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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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slide2

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
slide3

Complications Associated with Falciparum Malaria

  • cerebral malaria
  • anemia
  • hyperpyrexia
  • hypoglycemia
  • acidosis
  • GI and liver syndromes
  • pulmonary edema
  • blackwater fever
  • algid malaria (shock)
slide4

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)
slide5

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
slide6

avoidance of spleen

  • low oxygen tensions
  • better invasion
slide7

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

slide8

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
slide9

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
slide10

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
slide12

Sequestration

Hypothesis

cytoadherence

cerebral ischemia

hypoxia, metabolic effects

coma

death

slide14

Problems with Sequestration Hypothesis

  • rapid reversibility
  • lack of ischemic damage
  • low levels of permanent neurological damage
  • sequestration occurs in non-cerebral malaria cases
slide16

Cytokine Theory Problem

  • minimal lymphocyte infil-tration or inflammation
slide17

Severe falciparum malaria

  • potentially high parasitemias
  • sequestration
  • complex (and not fully understood) host-parasite interactions
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