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Flashcards in Malaria Deck (18):

Malaria life cycle

-Due to plasmodium sp
-2 phases: asexual (in humans-intermediate host) and sexual (in female anopheles mosquito- definitive host)
-Overview: mosquito salivary gland-> blood-> liver (replication)-> RBCs (replication)-> mosquito
-Human (asexual, schizogeny) phase broken up to exoerythrocytic (liver) and erythrocytic (RBC)



-Sporozoites enter blood and infect hepatocytes
-After replication (days-months), merozoites are released from hepatocytes
-Some malaria (only P vivax or P ovale) remains in hepatocyte, must be treated w/ primaquine to destroy and prevent relapse



-Merozoites (released from liver) infect RBCs and develop into trophozoites inside cell
-They will either mature into a schizont (which bursts to release many merozoites which then infect more RBCs), or mature into a gametocyte and be picked up by a mosquito


Alteration of host cells

-Shape and deformability of RBC
-Protrusion and knobs
-Expression of new surface molecules
-Adherence to normal RBCs and endothelial cells


Sexual phase

-In the female anopheles mosquito
-Female picks up gametocytes of both sexes
-The two gametocytes in the mosquito meet in the gut and sexually reproduce into ookinete, which invades gut epithelial cell
-Ookinete matures into Oocyst, which moves to mosquito salivary gland
-Oocyst ruptures and releases sporozoites, which are ready to infect a new human upon mosquito bite


Symptoms of malaria

-Non-specific: headache, fatigue, abdominal pain, myalgia, arthralgia, fever, chills, anorexia, nausea
-Classical paroxysmal fevers (intermittent, appear and disappear quickly): due to all organisms in RBCs lysing the cells at the same time every 48 hrs (not always regular)
-Lab findings: anemia, normal WBC, thrombocytopenia, elevated ACR protein, elevated bili and hepatic nzs


Pathogenesis of malaria

-RBC lysis, destruction by spleen, erythropoiesis suppression all lead to anemia
-Release of TNFa and IL1 by macrophages in response to glycosyl phosphatidylinositol, leading to fever, hypoglycemia, microvascular obstruction, and hypoxia


Resistance to malaria

-People who have abnormal RBCs or Hb sometimes have a selective advantage against malaria
-These include: SCD, thalassemia, G6PD deficiency, distribution of various RBC surface molecules (glycophorin, duffy Ag)
-These phenotypes are seen in higher prevalence in the malaria belt


Types of Plasmodium sp

-Plasmodium falciparum
-plasmodium vivax/ovale (these two are very similar)
-plasmodium malariae
-plasmodium knowleski
-Most important are the falciparum, vivax, and ovale
-Stable transmission: high rate of exposure (>10 inoculation/yr)
-Unstable transmission: rate of inoculation fluctuates over seasons and years (slows acquisition of immunity)


Plasmodium vivax/ovale

-Both found world wide, but ovale more in sub-saharan Africa and P vivax in other areas
-Rarely cause serious illness, resistance to drugs uncommon
-Likelihood of recurrence even if patient receives cholorquine (due to hypnozoites remaining dormant in hepatocytes)
-Frequency of paroxysms: tertian


Dx of malaria

-Light microscopy of blood smears (thick and thin)
-Thick smears tell you if the patient has malaria (look for ring-form and mature trophozoites, schizonts, gametocytes)
-Thin smears tell you what kind of malaria it is
-Can also do fluorescent microscopy, rapid diagnostic test (RDT, but these are vulnerable to high temp and humidity as they require fresh Abs on test strips)


Plasmodium falciparum

-Infects erythrocytes of all ages, leads to high parasite burden
-Able to sequester in the deep venous microvasculature, avoiding destruction by spleen
-Binds to endothelium w/ P falciparum erythrocyte membrane protein1 (PfEMP1)
-Found all over the world (worst type)
-Complications: cerebral malaria, severe anemia, respiratory failure, renal failure, hypoglycemia
-Causes acute distress then resolves, no recurrence w/out reinfection
-Drug resistance major problem
-Frequency of paroxysm: quartan


Cell interactions in P falciparum malaria

-Opsonization and phagocytosis of infected RBCs
-Soluble Ag-immune complexes lead to anemia, vasculitis, nephritis, splenomegaly
Immune cell responses: CD8, CD4, plasma/B cells (IgG, IgM)
-There is both innate (lack of adhesion receptor) and acquired (due to past exposure, Ab to PfEMP1) immunity to plasmodium, but acquired must be maintained by repeated exposure or it will be lost


Lab blood work findings

-Normal WBC
-Elevated acute phase proteins
-Elevated bili, liver nzs


Severe malaria

-Only caused by P falciparum
-Impaired consciousness, coma, seizures
-Due to cerebral malaria (lack of circulation in brain due to adherence of RBCs), hyperparasitemia


Dx and Rx

-In high transmission areas, confirmatory Dx is not required to begin Rx
-Rx for plasmodium except falciparum: chloroquine for 3 days, plus primaquine for 14 days (for vivax/ovale, to kill dormant organisms in liver)
-Primaquine is contraindicated in G6PD patients
-For all Rx: make sure it is not counterfeit


Rx for falciparum

-Due to drug resistance, and the fact that it can bind endothelial cells, falciparum requires special Rx
-Requires mixed Rx of Artemisinin-based plus lumefantrine Rx for 3 days, with daily blood draws during those 3 days to check for level of parasite
-Can also use atovoquone-proguanil (malarone)


Prevention and prophylaxis

-Prevention: mosquito nets, vaccine development
-Prophylaxis: mefloquine (can cause tremors, psychosis, depression, bad dreams), atovoquone-proguanil (malarone)