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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