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89 Cards in this Set
- Front
- Back
Malaria is caused by members of the genus ____ |
Plasmodium |
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The Plasmodium spp. belong to Phylum ____ |
Apicomplexa |
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The Plasmodium spp. are (metozoa or protozoa?) |
Protozoa |
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What is the definitive host of the Plasmodium spp.? |
Female Anopheles mosquitos |
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How many people are infected with malaria each year? How many die? |
300,000,000
1-2 million deaths |
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Where do 90% of malaria-related deaths occur? |
Sub-saharan Africa |
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Where is malaria endemic? |
Tropical and temperate regions of the world |
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How do US citizens acquire malaria? |
Travel to endemic areas |
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How many vertebrate hosts does each Plasmodium spp. have? |
One (human, mouse, etc.) |
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Which Plasmodium spp. cause malaria in humans? |
P. falciparum
P. vivax
P. ovale
P. malariae |
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Why is malaria only transmitted by female Anopheles mosquitos? |
Male Anopheles mosquitos feed on nectar, not blood |
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Why must female Anopheles mosquitos feed on blood? |
Nourishment of eggs |
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How many times will a female Anopheles mosquito lay eggs in its lifetime? |
4-5 clutches, each requiring a bloodmeal |
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Where do female Anopheles mosquitos lay their eggs? |
Stagnant water (discarded tires, puddles, ponds) |
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Describe the malaria life cycle |
1) Mosquito bite releases sporozoites into the bloodstream
2) Sporozoites invade hepatocytes and undergo several cycles of replication
3) Merozoites are released into the bloodstream, where they invade RBCs
4) Once inside RBCs, merozoites develop from the "ring stage" to the trophozoite stage
5) Trophozoites undergo schizogency, resulting in the release of merozoites that attack fresh RBCs
6) Some merozoites become gametes, which remain in RBCs and are taken up by mosquitos during a bloodmeal
7) In the mosquito, the male gamete exflagellates and fertilizes the female gamete, forming the ookinete
8) Ookinetes traverse the midgut wall and develop into oocysts
8) After 10-14 days of maturation, oocysts release sporozoites into the hemolymph
9) Sporozoites travel to the salivary gland to infect the next host during a subsequent bloodmeal |
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Which stage of Plasmodia asexual reproduction (exraerythrocytic or erythrocytic) is symptomatic in humans? |
Erythrocytic |
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What is the classical method for detecting the erythrocytic stages of malaria? |
Blood smear |
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What kind of stain is used for a malaria blood smear? |
Giemsa stain |
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Detection of erythrocytic stages of malaria in the blood is indicative of (active or inactive?) infection |
Active |
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Appropriate treatment of malaria requires... |
1) Identification of the species causing the infection (co-infections are possible)
2) Patient history (travel to endemic regions)
3) Knowledge of the drug sensitivity/resistance profile |
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The pre-patent period of a malarial infection is the time between... |
Time of infection (bite of an infected mosquito) to when the erythrocytic cycle commences |
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What is the basic symptom of erythrocytic malaria? |
High fever (40-41°C) with a defined periodicity |
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Tertian malaria (Definition) |
Malaria characterized by a fever with 48 hour periodicity (fever on days 1, 3, 5, etc.) |
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Quartran malaria (Definition) |
Malaria characterized by a fever with 72 hour periodicity (fever on days 1, 4, 7, etc.) |
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What is the relationship between the number of merozoites released from the liver and severity of disease? |
The higher the number of merozoites, the more severe the disease |
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Number of merozoites released per hepatocytes for each of the four Plasmodium spp. |
P. falciparum: 40,000/cell (5-7 days)
P. vivax: 10,000/cell (6-8 days)
P. ovale: 15,000/cell (9 days)
P. malariae: 2,000/cell (2 weeks) |
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What are the steps involved in the erythrocytic cycle of malaria? |
1) Invasion of the RBC
2) Ring stage
3) Early trophozoite
4) Mature trophozoite (accumulation of Malaria Pigment in the food vacuole)
5) Schizogeny (early shizont, schizont, mature schizont, release of merozoites)
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From where within RBCs do malarial trophozoites derive the bulk of nutrients required for growth? |
Hemoglobin |
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How do malarial trophozoites degrade hemoglobin? |
Endocytosis into the parasite food vacuole |
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What is the toxic end-product of hemoglobin degradation by malaria trophozoites? |
Heme |
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How do malarial trophozoites detoxify free heme? |
Polymerization of heme into hemozoin (Malarial Pigment) |
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Besides the degradation of hemoglobin, how else do Plasmodia modify erythrocytes? |
Membranous projections into the cytosol (Maurer's clefts, tubular vesicular network or TVN)
Surface projections called "knobs"
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What is the function of the knobs on the surface of infected erythrocytes? |
They provide erythrocytes with adhesive properties to bind endothelial cells and other RBCs (rosetting) |
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Which Plasmodium spp. is responsible for the vast majority of deaths due to malaria? |
Plasmodium falciparum |
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What is the geographic distribution of P. falciparum? |
Africa
South Asia
South east Asia
Brazil |
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F. falciparum causes what type of malaria? |
Severe malaria, Malaria Tropica, malignant tertian malaria |
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Incubation, pre-patent, and patent periods of P. falciparum |
Incubation: 8-24 days
Pre-patent: 4-12 days
Patent: 4-6 weeks if treated, 18 months if untreated |
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Relapses of P. falciparum are due mainly to organisms in the (extraerythrocytic or erythrocytic) stage |
Erythrocytic |
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P. falciparum is a (tertian or quartran) malaria |
Tertian, but it does not always follow this periodicity |
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Symptoms of P. falciparum malaria |
High fever that may follow a tertian pattern but may also be continuous
A phase of headache and general abdominal symptoms |
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P. falciparum malaria may progress to... |
Cerebral malaria |
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Why is it important to begin treatment for cerebral malaria immediately after the onset of symptoms? |
Coma and death can occur within 24 hours of the onset of symptoms |
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How is P. falciparum malaria diagnosed? |
Blood smear |
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Which erythrocytes are infected by P. falciparum? |
Mature erythrocytes |
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What is the typical parasite burden (parasitemia) in P. falciparum malaria? |
50-500,000 parasites/mL blood
Can be as high as 2.5 million/mL |
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Why is the parasite burden (parasitemia) in P. falciparum malaria so high? |
P. falciparum infects mature erythrocytes, which is the most abundant group |
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How does P. falciparum cause cerebral malaria? |
Infected RBCs have adhesive knobs that make them stick to the endothelial lining of blood vessels, which limits blood flow to the brain |
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Which knob protein is responsible for the adhesion of RBCs in P. falciparum malaria? |
P. falciparum Erythrocyte Membrane Protein 1 (PfEMP-1) a.k.a the Var family |
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How does P. falciparum avoid immune detection? |
Var proteins exhibit antigenic variation |
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How might P. falciparum affect pregnancy? |
Adhesive IE (infected erythrocytes) may block placental circulation to the fetus, leading to fetal anoxia, fetal and placental edema, and abortion after the first trimester
Often premature delivery, low birth weight, and anemia in the fetus |
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Does P. falciparum cross the placental barrier? |
No |
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When is the risk for P. falciparum-related complications during pregnancy the greatest? |
First pregnancy (and reduces with subsequent pregnancies) |
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How might P. falciparum infection affect the kidneys? |
Adhesive IE (infected erythrocytes) may occlude the renal tubules, resulting in dark-colored urine, hemoglobinuria, acute renal failure, and mortality (20-30% of cases) |
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What is the name for the renal complications that rarely accompany P. falciparum infection? |
Blackwater fever |
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What is the most commonly encountered form of malaria? |
Malaria caused by Plasmodium vivax |
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P. vivax causes what type of malaria? |
Malaria tertiana, benign tertian malaria |
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Geographic distribution of P. vivax |
South and south east Asia
Africa
The New World (was endemic in parts of the US, including KY, in the 19th century) |
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Is P. vivax usually fatal? |
No |
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Describe the fever pattern of P. vivax malaria |
Highly regular tertian pattern preceded by several hours of intense shivering |
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Incubation, pre-patent, and patent periods of P. vivax |
Incubation: 12-18 dyas
Pre-patent: 8-17 days
Patent: 5-7 years |
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P. vivax has (high or low?) potential for reactivation. Why? |
High
Long patent period |
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Reactivation of P. vivax malaria is due mainly to (RBC or liver?) stages of the parasite |
Liver (hypnozoites) |
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What is the typical parasite burden (parasitemia) in P. vivax malaria? |
20,000 parsites/mL of blood
Maximum of ~50,000/mL |
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Why is the parasite burden (parasitemia) of P. vivax so much lower than that of P. falciparum? |
P. vivax preferentially infects young (reticulo-endothelial) erythrocytes, which are fewer in the number than the mature erythrocytes infected by P. falciparum |
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What are some distinctive features of P. vivax erythrocytes? |
Enlarged erythrocyte
Schuffner's dots
Mature-ring form appears coarse |
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What is the rarest form of malaria? |
Malaria caused by P. ovale |
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What type of malaria is caused by P. ovale? |
Malria tertiana (same as P. vivax) |
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What is the mildest form of malaria? |
Malaria quartana, caused by Plasmodium malariae |
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Describe the characteristic fever caused by P. malariae infection |
Quartan pattern
Preceded by intense shivers |
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P. malariae preferentially infects ____ erythrocytes |
Old |
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P. malariae has an extremely (long or short?) patent period |
Long (up to 30 years) |
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Quartan malaria is often seen in what group of US patients? |
Vietnam vets |
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What challenges complicate malaria treatment/prevention? |
Increasing drug resistance (including multiple drug resistance)
Antigenic variation of Var and other immunogenic proteins complicate vaccine development
Vector control (mosquito resistance, environmental concerns)
Political and socioeconomic issues (poverty, civil war/political instability) |
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What genetic disease co-maps with malaria? Why? |
Sickle cell trait (heterozygotes)
Plasmodia cannot grow in sickle cell RBCs, which greatly reduces the severity of malaria |
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The Babesia spp. belong to Phylum ____ |
Apicomplexa |
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What is the definitive host/vector of the Babesia spp.? |
Ixodes spp. ticks (same vector as Lyme disease) |
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What is the intermediate host of the Babesia spp.? |
Mammals, including humans |
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Where do Babesia replicate within humans? |
Within erythroctes |
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Do Babesia have a liver stage in humans? |
No |
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How do Babesia reproduce in humans? |
Binary fission |
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Do Babesia degrade hemoglobin and produce hemozin? |
No |
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Most Babesia infections in the US are caused by what species? |
Babesia microti |
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Most Babesia infections are (symptomatic or asymptomatic?) |
Asymptomatic |
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When are symptoms typically seen with Babesia infection? |
Heavy infections
Infection of the immunocompromised
Infections in the aged (weaker immune response) |
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Babesia infection is typically fatal in ____ individuals |
Splenomectomised |
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When are Babesia infections most commonly seen? Why? |
Between May and September
Coincides with tick biting behavior |
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Main symptoms of babesiosis |
Continuous fever
Malaise
Abdominal symptoms
Flu-like symptoms |
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Incubation period, pre-patent period, and patent period of Babesia microti |
Incubation: 1-4 weeks
Pre-patent: 1 week
Patent: 1 year |
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How is babesiosis diagnosed? |
Giemsa stain of blood smear |