Malaria Flashcards

1
Q

Plasmodium parasite

A
  • lives in RBCs

- anopheles mosquito

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2
Q

Lifecycles

A
  • asexual in human host
  • sexual in moquito
  • cell replication of merozoites by schizogony
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3
Q

Signs and Symptoms

A

-incubation period of 7-30 days following bite
-fever, headache, chillls, vomiting
-

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4
Q

Geographical distribution

A

Half the worlds pop. at risk of malaria

-most malarial deaths occur in sub-saharan Africa (1 in 5 child deaths due to malaria)

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5
Q

Treatment for malaria

A
  • no vaccine
  • artemisinin-based combat therapy (ACT) is best treatment at present
  • vector control -bed nets/insecticide
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6
Q

Cerebral malaria

A
  • plasmodium falciparum (tertian peaks 48h)
  • not persistent in liver
  • sequestration of infected RBCs in brain
  • coma
  • death
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7
Q

ILO = the life-cycle of the malaria parasite (Plasmodium species), its vectors, the disease and its characteristic symptoms, the various approaches to control of the infection and its transmission, problems with vaccine development;

A

the life-cycle of the malaria parasite (Plasmodium species), its vectors, the disease and its characteristic symptoms, the various approaches to control of the infection and its transmission, problems with vaccine development;

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8
Q

Stages of growth

A
  • ring stage - early stage of infection
  • trophozoite (growing stage)
  • merozoite (multiplication)
  • gametocytes
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9
Q

Lifecycle- human

A
  • Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . -parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). -Merozoites infect red blood cells . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites
  • Some parasites differentiate into sexual erythrocytic stages (gametocytes)
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10
Q

Life-cycle mosquito

A
  • The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal
  • parasites’ multiplication in the mosquito is known as the sporogonic cycle
  • While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes
  • zygotes in turn become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts
  • oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. -Inoculation of the sporozoites into a new human host
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11
Q

Antigenic variation in P.falciparum

A

-rate of change -1-2% per division
VAR genes - red cell surface - double function - variant antigen for immune evasion and adhesion to endothelial cells of capillaries
-VAR genes –> Pfemp 1 family of proteins inserted into surface of RBCs
-brain and placenta - most Pfemp1 proteins are specific for adhesion to brain endotheliea, one or two specific for placenta
-The Pfemp1 antigens that bind to placenta are immunologically cross-reactive hence only first pregnancy is threatened

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12
Q

Genetic resistance to malaria

A
  • mutation in haemoglobin genes
  • sickle cell anaemia (single nucleotide polymorphism (A to T) of the B-globin gene, –> glutamic acid (E/Glu) being substituted by valine (V/Val) at position 6)
  • heterozygote advantage
  • blood groups - duffy antigen
  • HLA class I alleles (the MHC)
  • interleukin-4
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13
Q

Duffy blood group

A

-duffy negative and resistance to vivax malaria

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14
Q

Malaria and the placenta

A
  • infected RBCs can sequester in the venules of the placenta and brain resulting in stillbirth
  • reduced diameter of foetus head
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15
Q

Anti malarial drugs

A
  • quinine (tree bark cinchona)
  • chloroquine
  • proguanil
  • mefloquine
  • artemesinin (kills ring stage - before merozoites sequester in the brain)
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16
Q

Resistance

A
  • to insecticides

- to drugs

17
Q

Vaccine against P.falciparum

A
  • RH5 protein attaches to receptor (basigin) and allows parasite to invade cell
  • antibody raised to RH5