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61 Cards in this Set
- Front
- Back
T/F: the parasites that cause malaria are all intracellular protozoa
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True.
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Definitive host of Plasmodium
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Anopheles mosquito
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Life cycle of malaria parasites
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Mosquito injects SPOROZOITES into human --> sporozoites enter liver parenchyma and become MEROZOITES --> merozoites are released into circulation and infect red blood cells --> replication of merozoites within rbc's: RING STAGE --> cytoplasm synthesis --> nuclear replication --> cytoplasm division --> rbc lyses and releases metrozoites --> metrozoites differentiate into GAMETOCYTES --> gametocyte is taken up by mosquito --> gametocyte becomes GAMETES in the mosquito --> male (flagellated) and female gametes form zygote which produces SPOROZOITES that migrate to salivary gland
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Origin, target and progeny of sporozoite
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Comes from mosquito, infects liver cells, and progeny becomes merozoites
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Origin, target and progeny of merozoites
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Comes from liver cells or red cells, infects other red cells, and progeny is merozoites or gametocytes
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Origin, target and progeny of gametocytes
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Comes from red cells, infects mosquito, and progeny becomes sporozoites (following a number of intermediate stages, including gamete and zygote)
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This is the asymptomatic stage of Plasmodium infection
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Liver stage; sporozoites enter parenchymal cells of the liver. Asymptomatic bc one sporozoite infects just one hepatocyte.
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This is the symptomatic stage of Plasmodium infection
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Erythrocytic stage; merozoites enter red cells
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First stage that Plasmodium merozoite enters when it infects a red cell
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Ring stage
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This stage in the Plasmodium life cycle synthesizes a large volume of cytoplasm but remains uninuclear
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Ring stage as it undergoes cytoplasm synthesis
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When do we see multinucleate red cells?
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In plasmodium infection (merozoite in red cell), when cytoplasm synthesis is complete and multiple replications of the nucleus takes place
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How do merozoites replicate in red cells?
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First they enter a red cell, then enter a ring stage that synthesizes the cytoplasm of the future merozoites, then replicates its nuclei which will become the nuclei of the future metrozoites. Basically a soup of cytoplasm and nuclei is made, and these then divide off to become new metrozoites.
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Diagnostic stage of Plasmodium
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Erythrocytic forms observed in blood smears.
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Incubation period of malaria
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Typically 10-40 days. Up to 6-12 months in P. vivax. Up to years or decades in P. malariae (chronic asymptomatic erythrocytic phase).
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This disease is often misdiagnosed as influenza in non-endemic regions
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Malaria
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This disease causes anemia due to red blood cell destruction
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Malaria
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In the setting of chronic reinfection, this disease can result in splenomegaly
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Malaria
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Prodromal symptoms of malaria
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Headache, anorexia, fever, joint pain
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Symptoms of primary attack of malaria
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1 hour of shaking chills followed by a longer hot stage with headache and n/v. The cycle ends with a heavy sweat, which recurs with characteristic periodicity as blood stages become synchronized
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Why don't travelers with malaria present with characteristic periodic fevers?
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Because synchronous growth in the blood stage has not yet been established
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This species of malaria produces the most serious disease
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Plasmodium falciparum
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Incubation period of P. falciparum
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~2 weeks
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This species of Plasmodium infects red cells of all ages
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Plasmodium falciparum
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This species of Plasmodium preferentially infects reticulocyte (young red cells)
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Plasmodium vivax
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This species of Plasmodium preferentially infects ages red cells
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Plasmodium malariae
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Infection by this Plasmodium results in fever spikes every second day, then subsides in 3 weeks to low parasitemia; relapse with lower parasitemia may take place over next few months
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Plasmodium falciparum
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Microinfarcts are seen in infection with this parasite
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Plasmodium falciparum. Specific parasite proteins form "knobs" on the infected red cell membrane, binding endothelial cells and blocking capillaries.
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This parasite can cause cerebral disease (HA, coma, paralysis, death), intestinal hemorrhage, or tubular necrosis
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Plasmodium falciparum
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This species of malaria has no mechanism for relapse or delayed disease, thus it cannot survive mosquito-less winters of temperate zones.
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Plasmodium falciparum
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Diagnostic features of P. falciparum
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Only early forms (ring stages); later forms are not seen in peripheral blood because the knobs cause trapping in small vessels. Banana-shaped gametocytes.
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Banana-shaped gametocytes are pathognomonic for infection with this
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Plasmodium falciparum
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Alternative pathways for infection by malaria parasites
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Blood transfusion; perinatal, transplacental (rare)
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These parasites cause fever that spikes every second day
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P. falciparum, P. vivax
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T/F: all malaria can present with anemia
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True (due to rbc destruction)
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Hypnozoite
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Dormant stage of P. vivax
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This is the most common malaria of temperate zones
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P. vivax
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Schuffner's dots
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Prominent in late-stage infected cells of P. vivax; dots in other species of malaria are smaller and less distinct
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This is the most important feature of P. vivax on blood smear
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Schuffner's dots
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This parasite causes fever that spikes every third day
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P. malariae
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Incubation period of P. malariae
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(Longer than others) 5 weeks
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This malaria parasite can cause persistent infection decades-long (10-30 years)
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P. malariae
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This is a distinguishing feature of P. malariae on blood smear
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Band forms
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This is the most important feature of P. malariae on blood smear
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Yellow-brown malarial pigment
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This malaria parasite causes the lowest parasitemia
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P. malariae (just 6,000; vs. 300,000 and 20,000 in P. falciparum and P. vivax, respectively)
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Time before relapse for P. falciparum, vivax and malariae
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Weeks (f), months (v), years (m)
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This malaria parasite has the highest rates of resistance--chloroquine is useless against it
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Plasmodium falciparum
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This drug is used to eradicate the hypnozoite of P. vivax
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Primaquine
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This drug cannot be used in patients with a G-6-P dehydrogenase deficiency
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Primaquine
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T/F: malaria is a self-limiting disease
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True. Immunity is slow to arise, and requires repeat infections, but it is a self-limiting disease
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This is a non-malaria erythrocytic infection
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Babesiosis (Babesia microti)
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This disease has an endemic focus on Nantucket Island and elsewhere in the coastal northeast US
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Babesiosis (Babesia microti)
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This parasite can be mistaken for malaria on blood films because it has a similar ring stage
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Babesia
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These diseases are transmitted by dear ticks
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Lyme disease, Babesiosis
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Definitive host of Babesia
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Tick
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Infective stage of Babesia
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Parasites in salivary glands of tick
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Diagnostic stage of Babesia
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Trophozoites in stained blood film
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This parasite appears as tetrads of parasites in cross configurations on blood film
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Babesia
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Asplenia, old age and immunosuppression is a risk factor for this otherwise subclinical disease
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Babesiosis (Babesia microti)
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Symptoms of Babesiosis
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Hemolytic anemia, fevers, chills; severe complications are very rare
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This is why it is important to distinguish between Babesiosis and Malaria
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Chemotherapy differs. Babesiosis is also a less severe disease, whereas malaria can quickly progress to coma and death.
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5-20% of New Englanders are seropositive for this
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Babesiosis (Babesia microti)
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