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IHO Block 3 > Malaria Module > Flashcards

Malaria Module Flashcards

1
Q

Where is Malaria most prevalent?

A

-Africa, Asia, Latin America

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2
Q

How many people are affected by malaria each year?

A
  • 216 million ppl, 655,000 die each year
  • 90% of deaths in sub-saharan africa
  • 1500 cases in US each year
  • one child dies from malaria each minute in Africa
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3
Q

What causes malaria?

A
  • A mystery for many years!
  • mal (bad) + aria (air)
  • Symptom: weird recurrent fever
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4
Q

Alphonse Laveran:

A
  • Examined unstained, fresh blood smears and found malarial parasite in 1880
  • He found it be looking for pigment
  • The infected red cell containing parasite forms and hemozoin
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5
Q

Ronald Ross:

A

-Dissected thousands of mosquitos before finding the malarial parasite in 1897 (won nobel prize in 1902)

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6
Q

What is important about the anopheles mosquito?

A

-Type of mosquito that transmits malaria!

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7
Q

What is the parasite inside the mosquito?

A

Plasmodium (Protozoa) 1-50 um in size

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8
Q

What might an infected malarial red cell look like?

A

-Contains parasite forms & hemozoin (crystals)!

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9
Q

What do plasmodium trophozoites look like under the microscope?

A
  • Ring form of plasmodium

- Gray ring with red dot near the edge

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10
Q

What is important about Plasmodium vivax, P. ovale and P. malariae species?

A
  • Low parasite burden
  • mild anemia
  • relapses (in P. vivax and P. ovale)
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11
Q

What is important about Plasmodium falciparum?

A
  • High parasite burden
  • Severe anemia
  • Cerebral and multi-organ symptoms
  • High fatality rate
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12
Q

What is the infective stage of malaria?

A

Sporozoite!

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13
Q

What is the life cycle of plasmodium falciparum?

A
  1. Sporozoites go into the liver/hepatic cells first
  2. Form hepatic schizonts
  3. Exoerythrocytic cycle in hepatic cells
  4. Burst open and release merozoites
  5. Merozoites go into the red blood cell, goes into the ring form, becomes trophozoite
  6. Forms schizont,
  7. Cell bursts and releases merozoites –> some are released to infect other red cells and others become macro-gametocytes that go back into mosquito form
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14
Q

What type of organism infects red blood cells?

A

Merozoites!

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15
Q

What is unique about the life cycle of P. falciparum?

A
  • Trophozoites contain lots of rings!

- Gametocytes are crescent or banana-shaped gametocytes (rather than round)

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16
Q

What does falciparum come from?

A
  • Falci = falx cerebri = sickle-shaped

- Parum = giving birth to

17
Q

What is unique about P. malariae?

A

-Forms “rosette” arrangement of merozoites (in schizonts!)

18
Q

What is unique about P. ovale?

A
  • Enlarged red cells (OVAL SHAPED!) - trophozoites

- Schuffner’s dots - trophozoites

19
Q

What’s unique about P. vivax?

A

-Enlarged red cells (schizonts) and Schuffner’s dots (trophozoites)

20
Q

What is the only parasite that forms rings in RBCS?

A

MALARIA!!

21
Q

What are schizonts called when they are released?

A

Merozoites!!

22
Q

Why is P. falciparum worse?

A
  • Ability to infect red cell of any age!
  • Causes red cell pathology
  • -“rosettes”
  • -abnormal binding to endothelium
  • -blood flow is impeded
  • -main cause of death in children: cerebral ischemia
  • Stimulates high production of cytokines
  • -TNF, INF-gamma, IL-1
  • -how do the bugs do that?
  • -suppress red cell production, cause fever, tissue damage, and red cell binding to endothelium
23
Q

What do red blood cells have in P. falciparum?

A

-“knobs” on RBCs that bind to ligands on vascular endothelial cells (get stuck and make clots)

24
Q

What happens to the patient with malaria?

A
  • Spleen becomes enlarged (parasites in red cells, super-active macrophages, if chronic: fibrosis, grayish color)
  • Liver becomes enlarged and pigmented
  • Brain vessels get plugged (red cell rosettes, hypoxia around vessels, eventually, ischemia)
  • Heart, lungs may also be involved
25
Q

What is the timeline of malaria infection in the patient?

A
  • Incubation: 1-2 weeks
  • Prodrome: flu-like illness
  • Paroxysms! Fever/chills, sweating, myalgia
  • -Quotidian (daily!) - P. falciparum (worst)
  • -Tertian (every 48 hours) - P. vivax or ovale (every 3 days)
  • -Quartan (every 72 hours) - P. malaria (least worst - every 4 days)
26
Q

How have hosts (us!) developed resistance to malaria?

A
  1. Inherited red cell alterations
    - Hemoglobinopathies (e.g. sickle cell) - reduces disease severity
    - Thalassemias
    - G6PD deficiency
    - RBC antigens (ABO, Duffy)
  2. Partial immune-mediated resistance
    - Develops over time in patients in endemic areas
    - Reduces disease severity
    - P. falciparum uses antigenic variation
27
Q

How does blood type influence resistance?

A
  • Blood type (ABO) affects binding
  • Blood cells can be receptors for things
  • If you get infected and you’re type O, you’re less likely to get that interaction with the endothelium binding
28
Q

How do you diagnose malaria?

A
  • Clinical symptoms plus appropriate history (travel, contact with infected blood)
  • Identification of plasmodia in red cells on regularly stained blood smear (gold standard)
  • Rapid immunochromatographic tests sometimes used (quicker but less accurate)
29
Q

What do you see in a slide of P. falciparum?

A

TONS of ring forms

30
Q

What species could cause relapse? Where are they latent?

A

P. vivax and P. ovale - Latent forms in the liver!

31
Q

Where does primaquine work?

A
  • Axoalytic phase - ‘radical cure’ that treats and wipes out latent forms in the liver!
  • Used after initial drugs!
32
Q

In what species does resistance readily occur?

A

Vivax and Falciparum

33
Q

Most deaths from sever mail occur. . .

A

. . .within the first 24-48 hours.

-Need parenteral therapy and drugs that act quickly

IHO Block 3 (13 decks)

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