Questions and Answers
What is the first phase of malaria life cycle that occurs in humans?
During which phase do sporozoites reproduce asexually in the liver?
How long can the schizogonic phase last for P.falciparum?
What occurs to a proportion of intrahepatic parasites in P.vivax and P.ovale infections?
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What is the term for the dormant form of parasites in the liver during P.vivax and P.ovale infections?
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Which stage of malaria involves the formation of oocysts?
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What are the small motile forms of malaria that enter the human bloodstream from a mosquito bite?
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What is a possible method of malaria transmission besides mosquito bites?
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What is a common cause of recrudescence in malaria?
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Which Plasmodium species is associated with a 48-hour cycle causing benign tertian malaria?
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What is the primary infection target of Plasmodium malariae?
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Where is Plasmodium ovale predominantly found?
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What cycle is Plasmodium malariae responsible for?
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Which of the following statements is true about Plasmodium vivax and Plasmodium malariae?
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What process leads to the disappearance of RBCs from circulation due to parasitic attachment?
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Which species produces characteristic band forms as they mature?
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How long does the asexual life cycle take for P.falciparum?
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What do male and female gametocytes form after ingestion by mosquitoes?
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What is the term for the motile stage that penetrates the mosquito's mid gut walls?
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What is the typical duration for sporogony, depending on various factors?
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What unique feature is found in RBCs infected by P.vivax?
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How long does gametogony take in P.vivax infections?
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Which antigens are involved in the invasion of red blood cells by P.vivax?
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What genetic factor is associated with a reduced risk of malaria infection?
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What characteristic stage contributes to relapses in P.vivax and P.ovale infections?
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What is a primary clinical manifestation of malaria?
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What is the process by which merozoites multiply and release from infected hepatocytes?
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Which blood group antigen is associated with P.vivax infection susceptibility?
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How do P.falciparum infected RBCs avoid the immune response?
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Which genetic condition decreases the ability of RBCs to produce NADPH, inhibiting parasite growth?
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What is the first stage of development that merozoites undergo after invading a red blood cell?
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What surface feature is exhibited by P.falciparum-infected red blood cells after about 24-26 hours?
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What determines the outcome of malaria infection in individuals?
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Which Class 1 antigen is known to confer protection against severe malaria?
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Which species' ring forms display unique morphology that resembles earphones?
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What is the main component that merozoites consume from erythrocytes as they grow?
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What is the result of the simultaneous lysis of many RBCs during a malarial paroxysm?
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Which receptors are known for P.falciparum for attachment to red blood cells?
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Study Notes
Recrudescence
- Recrudescence can occur due to inadequate treatment or drug resistance, antigenic variation, or infection by different strains of parasites.
Plasmodium vivax
- Causes benign tertian malaria with a 48-hour cycle.
- Geographically wide distribution, more prevalent in South America, North Africa, and India; rare in Sub-Saharan Africa.
- Exhibits "true relapses" due to residual liver stages.
- Specifically infects young red blood cells (RBCs).
- Parasite density rarely exceeds 50,000 parasites per µl of blood.
Plasmodium ovale
- Also responsible for benign tertian malaria with a 48-hour cycle.
- Narrow geographic distribution, primarily found in West Africa and South Pacific islands.
- Infects young RBCs.
Plasmodium malariae
- Causes quartan malaria with a 72-hour cycle.
- Sporadic distribution and relatively uncommon outside of Africa.
- Infects older RBCs.
- Associated with recrudescence but does not cause true relapses.
- P. vivax and P. malariae infect 1-2% of RBCs; P. ovale infects less than 2%. P. falciparum can infect up to 30-40%.
- Parasite density typically around 10,000 parasites per µl of blood.
Introduction
- Nearly all malaria-related deaths and severe cases result from P. falciparum.
- Malaria can be imported and often misdiagnosed.
- Transmission may occur through blood transfusions or contaminated hypodermic needles.
Life Cycle Overview
- Malaria's life cycle consists of two main stages:
- Human stages: Pre-erythrocytic schizogony, erythrocytic schizogony, erythrocytic gametogony.
- Mosquito stages: Fertilization, meiosis, ookinete formation, oocyst formation, and sporogony.
- Malaria illustrates stage development specificity for invasion: sporozoites target liver cells, whereas merozoites infect RBCs.
Life Cycle: Pre-Erythrocytic (Hepatic Phase)
- Begins with female Anopheles mosquito inoculating plasmodial sporozoites into the bloodstream.
- Sporozoites home to liver cells, entering circulation within 45 minutes.
- Undergo schizogony, with duration varying from 5 days (P. falciparum) to 15 days (P. malariae).
- Some intrahepatic parasites enter a dormant state known as hypnozoites, leading to relapses in P. vivax and P. ovale infections.
Asexual Blood Stage Development
- Merozoites invade RBCs using specific surface receptors (e.g., Duffy blood group antigen for P. vivax).
- Morphological changes occur as merozoites develop from ring forms (trophozoites) to schizonts and back to merozoites.
- P. falciparum shows surface antigen variants that promote cytoadherence and sequestration in blood vessels.
Life Cycle: Sexual Stages and Development in the Mosquito
- After several asexual cycles, a subset of parasites transforms into gametocytes for reproduction.
- Gametogony duration varies; 4 days for P. vivax and over 10 days for P. falciparum.
- Upon ingestion by mosquitoes, gametocytes become activated, developing into zygotes that penetrate the mosquito’s midgut and form oocysts.
Human Genetics and Malaria
- Genetic polymorphisms affect malaria parasite invasion and survival in RBCs, influenced by specific surface molecules.
- Most black Africans are Duffy antigen negative, affecting susceptibility to P. vivax.
- Sickle cell trait carriers (Hbs or AS) show reduced malaria infection rates.
- Genetic conditions like G6PD deficiency and thalassemia can inhibit malaria parasite growth.
- Certain human leukocyte antigens (HLA) in West Africans provide protection against severe malaria.
Pathogenesis and Clinical Manifestations
- Malaria can manifest as uncomplicated or complicated.
- Common symptoms include fever, chills, and anemia.
- Malarial paroxysms correlate with the lysis of numerous RBCs and release of merozoites, leading to cyclical symptoms.
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Description
This quiz explores the concept of recrudescence in the context of malaria, focusing on the role of Plasmodium vivax. It examines causes such as inadequate treatment, antigenic variation, and infection by different strains. Test your knowledge about this important tropical disease and its geographic distribution.
