Parasitology & Malaria Flashcards

1
Q

Define parasite

A

An organism living in or on a host and dependent on the host for nutrition – causing damage

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2
Q

What are the two groups of endoparasites and what are the features of organisms within these two groups?

A
  • Protozoa
    • UNIcellular
    • Eukaryotes (membrane bound nucleus)
    • Some have insect vectors
    • No eosinophilia
  • Metazoa
    • MULTIcellular
    • They are helminths/worms
    • Free living, intermediate hosts and vectors
    • Cause eosinophilia if they invade the blood
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3
Q

What are the five types of plasmodium that cause malaria? List them from most common to least common

A
  • F MOV K*
  • Plasmodium falciparum
  • Plasmodium malariae
  • Plasmodium ovale
  • Plasmodium vivax
  • Plasmodium knowlesi
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4
Q

Discuss the asexual reproduction of P. falciparum

A

G-ZOO

Gametocyte –> Zygote –> Ookinete –> Oocyte

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5
Q

Outline the life cycle of P. falciparum is mosquitos

A

G-ZOOS

Gametocyte –> Zygote –> Ookinete –> Oocyte –> Sporozoite

  • Within a 15 day period, gametocytes sequester and develop within the bone marrow and, once mature, enter the peripheral circulation for ingestion by a mosquito where they emerge as extracellular male and female gametes in the midgut.
  • Mating occurs by fusion of micro- and macrogamete to form a zygote transforming over 24 hr into a ookinete that migrates through the mosquito midgut epithelium and encysts to become an oocyst where asexual sporogenic replication occur
  • Motile sporozoites are released into the hemocoel by oocyst rupture and pass into salivary glands where they can be injected into the next human host
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6
Q

Outline the life cycle of P. falciparum in the human

A

Sporozoites –> schizonts –> merosomes

Merozoite –> Gametocyte –> Zygote –> Ookinete –> Oocyte

  1. Malaria infection is initiated with the injection of sporozoites into the dermis by a feeding female anopheline mosquito.
  2. The sporozoites enter the vasculature and are transported to the liver, where they exit the sinusoids through Kupffer or endothelial cells and enter a hepatocyte.
  3. Active invasion is preceded by cellular traversal until a suitable hepatocyte is found.
  4. They form a parasitophorous vacuole membrane (PVM) and undergo exo-erthryocytic schizogony until tens of thousands of daughter merozoites are released in packets of merozoites into the vasculatur
  5. There they encounter erythrocytes and begin a chronic cycle of erthryoytic schizogony in the bloodstream.
    1. The merozoites that have infected the red blood cells and are feeding are known as trophozoites
      • These mature into schizonts
  6. A proportion of asexually reproducing merozoites are reprogrammed to undergo gametocytogenesis.
  7. Within a 15 day period, gametocytes sequester and develop within the bone marrow and, once mature, enter the peripheral circulation for ingestion by a mosquito where they emerge as extracellular male and female gametes in the midgut.
  8. Mating occurs by fusion of micro- and macrogamete to form a zygote transforming over 24 hr into a ookinete that migrates through the mosquito midgut epithelium and encysts to become an oocyst where asexual sporogenic replication occurs. Motile sporozoites are released into the hemocoel by oocyst rupture and pass into salivary glands where they can be injected into the next human host.
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7
Q

What are the two types of host for plasmodium?

A
  • Female anopheles mosquito
  • Humans
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8
Q

What are the two stages of malaria in humans?

A
  • Liver
  • Blood
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9
Q

Describe the symptoms of malaria.

A
  • Paroxysmal = sudden reoccurrence or intensification of symptoms
  • Occurs every 4-8 hours
  • Symptoms
    • Headaches
    • Vomiting
  • Fever
  • Chills
  • Muscle pain
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10
Q

State some complications of malaria.

A
  • Severe anaemia
    • due to intravascular haemolysis
  • Cerebral malaria
  • Kidney failure
  • Swelling and rupturing of the spleen
  • Liver failure
  • Shock
  • Pulmonary oedema
  • Abnormally low blood sugar
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11
Q

What are the treatments for uncomplicated malaria?

A
  • Chloroquine
    • Hemoglobin is composed of a protein unit (digested by the parasite) and a heme unit (not used by the parasite)
    • The parasite releases the toxic and soluble molecule heme
      • To avoid destruction by porphyrin ring of the heme group, the parasite biocrystallizes heme to form hemozoin, a non-toxic molecule
        • Hemozoin collects in the digestive vacuole as insoluble crystals
    • Chloroquine caps hemozoin molecules to prevent further biocrystallization of heme, thus leading to heme buildup
      • ​Chloroquine binds to heme forming a complex that is highly toxic to the cell and disrupts membrane function resulting in cell lysis and ultimately parasite cell autodigestion
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12
Q

What is the treatment for severe malaria?

A

Artemisinin-based combination therapy

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13
Q

How is malaria diagnosed?

A
  • Blood film + Giemsa stain
    • Stain specific for phosphate groups of DNA
    • Also used to stain chromosomes in chromosome banding
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14
Q

What is the vector for Malaria?

A
  • Females of Anopheles genus
    • Spread by bite of mosquito that was previously infected from a human blood meal - parasites multiply within liver cells and RBCs
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15
Q

How many malaria cases are there in the world?

A
  • About 3.3 billion people (half world’s pop) are at risk for malaria
  • 250 million malaria cases and nearly one million deaths each year
    • In Africa, 1 in 5 childhood deaths are due to effects of malaria - An African child has an average b/t 1.6-5.4 episodes of malaria fever each year
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16
Q

How long does it take for malaria to reach body system after bite? How long does it take to be symptomatic?

A
  • 1-2 hours
  • 2-5 weeks
17
Q

What does plasmodium vivax attack?

A
  • Reticulocytes
    • Immature red blood cells
18
Q

What does Plasmodium malariae attack?

A

Malariae = mature

  • Attacks mature red cells
19
Q

What is unique about Plasmodium ovale?

A

Ovale = old infection

  • Can be dormant for years
20
Q

What cells does Plasmodium falciparum invade?

A
  • invades all red cells irrespective of age of red cells
  • > cells agglutinate forming thrombi and emboli
21
Q

What are the compications of malaria?

A
  • Cerebral malaria
  • Acute renal failure
  • Severe anaemia
  • Thrombocytopenia
  • Liver dysfunction
  • Acute respiratory distress syndrome
22
Q

What is the insect vector for leishmania?

A

Sandfly

23
Q

What is congenital malaria and when should it be considered?

A
  • Febrile newborns and infants from women
    • Could have been infected during their pregnancy because the mother become infected during pregnancy or acquired months or years before
24
Q

What are ways to prevent malaria?

A
  • Vector control
    • Reduce stagnant water
    • Spraying with insecticide
    • Application of DEET
    • Mosquito nets
  • Vaccines
    • Under development
    • No completely effective vaccine
25
Q

What are the two forms of leishmania and how are they different?

A
  • Promastigotes
    • Found in the sandfly
    • Have a flagellum
    • Motile
  • Amastigotes
    • Found within macrophages in humans/other vertebrate hosts
    • Reabsorbed their flagellum
      • No longer motile
26
Q

How is transmission of leishmania in Europe changing?

A

It is spreading northwards

27
Q

Which type of leishmania causes the majority of cases of visceral leishmaniasis in Ethiopia?

A

L. donovani

28
Q

What type of leishmania are the majority of cutaneous leishmaniasis lesions caused by?

A

L. aethiopica

29
Q

What are the parasites that can cause trypansoma?

A
  • T. brucei
  • T. cruzi
  • L. major
30
Q

What is teh vector for trypansoma brucei?

A
  • Glossina species
    • Tsetse flies
31
Q

Outline the human stages for T. brucei

A
  1. Tsetse fly injects metacyclic trypsomastigotes
  2. Injected metacyclic trypsomastigotes transform into bloodstream trypsomastigotes which are carreid to other sites
  3. Trypsomastigotes multiply by binary fission in various body fluids
    • e.g. blood, lymph and spinal fluid
  4. Trypsomastigotes in blood
32
Q

Outline the fly stages of T. brucei

A
  • Tsetse fly takes a blodo meal
  • Bloodsteam trypsomastigotes transform into procycli trypsomastigotes in tsetse fly’s midgut
  • Procyclic trypsomastigotes multiply by binary fission
33
Q

What are the different forms of leishmanias?

A
  • Cutaneous leishmaniasis
    • Common
    • Causes skin sores
      • typically develop within a few weeks or months of the sand fly bite
      • can change in size and appearance over time.
      • may start out as papules or nodules and may end up as ulcers; skin ulcers might be covered by scab or crust.
      • usually are painless but can be painful.
      • Some people have swollen glands near the sores.
  • Visceral leishmaniasi
    • Usually spleen, liver, and bone marrow)
    • Can be life threatening.
    • Typically develops within months (sometimes as long as years) of the sand fly bite.
    • Symptoms:
      • fever,
      • weight loss
      • enlargement (swelling) of the spleen and liver,
      • anemia, leukopenia and thrombocytopenia).
  • Mucosal leishmaniasis
    • less common
    • can be a sequela of infection with some of the species of the parasite that cause cutaneous leishmaniasis in parts of Latin America: spreading from the skin and causing sores in the mucous membranes of the nose (most common location), mouth, or throat. The best way to prevent mucosal leishmaniasis is to ensure adequate treatment of the original cutaneous (skin) infection