Liver schizont

An anopheline mosquito inoculates plasmodium sporozoites to initiate human infection (Figure 52-1). Circulating sporozoites rapidly invade liver cells, and exoerythrocytic stage tissue schizonts mature in the liver. Merozoites are subsequently released from the liver and invade erythrocytes. Only erythrocytic parasites cause clinical illness. Repeated cycles of infection can lead to the infection of many erythrocytes and serious disease. Sexual stage gametocytes also develop in erythrocytes before being taken up by mosquitoes, where they develop into infective sporozoites. 

Secondary tissue schizonticides. Agents such as primaquine destroy exoerythrocytic tissue schizonts such as those developing in the liver. 

The intrinsic life cycle begins when a female mosquito takes a blood meal. At this time, sporozoites that have matured in the mosquito s salivary glands are inoculated into the blood stream. These sporozoites migrate to the liver where they infect hepato-cytes and progress from early trophozoites to mature schizonts. This process is referred to as the exoerythrocytic cycle. Schizonts in the liver contain thousands of merozoites that are able to infect... 

Over 100 Plasmodium species contribute to the spread of malaria, but only four of these (P. falciparum, P. vivax, P. ovale, and P. malariae) account for human infection, the deadliest being P. falciparum. The malaria life cycle exists first in a mosquito, and then it passes to a human host. An infected female Anopholes mosquito is the host of the parasite s sporogonic hfe cycle. Mature P. falciparum sporozoites reach the salivary glands of the mosquito, and the parasite is transmitted to a human host when the mosquito feeds. During this blood meal, sporozoites are released into the bloodstream where they penetrate hepatic cells and mature into schizonts. The liver cells rupture after approximately two weeks, discharging merozoites into the bloodstream whereupon they infect red blood cells (RBCs). Every 48 to 78 hours, mature merozoites rupture from... 

Sporozoites enter liver cells where they develop into schizonts which form large numbers of merozoites which, usually after 5-16 days but sometimes after months or years, are released into the circulation. Plasmodium falciparum differs in that it has no persistent hepatic cycle. 

Within minutes after being injected into the patient s blood, the sporozoites begin entering hepatocytes. where they become primary. schizonts and then merozoites. At this point, there are no symptoms. Depending on the Plttsniodittm species, the merozoites either rupture the infected hepato-cytes and enter the systemic circulation or infect other liver cells. The latter process is seen with P. vivax. P. malatiae. and P. ovale, but not P. falcipantm. and produces secondary schizonts. 

Which of the following drugs should be given later in order to eradicate schizonts and latent hypnozoites in the patient s liver ... 

Primaquine is the only antimalarial drug that reliably acts on tissue schizonts in liver cells. Starting about day 4 following an acute attack, primaquine should be given daily for 2 weeks. The answer is (C). 

Malaria is caused by four s Kcies of proto/,oa i lop left) that have part of their life cycle in ihe female Aiiophelex mosquito. When a mosquito bites a human, it injects spom/.oiles into a capillary (top left of figure. C 3 ) and these are carried in the blood to the liver, where they multiply and form tissue schizonts. This is the pre-erythrocytic or primary lissue stage of the disease (left half of the tigure). After days the sebizonts rupiure and release ((—) thousands of merozoiles ( )... 

Plasmodium vivax, the cause of benign tertian malaria, produces milder clinical attacks than those of P. falciparum, and death is uncommon even in untreated cases. The build-up of immunity in the host rapidly controls the infection and schizonts disappear from the blood stream. The exo-erythro-cytic forms in the liver, unaffected by immunity, continue asexual division and reinvade the circulation when immunity has fallen once more these relapses are characteristic of vivax malaria and occur for at least two years after the primary infection. Infections due to P. ovale also follow a tertian pattern, but are much milder and more responsive to therapy than those due to P. vivax and relapses are less frequent. Infections due to both these parasites often display a prolonged incubation period between the primary infection and the development of malarial symptoms. P. vivax is widely distributed north and south of the equator, extending from the tropics to the temperate zones, while P. ovale is restricted to tropical Africa and the western Pacific. 

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