Every year, millions of people are infected with malaria, resulting in significant economic losses to the developing and developed nations. The malaria parasite pursues a complicated life cycle in an invertebrate, mosquito and vertebrate host with several distinct stages. In the human host, it invades the liver and red blood cells to complete its life cycle. It is surprising that not only these two organs are under pressure and exhibit functional abnormalities; a large number of clinical studies also support the notion that malaria parasite propagation in the host affects several other organs and modulates functional outcomes of individual cells. Moreover, patients recovered from severe malaria may suffer throughout their life from impairments in organ function such as loss of eyesight, kidney failure, and much more. Thus, malaria infection leads to several pathological outcomes involving different organs and individual cells in the host. The sole purpose of the present article was to give an overview of pathological outcomes during severe malaria along with their molecular mechanisms. A large proportion of deaths associated with disease is contributed by the pathological effect in host due to parasite propagation and toxicity of antimalarials or combination of both. Hence, there is a need, not only to develop antiparasitic agents but also to discover lead molecules to take care of pathophysiological effects in the host. This may help a beginner to get involved with the topic and initiate research work towards improving adjuvant therapy or avoiding serious complications.
Keywords: Anaemia; cerebral malaria; diabetes; host; kidney; malaria.