Plasmodium vivax is one of four species of the genus Plasmodium that cause the disease malaria only among humans. Of the four, it is at the same time the most widespread and the least virulent.
The other three human pathogens of the genus are P. falciparum (the most virulent), P. malariae, and P. ovale; a fifth Plasmodium species, P. knowlesi targets macau monkeys but can also cause malaria in humans by zoonosis.
Plasmodium species are intraerythrocytic sporozoan organisms which have no obvious means of self-locomotions and are obligate endoparasitic. This means they need human erythrocytes in which to carry out their life-cycle, to the detriment of the larger host organism, in this case humans.
Malaria caused by P. vivax is the most common form seen outside of Africa and, therefore, the most common seen in subtropical and temperate regions such as the Southeastern United States. Prior to the “Age of Discovery”, P. vivax (along with P. malariae) did not exist in the Western Hemisphere (P. falciparum, however, was widespread in the tropics and subtropics) and is believed to have been imported by Europeans coming over the Atlantic Ocean beginning at the end of the fifteenth century.
At one time, P. vivax was endemic to the warmer, humid region of the Southeast, and the most common of the three forms mentioned above due to its ability to survive in more temperate climates which the other two, P. falciparum especially, cannot endure. Until the 1940’s in fact, its prevalence contributed significantly to much of the economic hardship suffered in the region. Malaria, mostly of the P. vivax variety, was until that time one of three chronic health deficiencies stereotypical of the South, along with pellagra and hookworm disease.
During World War II, however, the U.S. Army built several training camps in the area, and when medical personnel took note of the dangers from P. vivax and other Plasmodium species, the U.S. Public Health Service established the Office of Malaria Control (1942). Teams of workers from this agency began spraying all likely mosquito havens with large amounts of chlorophenothane (DDT), including private homes and buildings, and effectively reduced the American infection rate to a negligible amount within ten years.
The effectiveness of the eradication campaign was supported and enhanced by the better living standards the region’s people enjoyed with the advent of war-born prosperity (and a drastic decline in prevalence of poor living conditions such as those suffered by sharecroppers and similarly improverished people in the region).
The life cycle of P. vivax, and other Plasmodium species, is highly complex, including both asexual and sexual reproduction, along with three cycles within the bigger cycle: the sporogonic cycle, the exoerythrocytic cycle, and the intraerythrocytic cycle. The first of these takes place in female mosquitos of the Anopheles species which is the vector for the parasite infection of humans, the latter two take place within human hosts.
The easiest way to understand the complicated process is to begin with with an Anopheles mosquito biting a human host for a blood meal and injecting P. vivax sporozoites into his/her cutaneous bloodstream, beginning the exoeryrocytic cycle, which last one to two weeks.
The sporozoites then migrate to the liver where they invade hepatocytes and become cryptozoites and begin reproducing by asexually by dividing themselves rapidly to produce merozoites. The merozoites then develop into trophozoites which then form either schizonts for their return to the bloodstream or hypnozoites which can lie dormant within the liver for months or even years (a trait P. vivax shares with P. ovale but not other Plasmodium species).
Soon after reentering in the bloodstream, the schizonts burst, releasing their merozoites into the bloodstream to infect individual reticulocytes unlike other Plasmodium species, P. vivax only infects reticulocytes), entering the cell via the Fy6 Duffy antigen protein to begin the intraerythrocytic cycle.
Once inside the reticulocyte, the merozoites grow into immature trophozoites which develop into mature trophozoites, then become schizonts within 36 to 72 hours, each producing between 6 and 24 new merozoites. By then the schizont is large enough to burst the reticulocyte, releasing its merozoites to infect other cells.
After several cycles, some of the immature trophozoites leave their host cell to become gametocytes in the bloodstream, even as the previous cycle continues. The gametocytes then divide into macrogametocytes (female) and microgametocytes (male).
When a female of the Anopholes species feeds upon the infected human, she takes in the gametocytes along with her meal, beginning the sporogonic cycle. Inside her stomach, the microgametocyte penetrates the macrogametocyte, fertilizing it to become a zygote, or ookinete, which attaches itself to her stomach wall. The ookinete develops into an oocyst producing sporozoites until it bursts, realsing the organisms to travel to its host’s salivary glands to infect the next human.
P. vivax malaria, along with other forms of malaria, does not become symptomatic until the intraerythrocytic cycle.
This is the diagnostic stage of the disease. Symptoms include regularly occurring paroxysms of fever and chills, the periodicity of which in the case of P. vivax is every 48 hours, which is why P. vivax malaria is also called tertiary malaria; different species of Plasmodium have different periodicities. Other symptoms include splenomegaly (from the spleen absorbing the debris from destroyed RBC’s), hepatomegaly, and anemia from destruction of erythrocytes (especially in the case of P. vivax, which attacks immature reticulocytes as they enter the bloodstream), along with nausea, vomiting, and diarrhea.
Fatality from P. vivax infection is rare and in those cases most often occurs after the spleen bursts. While P. vivax is not as virulent as its cousin P. falciparum, the morbidity, or severity, of its symptoms is greater, particularly its paroxyms, with violent headaches and chills accompanying the fever along with profuse sweating.
In the laboratory, P. vivax malaria is diagnosed through the identification of trophozoites, schizonts, or gametocytes in in peripheral blood drawn between paroxyms. EDTA-preserved whole blood is the preserved specimen, and should be drawn immediately upon the patient’s admittance to the facility. The technician should examine both thick and thin smears, and take subsequent samples every 6 to 12 hours.
Giesma is the stain of choice but Wright’s can also be used. Paroxyms should also be timed since they are unique to each species of Plasmodium. Travel to areas where P. vivax should also be taken into account. If no indications are found in both morning and afternoon smears of blood taken during symptoms, the patient can be diagnosed as negative for infection by P. vivax.
Treatment for P. vivax malaria is chloroquine. If hynozoites are suspected, the liver should be sampled for their presence and if found, primaquine should be given, else the patient could have a recurrence months or even years after the primary infection has been cleared from their blood. Chloroquine should not be given to patients with G6PD deficiency because it will cause hemolysis nor should primaquine be given to pregnant women because it is not yet known if it is safe for the fetus.
Of note is the fact that most Africans and African-Americans lack the Duffy group of antigens on their erythrocytes and are thus immune to infection by P. vivax, a trait biologist believe comes from Darwinian selection to protect them against the pathogen as a result of endemic infection in the region.
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“Plasmodium vivax”. http://www.vivaxmalaria.com/index.htm