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Biology 9 Online
OpenStudy (anonymous):

Can anyone explain trophozoites and protozoal infections?

OpenStudy (anonymous):

@InYourHead

OpenStudy (agreene):

Protozoan infections tend to be rather complex and depend on the specific organism and the vector... everything is based on the life cycle stage. I'm not sure what exactly you're needing, but this might help: http://en.wikipedia.org/wiki/Apicomplexan_life_cycle

OpenStudy (anonymous):

I need it really dumbed down. I have a test Thursday and it's a minimal part but I'm trying to understand protozoan infections.

OpenStudy (anonymous):

its a vast topic i dk whaT u have to study.how mANY pages are there?in ur material?/text its a whole books part here.

OpenStudy (anonymous):

Malarial infections? Just the basic way they infect through mosquitos and humans and all the terms associated with it.

OpenStudy (anonymous):

terms? what do u mean?life cycle clinical terms?

OpenStudy (anonymous):

n Among the malaria species that infect humans, Plasmodium vivax and P. ovale can develop dormant liver stages that can reactivate after symptomless intervals of up to 2 (P. vivax) to 4 years (P. ovale). Pregnant women have increased susceptibility to Plasmodium falciparum malaria; in malaria-endemic countries, P. falciparum contributes to 8-14% of low birth weight, which in turn decreases the chance of a baby’s survival. After a single sporozoite (the parasite form inoculated by the female mosquito) of Plasmodium falciparum invades a liver cell, the parasite grows in 6 days and produces 30,000-40,000 daughter cells (merozoites), which are released into the blood when the liver cell ruptures. In the blood, after a single merozoite invades a red blood cell, the parasite grows in 48 hours and produces 8-24 daughter cells, which are released into the blood when the red blood cell ruptures. Under the microscope, Plasmodium knowlesi can resemble either P. falciparum or P. malariae. Thus PCR is often required to confirm infection.

OpenStudy (anonymous):

n The natural ecology of malaria involves malaria parasites infecting successively two types of hosts: humans and female Anopheles mosquitoes. In humans, the parasites grow and multiply first in the liver cells and then in the red cells of the blood. In the blood, successive broods of parasites grow inside the red cells and destroy them, releasing daughter parasites ("merozoites") that continue the cycle by invading other red cells. The blood stage parasites are those that cause the symptoms of malaria. When certain forms of blood stage parasites ("gametocytes") are picked up by a female Anopheles mosquito during a blood meal, they start another, different cycle of growth and multiplication in the mosquito. After 10-18 days, the parasites are found (as "sporozoites") in the mosquito's salivary glands. When the Anopheles mosquito takes a blood meal on another human, the sporozoites are injected with the mosquito's saliva and start another human infection when they parasitize the liver cells. Thus the mosquito carries the disease from one human to another (acting as a "vector"). Differently from the human host, the mosquito vector does not suffer from the presence of the parasites.

OpenStudy (anonymous):

bThe malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host 1. Sporozoites infect liver cells 2and mature into schizonts 3, which rupture and release merozoites 4. (Of note, in P. vivax and P. ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks, or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony A), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony B). Merozoites infect red blood cells 5. The ring stage trophozoites mature into schizonts, which rupture releasing merozoites 6. Some parasites differentiate into sexual erythrocytic stages (gametocytes) 7. Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal 8. The parasites’ multiplication in the mosquito is known as the sporogonic cycle C. While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes 9. The zygotes in turn become motile and elongated (ookinetes) 10which invade the midgut wall of the mosquito where they develop into oocysts 11. The oocysts grow, rupture, and release sporozoites 12, which make their way to the mosquito's salivary glands. Inoculation of the sporozoites 1into a new human host perpetuates the malaria life cycle.

OpenStudy (anonymous):

That was just what I needed. Thank you. Just to make sure I understand correctly: the protozoa undergoes sexual reproduction in mosquitos and asexual reproduction in humans? I also understand what merozoites are.. but is the reason they are so small SO THAT they can infect RBCs?

OpenStudy (anonymous):

yes sexual in mosq and asex in humans http://malaria.wellcome.ac.uk/interactive/parasitelifecycle/interactive.html Malaria Merozoite invasion process is complex and involved in the multi-step sequence which can be divided into four phases: Initial Recognition and Reversible Attachment of the Merozoite to the Erythrocyte membrane; Reorientation and Junction formation between the Apical end of the Merozoite (Irreversible Attachment) and the release of Rhoptry-Microneme substances with Parasitophorous Vacuole formation; movement of the Junction and Invagination of the Erythrocyte membrane around the Merozoite accompanied by removal of the Merozoite’s surface coat, and finally resealing of the PVM (Parasitophorous Vacuole Membrane) and Erythrocyte membrane after completion of Merozoite invasion The initial interaction between the Merozoite and the Erythrocyte is probably a random collision, which is highly dependent on specific molecular interactions between parasite ligands on the Merozoite and host receptors on the Erythrocyte membrane. However, these molecular interactions are not completely defined. Proteins on the surface and in the apical organelles of the Merozoites mediate cell recognition and invasion into the RBCs. This invasive process is conducted by an Actin-Myosin motor process, which involves four components, the MCP1 (Merozoite Cap Protein-1), Actin, MyosinA and MTIP (MyosinA Tail Interacting Protein). MSP1 (Merozoite Surface Protein-1), with GPI (Glycosyl Phosphatidyl Inositol) anchor; also called MSA1, gp195 or PMMSA could be involved in the initial recognition of the Erythrocyte in a Sialic Acid-dependent way. Three other P. falciparum-Merozoite Surface Proteins, named MSP2, MSP3 and MSP4, have been identified. Sialic Acid on Glycophorins are involved in receptor recognition for Merozoite invasion after initial attachment. The microneme derived 175-kD EBA175 (Erythrocyte-Binding Antigen-175) of P. falciparum also binds to Sialic Acids on Glycophorin. The gene structure of EBA175 has striking similarities with the Duffy-Binding Proteins of P. vivax and P. knowlesi. EBA175 seems to be the most important ligand for binding of Merozoites to GlycophorinA on the Erythrocytes; however, some P. falciparum Merozoites can utilize alternative pathways for invasion. GlycophorinB can also act as an Erythrocyte receptor. Furthermore malaria Merozoites can utilize independent pathways for invasion without Sialic Acid. Other vacuolar proteins, such as the ABRA (Acidic Basic Repeat Antigen) and SERA (Serine Repeat Antigen) are also found in Merozoite. Many apical organellar proteins in the Micronemes and Rhoptries, which include, AMA1 (Apical Membrane Antigen-1) and MAEBL (in Rodent Malaria) are also present in Merozoite. Components of the low molecular mass Rhoptry Complex, the RAP1 (Rhoptry-Associated Protein-1), RAP2 and RAP3, also occur in Merozoites. The high molecular mass Rhoptry protein Complex (RhopH), together with RESA (Ring-infected Erythrocyte Surface Antigen), which is a component of dense granules, is transferred intact to new Erythrocytes at or after Invasion and may contribute to the host cell remodeling process. RhopH1 (High Molecular Weight Rhoptry Protein-1), RhopH2 (High Molecular Weight Rhoptry Protein-2) and RhopH3 (High Molecular Weight Rhoptry Protein-3) are found in the Merozoite proteome. The Merozoite develops within the Erythrocyte through ring, Trophozoite and Schizont stages (Erythrocytic Schizogony) too much detail for me.....lol for u it maybe simple

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