**4. Diagnostic characteristics of the genus** *Plasmodium*

• Merogony occur both in erythrocytes and other tissues

Biology of Malaria Parasites 13

There is considerable variation in the appearance of the blood between individuals experimentally inoculated at the same time. Even within a single experimental individual there may be considerable variation in the maturity of the hepatic forms seen on liver biopsy.[12]

A proportion of the hepatic stages may remain within the liver for considerable time – a form known as hypnozoites. Reactivation of the hynozoites have been reported for up to 30 years after the initial infection in humans. The factors precipitating this reactivation are not known. In the species *Plasmodium ovale* and *Plasmodium vivax*. It is not yet known if hypnozoite reactivation occurs with any of the remaining species that infect humans but this

The development from the hepatic stages to the erythrocyte stages have, until very recently, been obscure. In 2006 it was showed that the parasite buds off the hepatocytes in merosomes containing hundreds of thousand of merozoties. These merosomes lodge in the pulmonary capillaries and slowly disintegrate there over 48 – 72 hours releasing merozoites. Erythrocyte invasion is enhanced when blood flow is slow and the cells tightly packed: both

After entering the erythrocyte, the merozoite lose one of their members, the apical rings, conoid and the rhopteries. Phagotropy commences and both smooth and granular

Within the erythrocytes the merozoite grow first to a ring-shaped form and then to a larger trophozoite form. In the schizont stage, the parasite divides several times to produce new merozoites. Which leave the red blood cells and travel within the bloodstream to invade new red blood cells. The parasite feeds by ingesting hemoglobin and other materials from red blood cells and serum. The feeding process damages the erythrocytes. Details of process have not been studied in species other than *Plasmodium falciparum.* so generalization may be

Erythrocytes infected by *Plasmodium falciparum* tend to form clumps – rosettes – and these have been linked to pathology caused by vascular occlusion. This rosette formation may be inhibited by heparin. This agent has been used in the past as part of the treatment of malaria but was abandoned because of an increased risk of haemorrhage. Low molecular weight heparin also disrupts rosette formation and may have a lower risk of bleeding in malaria.[17]

The budding of the merozoites from interconnected cytoplasmic masses (pseudocytomeres) is a complex process. At the tip of each bud a thickened region of pellicle gives rise to the apical rings and conoid. As development proceeds an aggregation of smooth membranes and the nucleus enter the base of the bud. The cytoplasm contains numerous large ribosomes. synchronous multiple cytoplasmic cleavage of the mature schizont results in the

Escape of the merozoites from the erythrocyte has also been studies. The erythrocyte swells under osmotic pressure. A pore opens in the erythrocyte membrane and 1-2 meorozites

endoplasmic reticulum because prominent. The nucleus may become lobulated.[16]

is presumed to be the case.[13,14]

**7. Erythrocyte stage** 

premature at this time.

**8. Merozoites** 

formation of numerous uninucleate merozoites.

of these conditions are found in the alveolar capillaries.[15,16]

