Page 53 - Medical Parasitology_ A Textbook ( PDFDrive )
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Types of Malarial Parasites and Their Morphology                45

              Blackwater fever is sometimes seen in falciparum malaria, in patients who have
            experienced repeated infections and inadequate treatment with quinine. Clinical
            manifestations include bilious vomiting and prostration, with passage of dark red
            or blackish urine (blackwater).The pathogenesis is due to massive intravascular
            haemolysis caused by anti-erythrocyte antibodies, giving rise to haemoglobinuria.
            Complications of blackwater fever include renal failure, acute liver failure, and
            circulatory collapse.
              Acute renal failure may occur in severe falciparum malaria most likely due to
            tubular necrosis. Acute renal failure has also been described in severe malaria
            caused by other species. Nephrotic syndrome has been reported in malariae malaria.
            Immune complexes may cause structural glomerular damage and the associated
            nephrotic syndrome.
              Tropical splenomegaly syndrome (TSS) or hyper-reactive malarial splenomeg-
            aly is a chronic benign condition seen in some adults in endemic areas. This results
            from abnormal immunological response to malaria and is characterized by spleno-
            megaly, high titres of anti-malaria antibodies and absence of malaria parasites in
            peripheral blood smears. Hypergammaglobulinemia (IgM) is its other feature. Liver
            is also enlarged, congested, with marked lymphocytic infiltration. TSS responds to
            anti-malarial treatment.
              Other complications of malaria are hypoglycemia and hyperparasitaemia.


              Immunity

            Immunity in malaria may be classified as innate immunity and acquired
            immunity.

              1.  Innate immunity
                 It is an inherent, non-immune mechanism of host resistance against malarial
              parasite. It could be due to Duffy-negative RBCs. The invasion of red cells by
              merozoites requires the presence of specific glycoprotein receptors on the eryth-
              rocyte surface. Persons negative with Duffy blood group antigen are found to be
              refractory to infection by P. vivax. This genetically determined blood group anti-
              gen is a specific receptor for P. vivax and P. knowlesi.
                 Nature of haemoglobin like haemoglobin E provides natural protection
              against P. vivax. Plasmodium falciparum does not multiply properly in sickled
              red cells containing HbS. Sickle cell anaemia trait is very common in Africa,
              where falciparum malaria is hyperendemic and offers a survival advantage. HbF
              present in neonates protects them against all Plasmodium species.
                 Innate immunity to malaria has also been related to glucose-6-phosphate
              dehydrogenase (G6PD) deficiency found in Mediterranean coast, Africa, Middle
              East and India. G6PD-deficient cells are more resistant to P. falciparum.
              2.  Acquired immunity
                 Malaria induces specific immunity involving both humoral and cellular
              immunity, which brings about clinical cure, but cannot eliminate parasites
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