Past two years Past Year Past 30 Days
Abstract Views 258 99 10
Full Text Views 5 1 0
PDF Downloads 3 1 0
 
 
 
 
 
 
 
 
 
 
 

Peripheral Vascular Pathophysiology of Plasmodium berghei Infection: A Comparative Study in the Cheek Pouch and Brain of the Golden Hamster

David R. FranzMalaria Research Group, United States Army Medical Research Unit, Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, Malaysia

Search for other papers by David R. Franz in
Current site
Google Scholar
PubMed
Close
,
Melinda LeeMalaria Research Group, United States Army Medical Research Unit, Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, Malaysia

Search for other papers by Melinda Lee in
Current site
Google Scholar
PubMed
Close
,
Lim Thuang SengMalaria Research Group, United States Army Medical Research Unit, Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, Malaysia

Search for other papers by Lim Thuang Seng in
Current site
Google Scholar
PubMed
Close
,
G. David YoungDepartments of Comparative Pathology

Search for other papers by G. David Young in
Current site
Google Scholar
PubMed
Close
,
Wallace B. BazeUltrastructural Studies, Division of Pathology, Walter Reed Army Institute of Research, Washington, DC 20307-5100

Search for other papers by Wallace B. Baze in
Current site
Google Scholar
PubMed
Close
, and
George E. Lewis Jr.Malaria Research Group, United States Army Medical Research Unit, Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, Malaysia

Search for other papers by George E. Lewis Jr. in
Current site
Google Scholar
PubMed
Close
View More View Less
Restricted access

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.

Save