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Microimm 2500 > (O) 29: Parasitology I > Flashcards

(O) 29: Parasitology I Flashcards

1
Q

What is a parasite?

A

any organism that takes METABOLIC ADVANTAGE of another organism
- not necessarily harmful

  • include animals, plants, fungi, bacteria and viruses (host-dependent guests)
  • parasitism is one of most successful ways of life
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2
Q

Forms of parasitism

A
  • facultative parasites
  • obligate parasites
  • endoparasites
  • ectoparasites
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3
Q

Facultative parasites

A

can live as parasites but are NOT dependent on parasitic mode of life

does not need to exploit host

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4
Q

Obligate parasites

A

organisms that cannot complete their life-cycle without exploiting a suitable host

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5
Q

Endoparasites

A

live WITHIN a suitable host

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6
Q

Ectoparasites

A

live on the SURFACE of a suitable host

ex. ticks, fleas

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7
Q

What domain is mostly studied in parasitology?

A

Eukaryota
- single-celled (protozoa) + multi-celled

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8
Q

Classification of eukaryotic parasites

A

Protozoa - MICROscopic, single-celled
Metazoa - MACROscopic, multi-cellular (helminths - worms, arthropods - insects and arachnids)

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9
Q

Parasitic Protozoa + Helminths

A

Eukaryotic parasites are different from viruses/bacteria by their higher complexity = slower reproduction + less genetic flexibility

Protozoa: single-celled eukaryotes (either free-living or parasitic) that feed on organic matter like organic tissues and debris

Helminths are worms (either free-living or parasitic)

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10
Q

Why are there so many parasitic diseases?

A

we come into contact w/ them

  • we drink to survive
  • we eat to survive
  • we mist interact w/ our environment to survive
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11
Q

Parasitic protozoa

A

all protozoans are EUKARYOTIC SINGLE-CELLED organisms

Classified based on mechanism of motility:
- flagellates (use flagella)
- amebae (use plasma memb + projections - pseudopodia)
- sporozoa or apicomplexa (gliding)
- ciliates (move cilia - hair-like projections)

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12
Q

Mechanisms of parasite entry

A
  • oral (Giardia lamblia)
  • sexual (trichomonads vaginalis)
  • inhalation (toxoplasma gondii) - widespread from cat litter
  • direct contact (trypanosoma cruzi)
  • arthropod vectors (plasmodium falciparum - causes MALARIA)
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13
Q

Division + Reproduction of parasites

A

Asexual, sexual and both

Life cycles
- monoxenous
- diheteroxenous
- triheteroxenous

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14
Q

Monoxenous

A

Life cycle

  • infects only one host
  • does whole life cycle in one host
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15
Q

Diheteroxenous

A
  • needs two hosts
  • asexual reprod. in intermediate host
  • sexual reprod. in final host
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16
Q

Triheteroxenous

A

has a first and second intermediate then final host

increased rate of survival

17
Q

Survival of parasites

A

Immune evasion
- antigenic variation (immune system doesn’t recognize it)
- niche selection
- inhibition of host protective immune responses
- entering long-lasting dormant stage

Non-immune evasion
- enter environmentally resistant stage

18
Q

Pathogenesis of parasites

A

causes
- cell death
- virulence factors (ex. enzymes)
- biproducts of parasite metabolism (ex. hemazoin)

19
Q

Malaria

A

“bad air” b/c ppl thought it was air-borne

  • passed by bite of infected mosquito
  • spread by Plasmodium (single-celled parasite - sporozoan)
20
Q

Plasmodium

A
  • a sporozoan (single-celled parasite)
  • parasite that causes MALARIA

4 species of Plasmodium infect humans
- P. FALCIPARUM (most fatal, in Africa)
- P. vivax (Asia + South America)
- P. ovale (Africa)
- P. malariae (causes CHRONIC infection)

P. knowlesi infects macaques which is a cause of zoonotic malaria in humans (progresses quickly(

21
Q

Anopheles mosquitoes

A
  • Human malaria is transmitted only be FEMALES of genus Anopheles
  • female mosquitoes TAKE BLOOD MEALS FOR EGG PRODUCTION + these blood meals link humans and mosquitoes
22
Q

Global distribution of malaria

A
  • presence of malaria depends mainly on climatic factors like temp, humidity and rainfall
  • transmitted in tropical/subtropicla areas

Malaria parasites can complete their growth cycle IN mosquitoes (extrinsic incubation period) - we are intermediate host

Mosquitoes reproduce in standing after
- humans facilitate reproduction w/ blood

23
Q

Malaria Life Cycle - Mosquito (Sporogony)

A

Definitive host

  1. Gametocytes in infected human blood
  2. Female mosquitoes ingest gametocytes ingested w/ bloodmeal from infected human. Gamete form sin the stomach
  3. Sexual Reproduction – male gametocytes undergo EXFLAGELLATION and fertilize female gametocytes creating diploid cells in the stomach of the mosquito called OOKINETES
  4. Ookinetes migrate between stomach lining and undergo asexual reproduction (sporogony) to
    form an OOCYST containing sporozoites (haploid).
  5. Sporozoites form and release occurs in the stomach
    - oocysts grow, rupture, and release sporozoites into the mosquito’s hemolymph.
  6. Within the hemolymph, sporozoites migrate to the salivary glands and into the salivary duct
  7. Sporozoites in the mosquitoes saliva is injected into another human when
    the infected mosquito takes a second blood meal
24
Q

Microgametocyte vs Macrogametocyte

A

Microgametocyte: MALE gametocyte
Macrogametocyte: FEMALE gametocyte

25
Q

P. Falciparum infection - Human

A
  1. Sporozoites are injected into human through the saliva of an Anopholes mosquito during a second blood meal.
  2. Sporozoites enter the bloodstream and invade liver cells where they reproduce asexually (schizogony) to form CRYPTOZOITES (sporozoites in the liver - can’t infect liver)
  3. The schizont in the infected liver cell grows and ruptures, releasing MEROZOITES (cryptozoites in blood) into circulation.
  4. Merozoites infect RBCs and become ring stage “signet” TROPHOZOITES.
    - trophozoites divide asexually (schizogony) in RBC to form a schizont.
    - some of the cells will differentiate into male (micro) or female (macro) gametocytes
    - When RBC ruptures, these cells are released into circulation—many infect other red blood cells in circulation
  5. Mosquitos who bite an infected human will ingest the gametocytes during the blood meal.
26
Q

Hemozoin

A

stacking of heme groups
- makes humans sick + releases free heme into the body

biocrystal made by Plasmodium in humans

merozoites (sporozoites in the blood) use RBCs as a source of nutrition
- heme is released to kill parasite but P. falciparum stacks heme = bursting of RBCs = spread of merozoites

27
Q

Other modes of malaria transmission

A
  • vertical transmission from mother to her fetus before or during delivery
  • blood transfusion
  • organ transplant
  • shared use of needles/syringes
28
Q

Symptoms of malaria

A

ANEMIA + JAUNDICE (caused by loss of RBCs by bursting + liver being affected)

  • also flu-like symptoms, nausea, vomiting, diarrhea
29
Q

Diagnosis of malaria

A
  • microscopic exam of thick and thin blood smears
  • PCR is more sensitive and specific than microscopy but results take longer
30
Q

Treatment of malaria

A

should be guided by these 4 factors:
- infecting Plasmodium species
- clinical status of patient
- expected drug susceptibility of infecting parasite based on geographical area
- previous use of antimalarials

31
Q

Incidence of malaria

A

dependent on biological and human factors:
- density of suitable habitats for mosquito vector breeding
- prevalence of infected humans that mosquitoes can feed on
- susceptibility of humans bitten by an infected mosquito

32
Q

Malaria antagonistic interactions

A

Sickle cell anemia (Hb mutation = malformed RBC) - clogs blood vessels

If one is heterozygous for sickle cell (no symptoms), they are at an advantage if infected w/ malaria
- not enough good RBCs for malaria to work well
- lower parasitic load b/c of lower number of healthy cells
- can still be infected but LESS symptoms

33
Q

Malaria Prevention

A

Vector control + personal protection
- case management
- insecticide-treated nets (ppl cannot touch net b/c mosquitoes can bite btwn)
- indoor residual spraying
- prophylaxis treatment (pregnant women + infants)

Microimm 2500 (29 decks)

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