in a mouse model of cerebral malariaDesruisseaux M, Nagajyothi F, Mukherjee S, Iacobas D, Tanowitz H, Spray D. Gene expression alterations in a mouse model of cerebral malaria BMC Proceedings 2008, 2: p15. DOI: 10.1186/1753-6561-2-s1-p15.
  • Thromboxane A 2 is a key regulator of pathogenesis during Trypanosoma cruzi infectionAshton A, Mukherjee S, Nagajyothi F, Huang H, Braunstein V, Desruisseaux M, Factor S, Lopez L, Berman J, Wittner M, Scherer P, Capra V, Coffman T, Serhan C, Gotlinger K, Wu K, Weiss L, Tanowitz H. Thromboxane A 2 is a key regulator of pathogenesis during Trypanosoma cruzi infection Journal Of Cell Biology 2007, 177: i4-i4. DOI: 10.1083/jcb1772oia4.
  • Human Parasitic Disease in the Context of the Blood‐Brain Barrier – Effects, Interactions, and TransgressionsDesruisseaux M, Weiss L, Tanowitz H, Mott A, Milner D. Human Parasitic Disease in the Context of the Blood‐Brain Barrier – Effects, Interactions, and Transgressions 2006, 671-700. DOI: 10.1002/9783527611225.ch27.