Cerebral malaria
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Cerebral Malaria. severe complication of falciparum malaria mortality of 30-50% associated with sequestration in micro-vasculature of brain a diffuse encephalopathy with loss of consciousness consciousness ranges from stupor to coma unresponsive to pain, visual, and verbal stimuli

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Cerebral Malaria

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Cerebral malaria

Cerebral Malaria

  • severe complication of falciparum malaria

    • mortality of 30-50%

  • associated with sequestration in micro-vasculature of brain

  • a diffuse encephalopathy with loss of consciousness

    • consciousness ranges from stupor to coma

    • unresponsive to pain, visual, and verbal stimuli

    • convulsions frequently observed

    • onset can be gradual or sudden


Cerebral malaria

Complications Associated with Falciparum Malaria

  • cerebral malaria

  • anemia

  • hyperpyrexia

  • hypoglycemia

  • acidosis

  • GI and liver syndromes

  • pulmonary edema

  • blackwater fever

  • algid malaria (shock)


Cerebral malaria

Features Indicating Poor Prognosis in Severe Malaria

  • impaired consciousness

  • repeated convulsions

  • respiratory distress

  • shock

  • acidosis/hyperlactemia

  • hypoglycemia

  • jaundice or other liver malfunctions

  • renal impairment

  • high parasitemia (>500,000/mm3)


Cerebral malaria

Higher Parasitemias in Falciparum Malaria

  • all erythrocytes invaded

    • Pv/Po = reticulocytes

    • Pm = senescent RBC

  • up to 36 merozoites

  • sequestration of infected erythrocytes

    • trophozoite and schizont stages

    • primarily in brain, heart, lungs, and gut

    • complications

    • immune evasion


Cerebral malaria

  • avoidance of spleen

  • low oxygen tensions

  • better invasion


Cerebral malaria

P. falciparum expresses ‘knobs’ on the surface of infected erythrocytes. Knobs mediate cytoadherence to endothelial cells.


Cerebral malaria

Several Parasite Proteins Are Associated with Knobs

  • KAHRP and PfEMP2 are believed to interact with the submembrane cytoskeleton of the host erythrocyte

  • reorganization of the membrane skeleton may result in knob formation

  • PfEMP1 crosses the erythrocyte membrane and is exposed on the surface


Cerebral malaria

PfEMP-1 Structure

  • family of 40-50 var genes

  • conserved intracellular C-terminus

    • acidic terminal segment (ATS)

    • binds cytoskeleton + KAHRP

  • transmembrane domain

  • variable extracellular domain composed of modules

    • 2-7 copies of Duffy-binding like domains

      • 5 sequence types (a, b, g, d, e)

    • 1-2 cys-rich interdomain regions

    • all have DBL1a + CIDR

  • participates in cytoadherence


Cerebral malaria

Possible Host Receptors

  • CD36

  • Ig super-family

    • ICAM-1

    • VCAM-1

    • PECAM-1

  • E-selectin

  • thrombospondin

  • chondroitin sulfate A

  • hyaluronic acid

  • Rosetting Receptors

    • CR-1

    • glycosaminoglycan

    • blood group A


Cerebral malaria

Sequestration

Hypothesis

cytoadherence

cerebral ischemia

hypoxia, metabolic effects

coma

death


Cerebral malaria

Problems with Sequestration Hypothesis

  • rapid reversibility

  • lack of ischemic damage

  • low levels of permanent neurological damage

  • sequestration occurs in non-cerebral malaria cases


Cerebral malaria

Cytokine Theory


Cerebral malaria

  • Cytokine Theory Problem

  • minimal lymphocyte infil-tration or inflammation


Cerebral malaria

  • Severe falciparum malaria

  • potentially high parasitemias

  • sequestration

  • complex (and not fully understood) host-parasite interactions


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