Micro- Malaria Flashcards

1
Q

What is algid malaria?

A

Complication of falciparum malaria where there is:

  1. vascular collapse
  2. shock
  3. drop in body temperature
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2
Q

What is bilious remittent fever?

A

Impairment of liver function an marked jaundice associated with falciparum malaria

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3
Q

What is “blackwater” fever?

A

Complication of falciparum malaria where there is massive hemolysis and hemoglobinuria.

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4
Q

What is cerebral malaria?

A

Complication of falciparum malaria where there is:

  1. cerebral capillary obstruction
  2. brain congestion
  3. brain swelling
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5
Q

What form of the malaria parasite is responsible for infecting more mosquitoes?

A

Gametocyte [male or female] in the RBC

*females are called macrogametocytes, males are called microgametocytes

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6
Q

What 2 strains of malaria have hypnozoites?

A

Hypnozoite is a dormant form of malaria in liver cells

  1. Plasmodium vivax
  2. plasmodium ovale
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7
Q

What is a merozoite?

A

form of the malaria parasite that results from asexual multiplication within the RBC
It is released from the mature schizont to infect other RBCs

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8
Q

What is the ring stage?

A

First stage of development of malaria parasites in the RBC.

It consists of a ring of cytoplasm and a dot of nuclear material surrounding a vacuole

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9
Q

What area is considered to be a zone of chloroquine-resistant P. falciparum?

A

at the present time, nearly ALL P. falciparum are chloroquine resistant except in:

  1. Haiti
  2. Central America north of the Panama Canal
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10
Q

What are the 5 species that can cause malaria in humans?

A
P. falciparum
P. vivax
P. ovale
P. knowlesi [S.E. Asia--Malaysia] 
P. malariae
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11
Q

P. knowlesi was prior thought to only be a primate pathogen but now it has been shown to infect humans in what area?
What does P. knowlesi resemble microscopically? How does it different from this strain clinically?

A

It infects humans in Southeast Asia, specifically Malaysia

Microscopically it resembles P. malariae but it has a MUCH more severe disease

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12
Q

Describe the pathogenesis of malaria protozoa parasites.

What vector transits the plasmodium to humans?

A
  1. Plasmodium sporozoites are transmitted to humans via Anopheles mosquitos that take a blood meal
  2. In liver cells, sporozoites mature into schizonts and mature into merozoites.
  3. Merozoites released from the liver invade RBCs and attach themselves to specific binding sites on RBC
  4. in RBC, merozoites feed on Hb and other proteins and mature into trophozoites
  5. Trophozoites undergo nuclear division [without cell division] to form 16-32 parasite nuclei [Schizonts] in a single RBC
  6. RBC ruptures, and schizonts release merozoites to infect new RBCs
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13
Q

What are the 4 developmental stages of malaria apparent in peripheral blood?

A
  1. ring stage - early, asexual stage in RBC, ring-shaped
  2. Trophozoites- further development asexual stage that is larger, less ring-shaped, with accumulation of malarial pigment [hemozoin]
  3. Schizonts- late asexual stage where the parasite has divided into merozoites each containing chromatin.
  4. Gametocytes- sexual stage. The forms have no relevance to disease, but are necessary for infection of mosquitos
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14
Q

Describe the appearance of P. vivax in trophozoite stage blood smears.

  1. RBC appearance
  2. trophozoite appearance
A
  1. Erythrocyte it lives in is usually younger and thus LARGER than other RBCs
  2. amoeboid appearance
  3. Schuffner’s dots = inclusion of RBC [little pink dots]
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15
Q

Describe the appearance of P. ovale in trophozoite stage blood smears.

A
  1. oval, tear drop or elongated RBC with “pulled out” fimbriated cell membranes
  2. James dots= inclusion bodies
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16
Q

What can the number of merozoites in the schizonts clue you in to?

A

identification of the plasmodial species

17
Q

Which peripheral blood stage is NOT important for disease pathogenesis, but is crucial for infection of mosquitoes?

A

gametocytes

18
Q

For what 2 species of plasmodium is it important to treat for the peripheral blood stages AND with primaquine to eradicate hypnozoites from the liver?

A

ovale and vivax

19
Q

Describe thick blood film for malarial detection.

A
  1. Lyse RBCs with distilled water or saponin to leave WBC, parasite, platelets
    - more sensitive than thin film because it has larger volume of sample
  2. stain with Giemsa or pH 7.2-7.4 stain
    - usually hematologic stains are lower pH but if you use these for malarial suspicion, you may not see Schuffners dots
20
Q

What are the 3 main things the thin blood film allows you to do?

A
  1. morphological differentiation between plasmodium species
  2. differentiate plasmodium from babesia
  3. estimate the percentage of parasitemia
21
Q

What plasmodium species is associated with:

  1. Schuffner’s dots
  2. James dots
  3. Maurer’s lefts
A
  1. P. vivax
  2. P. ovale
  3. P. falciparum
22
Q

In addition to thick and thin blood films, what techniques are used to diagnose malaria?

A
  1. EIA [used mostly outside the US]
    - P. falciparum vs the other species
    - Some can do P vivax
  2. PCR
    - used in reference laboratories
    - useful for identifying dual species infections
  3. Ab tests
    - reference labs
    - NOT useful for individual cases
23
Q

How many cases of malaria are there worldwide per year?
What age group/area has the highest mortality?
How much of the world’s population lives in an endemic zone?

A

300-500 million cases/year
Highest mortality in children under 5 in Sub-Saharan Africa
1/2 the word’s population lives in an endemic zone

24
Q

In parts of Africa and Southeast Asia, what drugs are P. falciparum resistant to?

A
  1. chloroquine
  2. sulfadoxine/proguanil
  3. proguanil
  4. mefloquine
25
Q

What is the only location [except for RARE exceptions] where P. ovale occurs?

A

Central and Western Sub-Saharan Africa

26
Q

What is the specific binding site on P. falciparum and P. vivax that merozoites bind to ?

A

P. falciparum = glycophorin antigen

P. vivax = Duffy blood group antigen

27
Q

What determines the clinical picture of malaria?

A
  1. age and immune status of the patient
  2. species of parasite
    - falciparum is most virulent
28
Q

One brood of parasites becomes dominant and is responsible for the synchronous nature of the clinical symptoms of malaria [cyclic paroxysms]. How do they elicit symptoms?

A
  1. replicate inside RBC and then induce cytolysis
  2. release toxic metabolic byproducts into the bloodstream
  3. since many RBCs rupture at the same time, the host experience :
    - flu like symptoms
    - anemia
29
Q

What are the 3 things plasmodium species do to cause anemia?

A
  1. RBC lysis
  2. suppression of hematopoiesis
  3. increased clearance of RBC by the spleen

[over time they also cause thrombocytopenia and hepatosplenomegaly]

30
Q

Why is the level of parasitemia higher for P. falciparum then the other plasmodium species?
What clinical effects does this lead to?

A

It infects ALL RBCs [young, middle age, old]
This means it makes more merozoites, destroying even more RBCs leading to:

lack of O2 to tissues

31
Q

Why does P. falciparum cause hypoglycemia and lactic acidosis?

A

P. falciparum uses glucose as their energy source and because they metabolize it 70x faster than the RBCs they live in, this causes hypoglycemia/lactic acidosis

32
Q

What 3 factors are considered when deciding treatment options for plasmodium?

A
  1. infecting species
  2. geographical area where infection was acquired
  3. severity of the disease
33
Q

What are the 3 “r” problems with management of malaria?

A
  1. recrudescence- controllable number of parasites remain latent in RBCs in the blood stream due to inadequate immune response or antimalarial therapy and reactivate with trauma or immunosuppression
  2. relapse- hypnozoites [vivax/ovale] in the liver reactivate
  3. resistance- anti malarial drugs become ineffective
34
Q

What is the drug of choice for non-resistant strains of Plasmodium?
Which plasmodium species does it kill?
What 2 situations do you need supplement/ a different drug?

A

Chloroquine is drug of choice for all 5 species if they are non-resistant.

  1. It does NOT kill hypnozoites so you need to use PRIMAQUINE to prevent drug relapse
  2. it does NOT kill resistant strains so you need MEFLOQUINE, malarone [atovaquone/proguanil] or quinine
35
Q

In EXTREME cases of falciparum malaria, what technique can be used?

A

Exchange transfusion to decrease the level of parasitemia

36
Q

What are the 2 reasons morbidity and mortality are greater for P. falciparum?

A
  1. increased parasitemia – lack of O2 to tissues, lactic acidosis, hypoglycemia
  2. cytoadherence- infected RBCs have proteinaceous knobs on the surface of the RBC that stick to endothelial cell lining in microvasculature of the CNS, kidney and lungs. This leads to aggregation [rosetting] of uninfected RBCs sequestering them and resulting in cerebral malaria/kidney failure
37
Q

What is prevention of malaria?

A
  1. DEET insect repellent
  2. premethrin-treated clothes and bed nets
  3. staying indoors at night/early morning
  4. if travelling to endemic areas
    - chloroquine if not resistant
    - if resistant area : mefloquine, malarone, proguanil, primaquine, doxy