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Kaplan Qbank USMLE



Author19 Posts
  #1

Several species of Plasmodium cause malaria. Some plasmodia cause a relatively mild form of malaria, while others cause malaria that is associated with severe complication and death. Which of the following factors will best explain the difference in the virulence of this species?

A. Age of the erythrocytes

B. Life cycle of plasmodia within the disease vector

C. Life cycle of plasmodia within the human host

D. Life cycle of the disease vector

E. Type of disease vector


  #2

C


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  #3

C


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  #4

C

  #5

C. Life cycle of plasmodia within the human host


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  #6




  #7

ok this one is a stumper and the explanation better be good cos i m seriously scratching my head.


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  #8

Whats the Answer please?

  #9

Ok - this was a toughie. The answer is A - age of the erythrocytes infected.

The different species of Plasmodium infect erythrocytes at different stages of development. Plasmodium vivax and Plasmodium ovale infect young erythrocytes, and Plasmodium malariae infects old erythrocytes. In contrast, Plasmodium falciparum infects erythrocytes at any age and can therefore parasitize a higher percentage of erythrocytes. As a result, infection with Plasmodium falciparum tends to be the most serious and may be associated with complications involving many visceral organs.


  #10

No

Though the predilection for young RBCs is seen in Vivax and Ovale speices its not that ability of the Species to result in extensive disease. Falciparum infection is mostly to the alteration in the RBC membrane by the parasite and its attachment to capillaries.

Therefore I disagree .

Severe disease is typically seen with P falciparum infection. This species is more virulent because it may create high levels of parasitemia and sequestration that contribute to end-organ damage. Sequestration is a specific property of this species. As it develops through the 48-hour life cycle, it demonstrates adherence properties, which result in the sequestration of the parasite in small postcapillary vessels. For this reason, only early forms are observed in the peripheral blood, before the sequestration property develops; this is an important diagnostic clue that the patient is infected with P falciparum.

Sequestration of parasites may contribute to mental status changes and coma, observed exclusively in P falciparum. In addition, cytokines and a high burden of parasites contribute to end organ disease. End organ disease may develop rapidly with P falciparum, and it specifically involves the central nervous system (CNS), lungs, and kidneys. These severe manifestations may occur in the nonimmune traveler or young children who live in endemic areas.


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FORUM RULES-- Those who believe in telekinesis, raise my hand. I get enough exercise just by pushing my luck --P4U World.." The pure and simple truth is rarely pure and never simple."

  #11

NNL

"Though the predilection for young RBCs is seen in Vivax and Ovale speices its not that ability of the Species to result in extensive disease. Falciparum infection is mostly to the alteration in the RBC membrane by the parasite and its attachment to capillaries." This is true however your response in entirety appears contradictory. The question is asking which best explains the difference of virulence? You said yourself..."This species is more virulent because it may create high levels of parasitemia and sequestration that contribute to end-organ damage. Sequestration is a specific property of this species." In order for the life cycle of falciparum to persist and trophoizoites formed, erythrocytes must be infected. Virulence is contigent on infected erythrocytes and since falciparum can infect them at any age, it makes sense that much more of them would be infected. - Which means more are sequestered and more adhered to the endothelium of capillaries of numerous tissues.

Here is the explanation for the incorrect option C: For the four Plasmodium species, the life cycle within humans is predominantly the same. All of the species have an erythrocye stage. However, P. vivax and P.ovale also have an exoerythrocytic (hypnozoite) stage and this accounts for their persistence and ability to cause relapses of disease. Antimalarial drugs that target the erythrocytic stage can cure malaria caused by P. falciparum or P. malariae. However, these drugs can cure malaria caused by P.vivax or P.ovale only if they are given in combination with a drug that targets the exoerythrocytic stage (a drug such as Primaquine)

Also, here is a link that will help provide more clarity. http://www.pnas.org/cgi/reprint/96/8/4563.pdf


  #12

A. nod

I had a question similar to this question on my step 1 exam.


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  #13

@ Tiff from the article you presented says the same thing which i m saying. You are saying that its the age of the RBC which dictates the severity of the infection. And i m saying that the property of sequestration and therefore the property of the parasite to adhere to endothelium is the cause of it and its only present in the life cycle of P falciparum.

My only contradiction to your statement is that its not the number of RBC that infected but its the adherence of the parasite infected RBCs to the endothelium which indicates the parasite density in the body and dictates the severity of the infection.

The ability of the parasite to infect all RBCs is not dictatum for its severity its the ability of the parasite to alter the RBC membrane and make it adhere in the capillaries.

Now I know you will say that property is though unique is done during its life in RBC which is no different from other species. But i took the option C as the alteration which occurs in the RBC in Falciparum is not Exhibited by any other species.






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FORUM RULES-- Those who believe in telekinesis, raise my hand. I get enough exercise just by pushing my luck --P4U World.." The pure and simple truth is rarely pure and never simple."

  #14

NNL - I see how you're thinking, but all the Plasmodium species have the same life cycle. Vivax and ovale may have a dormant stage and cause relapses, nevertheless it's the same cycle. Adherence of infected RBCs to the endothelium is indeed a very important property unique to Falciparum, but again, not part of the life cycle and not mentioned in the list of answer choices making A the best option.

Here are a couple of more links. The second one has a great illustration of the Plasmodium life cycle.

http://www.nature.com/nrmicro/journal/v4/n5/box/n...

http://www.dpd.cdc.gov/dpdx/HTML/Malaria.htm


  #15

Also NNL - would like to add that the fact that it infects all ages of erythrocytes is indeed extremely important for determining virulence. As said previously, the more RBCs that are infected, the more will adhere in capillaries which is also important for virulence.


  #16

look i get what you are trying to say but your first article says it best.

Evolutionary ecologists have an alternative view of the evolution of virulence (2–7). Both theoretical and recent empirical data demonstrate that pathogenicity can be maintained when it is a direct or indirect consequence of the parasite’s exploitation of the host during production of transmission stages. Parasite reproduction is balanced against host survival. In an attempt to better understand the processes that influence the evolution of virulence of P. falciparum in the human host, we have explored the molecular relationship between virulence and transmissibility in this host–parasite system.
During its life cycle P. falciparum develops and multiplies asexually within host erythrocytes (RBCs). RBCs infected with mature parasites, called trophozoites, sequester from the peripheral circulation by adhesion to capillary endothelium in a variety of tissues (8–10). Under conditions of blood flow, this adhesion is facilitated by the expression of knob-like protrusions under the infected RBC membrane (11).

Virulence of P. falciparum, measured by the clinical outcome of infection, has been associated with parasite density, which, in turn, is influenced by this ability to adhere to endothelium (12). A number of host receptors involved in the parasite adhesion process have been identified (reviewed in ref. 13). These include the leukocyte differentiation antigen CD36, thrombospondin, intercellular adhesion molecule 1, and chondroitin sulfate A. Trophozoite-infected RBCs from
the majority of wild-type parasites tested so far can bind to CD36, whereas adhesion to other receptors occurs less frequently (14–16).




This to me is the best explanation for the question. Again only my views


___________________
FORUM RULES-- Those who believe in telekinesis, raise my hand. I get enough exercise just by pushing my luck --P4U World.." The pure and simple truth is rarely pure and never simple."

  #17

Good Discussion though. nodnod


___________________
FORUM RULES-- Those who believe in telekinesis, raise my hand. I get enough exercise just by pushing my luck --P4U World.." The pure and simple truth is rarely pure and never simple."

  #18

nod


  #19

Damn you guys really got into the nitty gritty of it. which further proves me that i m dumb cos i never thought about this question in this way.








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