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Why doesn't the plasmodium falciparum not have shizonts?

  1. Jan 29, 2012 #1
    Hello everyone,

    I'm learning Malaria right now, and thought it would be good for me to differentiate plasmodium vivax and plasmodium falciparum.

    P.V
    Produces benign tertian malaria,
    Some sporozoites remain as hypnozoites,
    Merozoites enter new RBCS
    Ring stage, amoeboid, shizont, gametocyte can be identified using microscope

    P.F
    Produces malignant tertian malaria,
    Cause more severe infection
    No hynozoites,
    Merozoites enter RBC of all ages
    Only ring stage and gametocyte can be identifed using microscope

    Now my questions are,

    1. What is the difference between malignant and benign malaria? Malignant one obviously sounds bad but what is the exact difference.
    2. Now why are amoeboids and shizonts not seen with P.F. To complete the life cycle these stages must occur right, are these stages occuring with plasmodium falciparum, if so why can't we see it in peripheral blood.

    Also if there are any difference between too, please add. Thank you :smile:
     
  2. jcsd
  3. Feb 2, 2012 #2

    rhody

    User Avatar
    Gold Member

    Sammeeralord,

    You might find this TED Video I posted recently on Malaria transmission, infection progression interesting for general background, but not to address your question(s).

    Have a look.

    Rhody...
     
  4. Feb 3, 2012 #3

    bobze

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    Science Advisor
    Gold Member

    Sameer,

    P. vivax and ovale can establish "latent" infections via the dormant form: hypnozoites. Why doesn't P. falciparum do this? I don't know, take it up with evolution! :P

    PF still goes through a schizont form though, not sure where you heard that. Got a source?

    Here's a picture!

    P. falciparum schizonts;
    http://dpd.cdc.gov/dpdx/images/ParasiteImages/M-R/Malaria/falciparum/Pf_schizont_thinC.jpg

    PF causes more severe malarial parasitemia because it can invade all RBCs.

    P. vivax and ovale on the other hand, only like young, supple RBCs (immature RBCs)--I'm sure that probably has to do with how the parasite gains access to the cells and the different receptors it does it through--But the specifics of that kind of information is venturing into the land of low-yield for clinical medicine.

    P. malariae only invades senescent RBCs.

    The important thing to know about P. vivax is that it can remain dormant as the hypnozoites. As such, you have to add primaquine to a treatment regime (the typicals like chloroquine and mefloquine aren't active against hypnozoites, only erythrocytic forms). Hypnozoites stay in hepatocytes, while the other stages of malaria move to the plasma.

    I think you should probably just know the generals of the lifecycle like;

    Sporozoite→ attachment to hepatocyte and entry→ schizont (some for vivax and ovale can turn into hypnozoites here)→ differentiation into merozoites→ rupture and release into plasma→ attachment and invasion of RBCs→ ring stage → trophozoites→ differentiation into schizonts (repeat cycle) and gametocytes (small number, taken up by mosquitos where they finish life cycle).

    Really to differentiate falciparum and vivax via light microscopy you look for multiple ring forms in RBCs for PF and Schüffner's dots in young RBCs (like reticulocytes). Really differentiating between plasmodium species by microscopy is a terrible way to go about it. Its generally done by PCR in reference labs.
     
    Last edited: Feb 3, 2012
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