Abstract
Background: Malaria infection is a multisystem pathology with various clinical complications in both adults and children. The clinical manifestation originates in humans following the invasion of erythrocytes by merozoites. Methods: The relevant information and data was collated from scientific databases such as Google Scholar, Science Direct, PubMed, Mendeley, Springer Link, and Medline using keywords such as ‘severe malaria infection’, ‘pathophysiology of severe malaria’, ‘complications of severe malaria’ and ‘erythrocyte impairment in severe malaria’. Results: Generally speaking, the pathophysiology of severe malaria infection encompasses a succession of stages involving the metabolic products of the malaria parasites inclusive of hemoglobin digestion, damaged erythrocyte membrane components, the actions of the pro- and anti-inflammatory cytokines, and the cytoadherence of the malaria parasites to the vascular endothelium as well as sequestration and rosetting. The major complications connected with severe malaria infection include acute respiratory distress syndrome, neurological disorders resulting from cerebral malaria, liver and kidney dysfunction, anaemia and thrombocytopenia, and fatal placental malaria. Conclusion: The effective management of severe malaria infection involves a proper diagnosis followed by the subjection of the patient to suitable antimalarial treatment with the necessary medications depending on the various clinical manifestations of the infection.
Highlights
Malaria is one of the more widespread health issues worldwide 1 caused by the obligate intra-erythrocytic protozoa of the genus Plasmodium, of the following species, P. falciparum, P. vivax, P. ovale, and P. malariae and in addition, recently P. knowlesi infecting humans 2
The pathophysiology of severe malaria infection encompasses a succession of stages involving the metabolic products of the malaria parasites following hemoglobin digestion, damaged erythrocyte membrane components, the actions of the pro- and anti-inflammatory cytokines, and the cytoadherence of the malaria parasites to the vascular endothelium as well as sequestration and rosetting
The cytokines and membrane products released during the process of erythrocyte lysis have been reported to be accountable for most of the complications that are connected with malaria, such as a fever, headache, weakness, pain in the muscles and joints, diarrhea, central nervous system disorders, stomach discomfort, vomiting, a low blood platelet level, blood clotting impairments, the suppression of the immune system, etc. (Figure 1) 23,24
Summary
Malaria is one of the more widespread health issues worldwide 1 caused by the obligate intra-erythrocytic protozoa of the genus Plasmodium, of the following species, P. falciparum, P. vivax, P. ovale, and P. malariae and in addition, recently P. knowlesi infecting humans 2. It is noteworthy to mention that the most severe complications and deaths connected with malaria are caused by the P. falciparum species. After the development of the parasite within the erythrocyte, various waste substances, including the hemozoin pigment and other toxins, accumulate in the infected erythrocyte These substances are transferred into the vascular system following the lysis of the infected erythrocyte alongside the discharge of the invasive merozoites. There is the activation of the macrophages and other cells by hemozoin and other malaria parasite toxins This eventually leads to the generation of cytokines and other soluble factors that play a major role in the initiation of a fever and other pathologies connected with severe malaria 9. Asian Journal of Health Sciences, 2021; 7(2): factors play a major role in the origin and development of severe malaria infections. The present review summarizes the pathophysiology of severe malaria and the varying complications connected with the disease
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