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Peripheral Vascular Pathophysiology of Plasmodium berghei Infection: A Comparative Study in the Cheek Pouch and Brain of the Golden Hamster
David R. Franz
David R. Franz
Malaria Research Group, United States Army Medical Research Unit, Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, Malaysia
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Melinda Lee
Melinda Lee
Malaria Research Group, United States Army Medical Research Unit, Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, Malaysia
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Lim Thuang Seng
Lim Thuang Seng
Malaria Research Group, United States Army Medical Research Unit, Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, Malaysia
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G. David Young
G. David Young
Departments of Comparative Pathology
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Wallace B. Baze
Wallace B. Baze
Ultrastructural Studies, Division of Pathology, Walter Reed Army Institute of Research, Washington, DC 20307-5100
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George E. Lewis Jr.
George E. Lewis Jr.
Malaria Research Group, United States Army Medical Research Unit, Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, Malaysia
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Four- to six-week-old hamsters were infected with 1.5 × 107 Plasmodium berghei-parasitized hamster red blood cells by intraperitoneal injection. Cheek pouch circulation was observed microscopically in the anesthetized animal; the brain and contralateral pouch were collected for histopathologic examination on days 3–12 post-challenge. Cheek pouch vascular lesions, observed in vivo, appear to involve three phenomena; early (beginning 3–4 days) adhesion of pigment-laden mononuclear cells to endothelium within venous vessels and loss of function of the small capillaries supplying the skeletal muscle fibers and, later (6–9 days), the apparent attraction of erythrocytes to venular and venous endothelium and to adherent monocytes. The aggregation of formed elements on endothelial walls leads to progressive occlusion of venules and small veins and contributes to the observed disruption of flow through capillary networks. Histopathology of the brain and pouch shows vascular changes similar to those seen in vivo; in addition, multifocal hemorrhages are seen commonly in the brain and occasionally in the pouch on postmortem. In severe disease, evidence of cerebral edema is seen in the brain. The data suggest that failure of capillary flow and disruption of venous outflow tracts by cell aggregates are central to vascular failure in both the cheek pouch and brain of the P. berghei infected hamster. This hamster model of human cerebral malaria allows the in vivo observation, still and video photomicrography, and manipulation of the peripheral vascular pathogenesis of a disease process similar to that seen in humans.
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