Malaria: Life Cycle and Species

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Questions and Answers

In cases of malaria caused by Plasmodium falciparum, which of the following complications is most directly associated with the parasite's ability to induce the expression of parasite antigens on the surface of infected erythrocytes?

  • Nephrotic syndrome due to immune-complex deposition.
  • Cerebral malaria, resulting from the adherence of infected erythrocytes to blood vessel endothelium. (correct)
  • Black water fever, characterized by massive intravascular hemolysis.
  • Algid malaria, leading to hypotension and circulatory collapse.

A patient presents with repeated malaria attacks despite prior treatment with chloroquine, and lab tests confirm the presence of Plasmodium falciparum. Which of the following best describes the most likely underlying cause for the recurring symptoms?

  • Reactivation of persistent hypnozoites in the liver.
  • Incomplete quinine therapy leading to drug resistance. (correct)
  • Re-infection due to presence of low parasitemia.
  • Autoimmune reaction against infected red blood cells.

Why are individuals with sickle cell anemia often resistant to Plasmodium falciparum infection?

  • Individuals with sickle cell anemia produce antibodies that neutralize the parasite.
  • The altered red blood cell environment in sickle cell anemia impairs parasite development. (correct)
  • Sickle cell anemia enhances the efficacy of antimalarial drugs.
  • Sickle cell anemia prevents the mosquito vector from transmitting the parasite.

Following diagnosis of malaria, a patient is prescribed primaquine. What is the primary goal of this medication in the context of malaria treatment?

<p>To eliminate the parasite from the liver and prevent relapse, particularly in <em>P. vivax</em> and <em>P. ovale</em> infections. (A)</p>
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A patient who has been living in a malaria-endemic area presents with dysentery, gastrointestinal bleeding and anemia. Considering the complications associated with malaria, which pathological process is most likely contributing to these symptoms?

<p>Anoxia and necrosis of internal organs stemming from cytoadherence of infected erythrocytes. (B)</p>
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How does chemoprophylaxis primarily function in preventing malaria infections?

<p>By preventing the development of clinical symptoms through the use of medications that target blood schizonticides. (D)</p>
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A patient is suspected of having a malaria infection. After performing a rapid diagnostic test (RDT), the result comes back negative. Given this result, what is the most appropriate next step in confirming or ruling out the diagnosis?

<p>Perform a Giemsa-stained blood film to directly visualize the parasite. (B)</p>
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In the context of malaria, what is the significance of the Duffy antigen concerning Plasmodium vivax infections?

<p>The absence of the Duffy antigen confers resistance to <em>P. vivax</em> infection. (D)</p>
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During which stage of the malaria parasite's life cycle does the mosquito become infected?

<p>When the mosquito ingests gametocytes during a blood meal from an infected human. (C)</p>
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In the pathogenesis of malaria paroxysm, what triggers the cyclical pattern of cold, hot, and sweating stages?

<p>The synchronous rupture of infected red blood cells, releasing parasites and metabolites. (C)</p>
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Flashcards

Malaria Vector

Female Anopheles mosquito

Malaria Diagnostic Stage

Gametocytes or merozoites

Malaria Infective Stage

Sporozoites

Malaria Paroxysm Pathogenesis

Rupture of infected RBCs and release of parasite metabolites evoking host immune response.

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P. vivax

Benign tertian malaria

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P. falciparum

Malignant malaria, subtertian or irregular

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Severe Anemia (Malaria)

P. falciparum invades at any age of RBC

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Hyper-reactive splenomegaly

Reduction of T-suppressor cells

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Black Water Fever

Massive intravascular hemolysis

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CBC results for Malaria

Pancytopenia due to splenomegaly

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Study Notes

  • Malaria is a parasitic disease transmitted by female Anopheles mosquitoes.

Malaria Life Cycle

  • The life cycle includes stages in both the mosquito and human hosts.
  • In the mosquito, the stages are oocyst, ookinete, and sporozoites.
  • The mosquito takes a blood meal and injects sporozoites into the human host.
  • In the human liver, the parasite undergoes exo-erythrocytic cycle producing schizonts.
  • Schizonts rupture, releasing merozoites that infect red blood cells (RBCs).
  • In RBCs, the parasite goes through erythrocytic cycle, developing into trophozoites and schizonts, eventually producing gametocytes.
  • Mosquitoes ingest gametocytes from infected humans, completing the cycle.
  • Infective stage: sporozoites.
  • Diagnostic stage: gametocytes or merozoites.

Malaria Species

  • Plasmodium vivax: causes benign tertian malaria.
  • Plasmodium ovale: causes ovale tertian malaria.
  • Plasmodium malariae: causes benign quartan malaria.
  • Plasmodium falciparum: causes malignant malaria.

Clinical Presentation

  • Malaria paroxysm is the immediate attack.
  • Immune responses are evoked by the rupture of infected RBCs and release of parasite metabolites.
  • Cold stage: lasts for 15 minutes.
  • Hot stage: lasts for 2-6 hours.
  • Sweating stage: lasts for 2-6 hours.

Hemolytic Anemia

  • P. vivax invades reticulocytes only, leading to restricted anemia.
  • P. ovale invades reticulocytes only, leading to restricted anemia.
  • P. malariae invades old RBCs only, leading to restricted anemia.
  • Severe anemia occurs when P. falciparum invades RBCs at any age.
  • Hepatosplenomegaly results from enhanced phagocytosis of remnants of ruptured red cells and schizonts.

Complications

  • Nephrotic syndrome:
    • Type III hypersensitivity reaction occurs after chronic P. malariae infection
    • Immune complexes deposit on the glomeruli and kidneys
  • Knobs Formation: Occurs with P. falciparum infections (types 2, 3, and 4)
    • Parasite antigens are expressed on the surface of infected RBCs, forming knobs.
    • These knobs adhere to receptors on endothelium of blood capillaries, leading to anoxia and necrosis of internal organs
  • Clinical signs and symptoms:
    • Brain: headache, drowsiness, convulsions, coma.
    • GIT: diarrhea, dysentery, gastrointestinal bleeding.
    • Lungs: pulmonary edema, difficulty in breathing.
    • Algid malaria: hypotension, circulatory collapse, shock.
    • Kidneys: acute renal failure.
    • Liver: hypoglycemia.
  • Hyper-reactive splenomegaly: tropical splenomegaly syndrome
    • Is due to the reduction of T-suppressor cells, leading to a markedly enlarged spleen with increased IgM
  • Black water fever:
    • Caused by repeated attacks of P. falciparum infection and incomplete quinine therapy
    • Autoimmune reaction occurs (antibodies against infected RBCs), leading to massive intravascular hemolysis
    • Is characterized by anemia, hemoglobinuria, and jaundice

Diagnosis

  • Pancytopenia due to splenomegaly
  • Diagnosis can be determined through rapid diagnostic test (RDT)
  • Giemsa-stained blood films are used to demonstrate the parasite.
  • Serology detects circulating parasite antigens and antibodies.
  • DNA and RNA probes detect parasite DNA and RNA in patient's blood.

Treatment

  • During clinical attack: Chloroquine (blood schizonticides + blood gametocytes).
  • Prophylaxis of relapse: Primaquine (Tissue schizonticides + blood gametocytes).
  • Drug resistant cases: Coartem (combined drug).
  • Chemoprophylaxis: Tissue schizonticides + blood schizonticides.

Control

  • Is done by treatment of cases, Mosquito control, chemoprophylaxis, vaccination trials, wire screens and nets, mosquito repellents
  • Tissue schizonticides: pyrimethamine or primaquine.
  • Blood schizonticides: chloroquine or mefloquine.
  • Blood gametocytes: chloroquine or primaquine.

Notes

  • Sickle cell anemia provides resistance to P. falciparum.
  • Duffy antigen is essential for P. vivax infection.
  • Relapse involves reactivation of persistent hypnozoites in the liver (occurs in P. ovale and P. vivax).
  • Recurrence is reinfection with malaria due to presence of low parasitemia (occurs in P. falciparum and P. malariae).

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