Systemic Review: The Pathogenicity of Plasmodium berghei in The Liver and Spleen of the Experimental Mice

Abstract

Malaria is still one of the most prevalent tropical and parasitic diseases throughout the world representing a global health concern. Even with all efforts to restrict disease transmission and national malaria control programs, malaria infection continues to cause considerable morbidity and mortality in resource-poor countries. Malaria infection occurs in two stages, the Exoerythrocytic and Erythrocytic stage. The exact biology of malaria parasite in human hosts is likely relatively similar, with the main differences being attributable to the human immune response, the number of previous infections and the exposure profile. The disease severity can be determined by the balance between the pro-inflammatory and anti-inflammatory cytokines. Although, research about the clinical characterization and histology of malaria has shown some information regarding the pathogenesis, the actual mechanisms by which malaria parasites produce severe disease, the immunity defends against infection is remained unknown. Studies in animal models can reveal details about the processes of severe malaria infection and human defense mechanisms. Because of its similarities to the Plasmodium species that cause human malaria, Plasmodium berghei is used as a model organism for the experimental research. In addition, of affecting the central nervous system, Plasmodium berghei infection in the Swiss Webster mouse causes systemic damage, and affects numerous organs including the liver and lymphoid organs. The infected spleen demonstrations includethe splenomegaly, re-modelling and other basic changes consist of the red pulp’s expansion, marginal zone’s slight damage, enlarged vasculature and the barrier cells activities. Moreover, the liver shows hyperplastic Kupffer cells, fatty change, portal tract inflammation, cholestasis, liver cell necrosis, sequestration of Parasitized Red Blood Cells (PRBCs) and deposition of hemozoin pigments.