Life cycle of plasmodia in the human body
The development of the malaria parasite in the human body (schizogony) is an asexual cycle traditionally divided into three main stages:
- Exo-erythrocytic schizogony (EES). Along with the mosquito's saliva, sporozoites enter the bloodstream and reach the liver in literally 15–30 minutes. There, they actively invade hepatocytes, initially without causing damage. The causative agents of malaria falciparum, malariae, as well as some sporozoites of vivax and ovale (tachysporozoites), immediately begin to divide. A single Pl. falciparum sporozoite can yield up to 40,000 merozoites. This stage concludes with the destruction of liver cells and the release of merozoites into the blood. The duration of EES ranges from 6 days (Pl. falciparum) to 15 days (Pl. malariae).
- Erythrocytic schizogony (ES). Merozoites penetrate erythrocytes, where they go through trophozoite, schizont, and morula stages. Eventually, the erythrocyte ruptures, and new merozoites enter the plasma to infect other cells. This process is cyclical: 48 hours for most species and 72 hours for Pl. malariae.
- Gametocytogony.
Dormant stage (hypnozoites)
Special attention should be paid to Pl. vivax and Pl. ovale. When a mosquito bites, not only fast-developing tachysporozoites but also slow-developing ones — bradysporozoites — can enter the body.
Upon reaching the liver, bradysporozoites transition into an inactive form — hypnozoites. In this "dormant" state, they can remain in hepatocytes without dividing for anywhere from several months to several years.
The activation of hypnozoites is precisely what drives the prolonged incubation period (up to a year or more) and causes delayed exo-erythrocytic malaria relapses.
Mechanisms of severe falciparum malaria
Malaria caused by Pl. falciparum leads to severe complications more often than other species. This is due to the unique features of this species' erythrocytic schizogony:
- Sequestration. Infected erythrocytes (starting from the amoeboid trophozoite stage) accumulate in the capillaries of internal organs: the brain, kidneys, liver, intestines, and placenta.
- Rosetting. Affected erythrocytes clump together with healthy ones, forming conglomerates.
These processes lead to severe microcirculatory disorders, tissue hypoxia, and metabolic acidosis (due to lactic acid accumulation). Additionally, the macrophage-phagocytic system is activated, releasing cytokines (TNF-α, IFN-γ, IL-1) that damage the vascular endothelium. Excessive synthesis of nitric oxide (NO) by the cerebral vascular endothelium plays an important role in the development of the cerebral form.
A key pathophysiological link in severe forms is hypoglycemia, caused by reduced gluconeogenesis, active glucose consumption by the parasite, and stimulation of insulin secretion (including under the action of quinine).
Pathogenesis of febrile paroxysms
The classic symptom of malaria — fever attacks — is directly linked to the erythrocytic schizogony cycle. The paroxysm develops via the following cascade:
- Massive erythrocyte hemolysis and release of merozoites into the blood.
- Some merozoites are destroyed, while others invade new erythrocytes.
- In response, the mononuclear phagocytic system is activated.
- Intensive synthesis of endogenous pyrogens occurs — cytokines IL-1, IL-6, TNF-α.
- These cytokines affect the thermoregulation center in the hypothalamus, causing a sharp spike in temperature.
Briefly: answers to topical questions
What stages of development does the sporogony of the malaria parasite include in the mosquito body?
Sporogony in the mosquito body includes the formation of an oocyst, the generation of sporozoites within it, and their subsequent migration. The process consists of the following stages:
- Oocyst formation — an ookinete penetrates through the wall or beneath the outer membrane of the mosquito's stomach, rounds up, becomes encapsulated, and turns into an oocyst.
- Sporozoite generation — multiple division occurs inside the oocyst, resulting in the formation of thousands (up to 10,000) of sporozoites.
- Sporozoite migration — following the rupture of the oocyst, sporozoites enter the hemolymph and migrate to all organs, accumulating in the mosquito's salivary glands for further transmission.
What are the mechanisms of anemia development in malaria, aside from direct intracellular destruction of erythrocytes by the parasite?
The development of anemia in malaria, aside from intravascular hemolysis of infected erythrocytes, is associated with the following mechanisms:
- Phagocytosis — reticuloendothelial cells of the spleen destroy both infected and uninfected erythrocytes.
- Sequestration (accumulation) — erythrocytes with mature parasites accumulate in the bone marrow, leading to suppressed hematopoiesis.
- Immune mechanism — destruction of unaffected erythrocytes occurs due to the adsorption of immune complexes containing the C3 complement fraction onto their membrane.
Class and exam questions
Why are newborns relatively resistant to malaria?
Resistance is due to the presence of fetal hemoglobin (poorly suited for parasite nutrition) as well as passive immunity from the mother (transplacentally and via breast milk).
What determines the severity of the disease course?
The severity of the course is directly proportional to the level of parasitemia — the number of parasites per 1 µL of blood. The highest level (up to 100,000 or more) is characteristic of falciparum malaria.
What are the characteristics of immunity in malaria?
Immunity is non-sterile, species- and strain-specific, and unstable. To maintain it, constant antigenic stimulation — i.e., repeated infections — is required.
What specific complication is characteristic of malariae malaria?
In the case of prolonged untreated infection, nephrotic syndrome may develop due to the deposition of immune complexes containing parasite antigens on the glomerular basement membrane of the kidneys.
What else to study on this topic
- Features of the immune response (cellular and humoral, role of macrophages)
- The effect of para-aminobenzoic acid on parasite development in children over 3 months of age
- Laboratory diagnostic methods and determination of parasitemia levels
- Differences in immunity dynamics against different species of plasmodia (falciparum vs vivax/malariae)
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