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IHO Week 3 - WLB > Malaria Module - Krafts/Regal > Flashcards

Malaria Module - Krafts/Regal Flashcards

1
Q

Where is malaria most prevalent?

A

Africa, Asia, Latin America

(90% of deaths occur in sub-Saharan Africa)

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2
Q

How many cases of malaria occur in the USA each year?

A

1500

(mostly from blood transfusions, few from mosquito bites)

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3
Q

How many people total die from malaria each year?

A

655,000 die each year

(one child dies from malaria each minute in Africa)

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4
Q

What organism is a vector for malaria?

A
  • Anopheles mosquito (not native to U.S.) carries Plasmodia (only female bites humans)
  • Culex = what we have in the U.S. (harmless)
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5
Q

What is the causative agent of malaria?

A
  • Plasmodium
    • protozoan parasite
    • infectious in the blood!
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6
Q

What are the different species of Plasmodium?

A

Remember:

  • most common = P. vivax, P. falciparum
  • most deadly = P. falciparum
  • relapses = P. vivax and P. ovale
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7
Q

What species of Plasmodium has a low parasite burden, “rosette” arrangement of merozoites, and causes mild anemia?

A

P. malariae

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8
Q

What species of Plasmodium has a low parasite burden, results in enlarged red cells/Schuffner’s dots, has potential for relapse, and causes mild anemia?

A

P. vivax and P. ovale

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9
Q

What species of Plasmodium has a high parasite burden, causes severe anemia, may lead to cerebral and multi-organ sx, and has a high fatality rate?

A

P. falciparum

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10
Q

What is the life cycle of Plasmodium falciparum?

A
  • sporozoite (infected stage) → goes to liver (min-hr) first
  • becomes schizont (divided into little babies) →
  • busts open liver cell→
  • releases merozoites into blood → infect RBCs
    • In RBC: ring form → trophozoite → schizont → releases merozoites
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11
Q

What are the morphologic features of P. falciparum?

A
  • can have lots of ring forms within a single cell
  • gametocytes are crescent/banana-shaped
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12
Q

How does P. falciparum affect RBCs and blood flow?

A
  • Able to infect red cells of any age
  • Blood flow is impeded
    • Forms “Rosettes” – RBC clump together around infected cell → can block blood flow in small vessels and brain
  • Abnormal binding to vascular endothelium (knobs on RBC membrane) → impedes blood flow
    • important in brain and in children
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13
Q

What is the main cause of death in children with malaria?

A

cerebral ischemia

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14
Q

P. falciparum stimulates high production of what cytokines? What is the result?

A
  • TNF
  • INF-Υ
  • IL-1

***Suppresses RBC production, cause fever, tissue damage, and RBC binding to endothelium

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15
Q

What is the incubation period for malaria?

A

1-2 weeks

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16
Q

What is the malaria prodrome?

A

flu-like illness

17
Q

What happens in a patient with infected 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
18
Q

What are the episodic Paroxysms of malaria infections?

A
  • fever/chills, sweating, myalgia
  • depends on species
    • *Quotidian (daily) = P. falciparum
    • Tertian (every 48 hrs) = P. vivax or ovale
    • Quartan (every 72 hrs) = P. malariae
19
Q

What are the two types of host resistance to malaria?

A
  • Inherited RBC alterations: hemoglobinopathies (sickle cell), thalassemias, G6PD deficiency
    • RBC antigens (ABO, Duffy) – blood type affects binding (O is least adhesive)
    • Doesn’t necessarily prevent infection, but you just won’t get as sick (RBC die off sooner)
  • Partial immune-mediated resistance: develops over time in patients in endemic areas
    • Reduces severity of disease (kids have it worse due to development of immune system)
    • P. falciparum uses antigenic variation – changes antigen just when you get used to it (PfEMP proteins that stick out of RBC, every generation 2% make new PfEMPs)
20
Q

How do you diagnose malaria?

A
  • Clinical sx + appropriate hx (travel, contact with infected blood)
  • Gold standard: identification of plasmodia in red cells on regularly-stained blood smear (tons of ring forms)
  • Rapid immunochromatographic tests sometimes used (quicker but less sensitive/specific) – can use in the field
21
Q

What is the best treatment plan for malaria?

A
  • Don’t get bit – netting & insect repellents; avoid mosquito areas & exposure during periods of high insect activity
  • Plan B:
    • Take advantage of drugs used for prophylaxis – if you are planning a trip to a malaria area, take prophylactic drugs
    • Treat active malaria with the appropriate drug, depending on resistance, etc.
    • Use the ‘radical cure’ if indicated
22
Q

What are important considerations to make when treating malaria?

A
  • Which area is visited? Resistance or not?
    • Places will be listed as chlorquine resistant or not (P. falciparum and P. vivax)
  • Previous use of antimalarials?
  • Severity of DZ?
    • dictates how aggressive the therapy will be (P. falciparum)
    • possibility of relapse (P. vivax and P. ovale)
  • What is the probability of persistent hepatic forms of the organism?
  • Clinical status of the disease? Uncomplicated disease?
    • Severity of the DZ and necessity to achieve therapeutic levels quickly
      • Most deaths from severe malaria occur within the first 24-48 hrs
23
Q

What is the “radical cure” for malaria?

A

only drug to act in exoerythrocytic stage

24
Q

What are the two types of Plasmodium infection result in latent forms in the liver? Tx?

A

P. vivax and P. ovale

Primaquine: eradicates hypnozoite forms dormant in liver

25
Q

How should you treat someone going into an area with malaria?

A
  • suppressive prophylaxis
    • lower doses, fewer side effects
  • If going to chloroquine-resistant area DON’T treat with chloroquine (DUH) BUT chloroquine is first line in all other areas
26
Q

What is the basis for selection of Chloroquine?

A
  • Selective accumulation by the parasite in erythrocytes
    • parasitized RBC concentrates Chloroquine at least 25xmore than unparasitized RBC
    • Chloroquine accumulates in the acid pH of the food vacuole
27
Q

What is the MOA for Chloroquine?

A
  • interferes with heme handling, disrupts sequestration of heme as hemozoin
    • Parasite digests host Hb within the acidic food vacuole of plasmodia → results in production of large amounts of ferriprotoporphyrin IX (FPIX) inside the food vacuole
      • FPIX is toxic to the parasite so the parasite uses heme polymerase to convert it to hemozoin
      • Chloroquine binds to FPIX and prevents its conversion to hemozoin
      • Either free FPIX or chloroquine bound to FPIX is toxic to the plasmodium
28
Q

What are the adverse side effects of Chloroquine?

A
  • Low dose suppressive therapy used in prophylaxis – no significant toxicity
  • Acute attack doses = dizziness, headache, itching, vomiting, skin rashes, difficulty in visual accommodation
  • Large doses for prolonged periods can cause severe eye damage and even blindness
  • Less toxicity than quinine and quinidine
29
Q

When should you use Quinine to treat malaria?

A
  • used in chloroquine resistant P. falciparum
    • more toxic than chloroquine but resistance has not readily developed
30
Q

What is the MOA of Quinine?

A

Unknown

(probably the same as chloroquine)

31
Q

What are the adverse side effects of Quinine?

A
  • acute attack doses
    • cinchonism – tinnitus, blurred vision, nausea, HA, decreased hearing acuity
  • Permanent damage to vision, balance and hearing can result
32
Q

When should you use Quinidine to treat malaria?

A

IV for severe malaria

33
Q

What is the MOA of Quinidine?

A
  • anti-arrhythmic drug that blocks Na+ and K+ currents
    • used to maintain sinus rhythm for atrial flutter/a fib & to prevent recurrence of ventricular tachycardia
34
Q

What are the adverse side effects of Quinidine?

A

cardiac problems – patients need cardiac monitoring

35
Q

When is Mefloquine indicated?

A
  • Only for the treatment and prevention of Chloroquine resistant P. falciparum
36
Q

What is the MOA of Mefloquine?

A

Unknown

(probably acts like chloroquine)

37
Q

What are the adverse side effects of Mefloquine?

A
  • sometimes nausea, vomiting, dizziness, visual or auditory disturbances
  • may cause disorientation, hallucinations and depression
    • due to possibility of neuropsychiatric rxns, chloroquine is preferred if resistance is not a problem
38
Q
A

IHO Week 3 - WLB (10 decks)

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