THE PARASITE OF MALARIA - HUMAN PLASMODIUM


A. Plasmodium vivax;
Plasmodium vivax causes benign or vivax malaria. The development of this plasmodium, includes; the pre-erythrocytic and exco-erythrocytic cycles in the liver. Morphogically unstained preparations show the vivax trophozoite to appear in the red blood cells as a small disc, which becomes amoeboid with characteristic rapid movement that justifies the name vivax.

        The gametocyte show no evidence of segmentation P. vivax has a striking effect on the invaded red blood corpuscles that gradually enlarge and becomes decolourized. 

 B. Plasmodium falciparum
facliparum is the parasite responsible for most cases of malaria. It is the most severe, often fatal forms of the disease and deeply entrenched in tropical Africa. It is the most highly pathogenic as indicated by the name malignant often associated with it. It causes the most devastating malaria because it can infest the Red- blood cell of all ages. It is responsible for nearly all the cases of congenital malaria, cerebral malaria and this is the specie of malaria parasite that antidrug resistance is the highest. 

Majority of death in sub-Saharan-Africa as well as in Ebonyi State is as a result of P. facliparum infect. One of the reasons why it continued to thrive is because the most dangerous vectors of malaria parasite are Anopheles funestus and Anopheles gambiae exist here. Pre-erythrocytic schizonts of P. falciparum release more menozoites than those of other species affecting man. It is the Chief infection in areas of endemic malaria in Africa because development in the mosquito is retarded when the temperature falls, below 200C. Even at this temperature about 3 weeks are required for the maturation of the sporozoites. 

The asexual development of P. falciparum in the liver involves a pre-erythrocytic phase there is no exo-erythrocytic phase giving rise to long term relapses, such as occur in vivax and ovale. The young ring (trophozoites) form of P.falciparum as seen in the peripherial blood are very small, measuring about 1/6 of the diameter of a red blood corpuscle. The mature schizont of P. facliparum is smaller than that of any malaria parasite. 

The distribution of the parasite in organs of tissue of the human body varies on different cases, this accounts for the diversity of clinical manifestation observed in falciparum malaria. Most of the severe and fatal cases are due to blocking of the capilliaties by clumps of red blood corpuscles harbouring developing parasites.

C. Plasmodium malariae     
This is the causal organism of quartan malaria because the paroxysms of fever occur every fourth day after two days interval. This parasite differs from the other species affecting man by it morphological characters which indicates that it is characterized by a compact parasite (call stages) and does not alter the host erythrocyte or cause enlargement or development in both human and insect host. The cause of the disease is not unduly severe but its long persistence is notorious. It causes glomeruloephritis and nephritic syndrome in children. Atkinson (1987) described the fine structure of the erythrocytic stages of P. malaria.

D. Pasmodium ovale;
        This is the least common of the species that affect man. Diagnostically, the sporozite stage is plump, elongated and pointed at one end. The schizonts are large and quite distinctive. It has numerous nuclei. P. ovale produces fever similar to that of vivax malaria but often with prolonged latency lesser tendency to relapse and generally milder clinical symptoms.
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