Plasmodium

Abstract

Plasmodium is a genus of parasitic protozoa which infect erythrocytes of vertebrates and cause malaria. Their life cycle alternates between mosquito and vertebrate hosts. Parasites enter the bloodstream after a mosquito bite, and multiply sequentially within liver cells and erythrocytes before becoming male or female sexual forms. When ingested by a mosquito, these fuse, then the parasite multiplies again to form more invasive stages which are transmitted back in the insect's saliva to a vertebrate. All invasive stages have specialized secretory structures (apical organelles) typical of the protozoan subphylum Apicomplexa, enabling them to invade cells and tissues. Parasites exploit erythrocytes by ingesting haemoglobin and exporting molecules which change erythrocyte membrane properties. Five species infect humans, the most lethal being Plasmodium falciparum which can cause pathology and death by clogging blood vessels in brain, viscera and placenta. Many hundreds more species infect other mammals, birds and lizards. Key Concepts: Intracellular parasitism. Many apicomplexan protozoa invade and exploit the cells of their hosts, situated in a nutrient‐rich environment and protected from attack by their host's immune system. Alternation of hosts. All parasites of the genus Plasmodium have two different types of host which they parasitize alternately, a vertebrate and a mosquito. This arrangement enables the parasite to multiply numbers greatly in the richly nutrient environment of the vertebrate host, and also to find new hosts via the mosquito vector. The parasitophorous vacuole. Blood stage parasites are enclosed in a cavity within the erythrocyte (parasitophorous vacuole) lined by membrane (parasitophorous vacuole membrane) derived from the erythrocyte surface membrane. The parasite is therefore not in direct contact with the erythrocyte cytoplasm. Life‐cycle stages. The structure, molecular composition and behaviour of Plasmodium parasites change constantly throughout its life cycle, as the expression patterns of its genes vary within both vertebrates and mosquito hosts, enabling parasites to exploit different aspects of the host's biology. Intracellular invasion. Intracellular life requires the ability to selectively capture and enter host cells, seen in the invasion by merozoites into erythrocytes and of sporozoites into liver hepatocytes. In both cases this depends on the secretion of adhesive proteins and membrane‐altering substances by the parasite, and on its actin–myosin driven locomotion. Host cell transformation. Intracellular parasites export various molecules into the host cell to transform its properties. In erythrocytes this increases permeability to nutrients and in some species causes the erythrocyte membrane to adhere to blood vessel walls. The parasite also consumes host cell cytoplasm. Malaria. This is a generic name given to diseases in vertebrates caused by species of Plasmodium . They are typified in mammals by cyclic episodes of fever and may have many other complications including anaemia, spleen pathology, placental dysfunction, neurological complications and in severe malaria, coma and death. Parasite evolution. Molecular studies indicate that the evolution of Plasmodium species is closely linked to the evolution of terrestrial vertebrates and has impacted significantly on the human genome.

Injury and immune response: applying the danger theory to mosquitoes

“…It possesses an apicoplast (a plastid-like organelle) and an apical complex, which are present in its three invasive stages. While in the vertebrate host the parasite is mainly intracellular, in the mosquito it is primarily extracellular, invading cells solely because of its need to cross tissue epithelia (Bannister and Sherman, 2009). After a mosquito ingests Plasmodium parasites (through infected blood meal), the arrested gametocytes mature and emerge from the erythrocytes within minutes.…”

An Ancient Protein Phosphatase, SHLP1, Is Critical to Microneme Development in Plasmodium Ookinetes and Parasite Transmission

“…Development of mammalian Plasmodium species proceeds via asexual exoerythrocytic proliferation and intraerythrocytic multiplication occurring in mammalian liver hepatocytes and erythrocytes, respectively, whereas sexual development and sporogony occur in the mosquito. Plasmodium belongs to the phylum Apicomplexa, which is characterized by the presence of distinct apical organelles consisting of micronemes, dense granules, and rhoptries that are used by the parasite for host invasion and gliding motility (Bannister and Sherman, 2009). Of the three invasive stages (sporozoites, merozoites, and ookinetes), the ookinete uniquely lacks rhoptries and dense granules.…”

Influence of midgut microbiota in Anopheles stephensi on Plasmodium berghei infections

“…Five Plasmodium species are capable of infecting human host, namely Plasmodium falciparum , Plasmodium vivax , Plasmodium ovale , Plasmodium malariae , and Plasmodium knowlesi . Malaria is considered as an important public health burden, especially in sub-Saharan Africa, with an estimated 216 million cases reported worldwide in 2016 [ 1 , 2 ]. Malarial parasites have a complex life cycle, which alternates between the vector mosquito and the vertebrate host [ 2 ].…”