Flashcards in Malaria Deck (32)
There are many risk factors for getting Malaria. Which ones double your chances of getting Malaria?
- Missing ANY prophylaxis
- Not using bed nets regularly
- Junior enlisted rank
- Failure to keep sleeves down
- Guard duty along river more than 7 nights
Who is at risk for getting severe disease if they contract Malaria?
- Non-immune individuals (yea no shit)
- Children under 5 years old
- pregnant women
- asplenic patients
Why was Malaria referred to as the hidden plasmodia in the 1930s and 40s?
The fact that after infection of volunteers with mosquitoes, the sporozoites circulated free for only about half an hour, and then vanished for several days (based on classic experiments by Fairley in Australia)
Shortt and Garnham solved this in 1948: infected monkeys with P. cynomolgi, did thorough autopsies a few days later, and found parasites in liver cells
Discuss the forms of Malaria once it is in you.
Merozoites infect RBCs where they form ring-stage trophozoites .
(these mature into schizonts which rupture and release merozoites, which infect more RBCs)
What is a hypnozoite?
Dormant liver stage in P. vivax and P. ovale
Release blood stage parasites weeks to months after primary infection
How long after infection does one develop symptoms?
P. falciparum: 8-11 days
P. ovale: 10-17 days
P. vivax: 10-17 days
P. malariae: 18-40 days
What determines the time between infection and onset of symptoms
Onset of symptoms coincides with the start of the erythrocytic cycle.
P. ovale and P. vivax, if untreated, will cause repeated bouts of fever due to eruption of hypnozoites from hepatocytes
incubation period with P. malariae can be up to 20 years (due to chronic, subclinical erythrocytic stage)
One way some people have evolved against malaria is to become Duffy Antigen negative.
The fuck is Duffy antigen, and which malaria uses this
Duffy antigen/chemokine receptor (DARC), also known as Fy glycoprotein (FY) or CD234 (Cluster of Differentiation 234), is a protein that in humans is encoded by the DARC gene. The Duffy antigen is located on the surface of red blood cells, and is named after the patient in which it was discovered.
P. vivax uses Duffy Ag to enter RBCs
What trait helps us not get Malaria and why
Sickle cell trait (increases survival during P. falciparum infection, perhaps by selective sickling of infected RBCs)
G6PD deficiency is bad. How does it help though with malaria?
malaria parasites grow poorly in G6PD deficient RBCs, perhaps b/c this results in an overall increase in reactive oxygen species in RBCs
How do symptoms for Malaria begin?
RARELY does it cause sore throat, lymphadenopathy, or rash
What signs on exam will we see for Malaria?
1/3 of patients will have a temp greater than 39 degrees and 1/4 of patients will have splenomegaly
Typical lab values for Malaria
Platelets down, Hgb down.
Classic presentation of uncomplicated (mild) malaria
1. cold stage with shaking
2. hot stage with high temperature (>104°F)
3. sweating stage with resolution of fever
episodes last 6-10 hours, and then recur:
- every 2 days with P. vivax and P. ovale (tertian fever) and for P. falciparum (malignant tertian fever)
- every 3 days with P. malariae (quartan fever)
Which strand gives us complicated malaria and how does it present?
• Cerebral malaria (change in mental status, coma)
• Respiratory distress
• Severe anemia (hct 2%
Two most important prognostic factors for a patient with malaria
Degree of acidosis and degree of parasitemia
Why is falciparum so bad?
Can grow and replicate in RBCs of ANY age, not just mature ones. So there is NO limit to the amount of parasitemia
Wait, why do we get hypoxia and lactic acidosis with malaria?
Erythrocytes containing mature P. falcip. parasites develop “knobs” and express adhesion molecules that bind to endothelial cells of capillaries and post-capillary venules.
Additionally, there is decreased deformability of infected AND non-infected RBCs, contributing to sludging, rosetting, aggregation, and eventual blockage of blood vessels.
This causes tissue hypoxia and organ failure.
What defines cerebral malaria?
acute encephalopathy not attributable to other causes in a patient with malaria
- decreased consciousness
cerebral malaria is driven by sequestered RBC in brain blood vessels
What are the outcomes of cerebral malaria
mortality: 100% without Rx, 20% with Rx
gross neurologic sequelae in 10% of survivors
-->2/3 of neurologic sequelae in children occur in large vessel distributions (ex. hemiplegia)…a bit of a mystery.
What 4 hypotheses outline the drive of Cerebral Malaria symptoms
venous obstruction hypothesis
- Sequestered RBCs in post-capillary venules cause vascular obstruction leading to vascular congestion
inflammation and vasogenic edema hypothesis
- Malaria toxin (probably glycophosphoinositol) activates monocytes to secrete proinflammatory cytokines such as IL-1, IL-6, M-CSF, and TNF, disrupting blood-brain barrier
cytotoxic edema hypothesis
- Impaired perfusion causes metabolic injury & cell death, disrupting BBB.
hemostasis dysfunction hypothesis
- Coagulation dysfunction contributes to pathology.
How good is Antigen capture for diagnosing Malaria?
BINAX Now malaria card test (tests for malaria antigens)
- approved by FDA in 2007
- sensitivity 95%
P vivax and ovale have two histological features of smear. What are they?
-enlarged infected cells
P Malriae has two histological features all to itself, what are they?
- Band forms
- Owl eye trophozoite
Smaller infected cells with yellow brown pigment
P Falciparum has special feature on histology, you guessed it, two in particular. What do they look like?
- Multiple ring-shaped trophozoites
- Banana shaped gametocyte
How do we prevent Malaria?
Personal protection measures
- Chloroquine (in chloroquine-sensitive areas)
What antimalarials can we use to treat someone who now has Malaria?
- artemesin compounds
- quinoline derivatives (incl. quinine, chloroquine, mefloquine, and primaquine)
- antifolates (incl. proguanil and pyrimethamine/sulfadoxine)
- other (incl. tetracycline, atovaquone/proguanil)
Something to consider when treating patients with P vivax or P. ovale
Patients with P. vivax and P. ovale should receive therapy (primaquine) to eradicate any remaining hypnozoites after treatment for intraerythrocytic stage.
When do we shift to IV therapy in those with Malaria?
In the presence of depressed sensorium, vomiting, organ dysfunction or parasitemia more than 5%, intravenous therapy should be used