Malaria Module - Krafts/Regal Flashcards
Where is malaria most prevalent?
Africa, Asia, Latin America
(90% of deaths occur in sub-Saharan Africa)
How many cases of malaria occur in the USA each year?
1500
(mostly from blood transfusions, few from mosquito bites)
How many people total die from malaria each year?
655,000 die each year
(one child dies from malaria each minute in Africa)
What organism is a vector for malaria?
- Anopheles mosquito (not native to U.S.) carries Plasmodia (only female bites humans)
- Culex = what we have in the U.S. (harmless)
What is the causative agent of malaria?
-
Plasmodium
- protozoan parasite
- infectious in the blood!
What are the different species of Plasmodium?
Remember:
- most common = P. vivax, P. falciparum
- most deadly = P. falciparum
- relapses = P. vivax and P. ovale
What species of Plasmodium has a low parasite burden, “rosette” arrangement of merozoites, and causes mild anemia?
P. malariae
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?
P. vivax and P. ovale
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?
P. falciparum
What is the life cycle of Plasmodium falciparum?
- 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
What are the morphologic features of P. falciparum?
- can have lots of ring forms within a single cell
- gametocytes are crescent/banana-shaped
How does P. falciparum affect RBCs and blood flow?
- 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
What is the main cause of death in children with malaria?
cerebral ischemia
P. falciparum stimulates high production of what cytokines? What is the result?
- TNF
- INF-Υ
- IL-1
***Suppresses RBC production, cause fever, tissue damage, and RBC binding to endothelium
What is the incubation period for malaria?
1-2 weeks
What is the malaria prodrome?
flu-like illness
What happens in a patient with infected with malaria?
- 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
What are the episodic Paroxysms of malaria infections?
- 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
What are the two types of host resistance to malaria?
-
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)
How do you diagnose malaria?
- 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
What is the best treatment plan for malaria?
- 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
What are important considerations to make when treating malaria?
- 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
- Severity of the DZ and necessity to achieve therapeutic levels quickly
What is the “radical cure” for malaria?
only drug to act in exoerythrocytic stage
What are the two types of Plasmodium infection result in latent forms in the liver? Tx?
P. vivax and P. ovale
Primaquine: eradicates hypnozoite forms dormant in liver
