Lecture 6: Parasitology 1 Flashcards

1
Q

What is a parasite?

A

a eukaryotic organism that is using another for a variety of purposes

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2
Q

T/F

all parasites are worms

A

false

not all parasites are worms. some can be amoebas, protozoa, etc.

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3
Q

T/F

Parasitic infections can manifest in many different ways.

A

true

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4
Q

Why do the complex life cycles of parasites make diagnostics and treatment challenging?

A
  • there are multiple stages for the parasite, which can target multiple locations within the body
  • makes diagnostics, drug and vaccine development challenging
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5
Q

T/F

Most parasitic infections are not clinical.

A

true

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6
Q

infections are generally ____ –> most effective parasites are only ____ _____. that is to say, they will ____ but not ____

A
  • chronic
  • moderately virulent
  • infect
  • kill
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7
Q

parasites have the biological imperative to ____, ____, and ___, so not killing the host is beneficial to their existence.

A

reproduce, find nutrients, and shelter

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8
Q

If you are not the right host, how will a parasite respond?

A

it will try to get out of you by any means. Often kills the incidental host

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9
Q

T/F

parasites have maintained their responses to the host body since their inception.

A

false

parasites have evolved to manipulate host immune responses and host

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10
Q

routes of parasitic infection

A
  • ingestion
  • arthropod bite
  • transplacental penetration
  • direct penetration
  • transmammary
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11
Q

organisms that use ingestion to infect host

A
  • Giardia
  • E. histolytica
  • Cryptosporidium spp.
  • cestodes
  • nematodes
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12
Q

organisms that use arthropod vectors to infect host

A
  • Malaria
  • Babesia
  • filaria
  • Leishmania spp.
  • Trypanosomes
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13
Q

Organisms that use transplacental penetration to infect host

A

Toxoplasma gondii

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14
Q

organisms that use direct penetration to infect host

A
  • hookworm
  • Strongyloides
  • Schistosomes
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15
Q

how can parasites harm their hosts?

A

toxic products
- proteases, phospolipase, lytic enzymes, collagenase, elastase

mechanical tissue damage
- intestinal and organ blockage, pressure atrophy, tissue migration

immunopathology
- hypersensitivity reactions, autoimmunity, metaplastic changes, chronic inflammatory changes

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16
Q

Type 1 Reaction: ??
Mechanism: ??
Organism: ??

A
  • anaphylactic
  • Ag + IgE –> histamine
  • helminths, trypanosomes
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17
Q

Type 2 Reaction: ??
Mechanism: ??
Organism: ??

A
  • cytotoxic
  • Ab + Ag + C’ (ADCC)
  • T. cruzi
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18
Q

Type 3 Reaction: ??
Mechanism: ??
Organism: ??

A
  • immune complex
  • Ab + Ag complex
  • Malaria, schistosomes, trypanosomes
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19
Q

Type 4 Reaction: ??
Mechanism: ??
Organism: ??

A
  • delayed
  • T cells
  • Leishmania, Schistosomes, trypanosomes
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20
Q

What can a type 1 reaction result in?

A

anaphylactic shock, bronchospasms, local inflammation

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21
Q

what can a type 2 reaction result in?

A

Ab + Ag on cell surface –> complement activation or ab-dependent cellular cytotoxicity. results in the lysis of cell-bearing microbial antigens

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22
Q

What can a type 3 reaction result in?

A

inflammation and tissue damage; complex deposition in glomeruli, joints, skin vessels, brain; glomerulonephritis and vasculitis

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23
Q

what can a type 4 reaction result in?

A

sensitized T-cell reaction with antigen, liberation of lymphokines, triggered cytotoxicity –> results in inflammation, mononuclear accumulation, macrophage activation, tissue damage

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24
Q

What is released when a parasite is destroy and what can it cause?

A

proteases and phospholipases are released

can cause cell destruction, inflammatory response, and gross tissue pathology

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25
Q

differentiate between parasitic infection and parasitic disease.

A

parasitic infection is the presence of a parasite in the host; parasitic disease results when the parasitic infection damages the cells or body, thereby harming the host

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26
Q

T/F

most parastic infections are acute

A

False

most parasite infections are sub-acute or chronic

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27
Q

What determines the outcome of parasitic disease?

A
  • route of exposure
  • inoculum size and infective dose
  • tissue tropism
  • disruption, evasion, and inactivation of host immune system
  • host age and immune status
  • disease progression –> in for the long haul (unless immunocompromised)
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28
Q

How does Chagas disease demonstrate that parasitic complications can occur YEARS after initial infection?

A
  • can initially see minor skin lesions at time of infection, but years later, the infected can develop complications from damage to cardiac muscle and nerve damage, leading to heart disease, GI issues, etc.
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29
Q

How do schistosome infections demonstrate that parasitic complications can occur YEARS after initial infection?

A

initial infections may have minor bleeding in the GI or urinary tract from beginning, but years of it develops into obstructions, cancer, etc.

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30
Q

How do eosinophils aid in parasite infections?

A
  • these are the leukocytes that help neutralize infection with worms
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31
Q

what occurs in response to parasites’ surface proteins?

A
  • eosinophilia

- -> accompanied by increased levels of IgE and is triggered by increased IL-5

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32
Q

eosinophilia helps to identify parasitic infection with ___, but doesn’t help much with ____

A
  • helminths

- protozoa

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33
Q

T/F parasites are only a type 2 response.

A

false

parasites can be either type 1 or type 2

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34
Q
Th Group: Th1
Cell products: ??
Cell receptor: ??
Cell target: ??
Infectious agent(s): ??
A
  • interferon-gamma, IL-2
  • IL-12R
  • macrophages, DCs
  • intracellular bacteria, fungi, viruses, INTRACELLULAR PARASITES
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35
Q
Th Group: Th17
Cell products: ??
Cell receptor: ??
Cell target: ??
Infectious agent(s): ??
A
  • IL-17A, IL-17F, IL-21, IL-22
  • IL-23R
  • Neutrophils
  • Extracellular bacteria, fungi, EXTRACELLULAR PARASITES (?)
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36
Q
Th Group: Th2
Cell products: ??
Cell receptor: ??
Cell target: ??
Infectious agent(s): ??
A
  • IL-4, IL-13, IL-5
  • IL4R
  • Eosinophils, basophils
  • parasites
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37
Q

Types of interference/avoidance

A
  • antigenic variation
  • molecular mimicry
  • concealment of antigenic site (masking)
  • intracellular location
  • immunosuppression
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38
Q

mechanism of antigenic variation

A

variation of surface antigens within the host

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39
Q

mechanism of molecular mimicry

A

microbial antigens mimicking host antigens leads to poor Ab response

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40
Q

mechanism of masking (concealment of antigenic site)

A

acquisition of coating host molecules

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41
Q

mechanism of intracellular location

A
  • failure to display microbial antigen on host cell curface
  • inhibition of phagolysosomal fusion
  • escape from phagosome into cytoplasm with subsequent replication
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42
Q

mechanism of immunosuppression

A
  • suppression of parasite-specific B- and T-cell responses

- degradation of immunoglobulins

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43
Q

trophozoite

A

motile, feeding stage, causes pathogenesis

  • these are the ones interfering with cell lining in the gut, blocking absorption
  • “out and about,” so the immune response can recognize them
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44
Q

cyst

A

infectious (immediately), non-motile, passed in feces (or in tissue and consumed to cause infection)

  • often very resistant to immune system or to chemicals
  • stage isn’t really doing anything
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45
Q

oocyst

A

protozoan version of egg; passed in feces; often takes 1-2 days to sporulate and be infectious

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46
Q

sporulate

A

when oocysts develop from undifferentiated cellular material to sporozoites

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47
Q

merozoite

A

stage that undergoes asexual reproduction; feeding stage (seen with malaria and coccidia)

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48
Q

schizont

A

whole cell full of multiplying merozoites; schzogeny is the process by which asexual reproduction may occur

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49
Q

what are the 3 main geohelminths?

A
  • hookworms
  • roundworms
  • whipworms
50
Q

T/F

eggs are immediately infectious

A

false

51
Q

At which stage is a parasite infectious

A

L3 stage

52
Q

Are eggs environmentally resistant or labile

A

resistant

53
Q

examples of nematodes

A

ascarids, strongylids, filarids

54
Q

ascarids, strongylids, and filarids are examples of what?

A

nematodes

55
Q

examples of cestodes

A

tapeworms

56
Q

tapeworms are examples of what

A

cestodes

57
Q

flukes are examples of what

A

trematodes

58
Q

examples of trematodes

A

flukes

59
Q

What is one of the leading causes of death in children under 5 years of age

A

diarrheal illness

60
Q

what percent of childhood mortality is attributed to diarrhea?

A

10%

61
Q

what are the 3 main protozoa that cause diarrhea?

A
  • Giardia
  • Cryptosporidium
  • Entamoeba histolytica
62
Q

T/F

illness in early childhood has no longterm physical and cognitive development effects

A

false

it does

63
Q

what is the most common intestinal parasite in humans/

A

Giardia lamblia

64
Q

what is the route of contamination for giardiasis?

A

fecal-oral contamination (cysts in feces)

65
Q

what is the distribution of giardia?

what is it generally associated with?

A
  • world-wide distribution

- water contamination

66
Q

what is the prevalence of giardia in developed countries?

A
  • 2% in adults, 6-8% of children
67
Q

what is the prevelance of giardia in developing countries?

A

33% prevalence

68
Q

T/F

Giardiasis is rarely zoonotic

A

true

69
Q

what could be a reason for the difference in prevalence between developed and developing countries

A

water purifying systems

70
Q

What is more likely to affect whether one has Giardiasis: immune status or infectivity?

A

immune status

71
Q

which stage of giardia is responsible for transmission of giardiasis?

A

cysts

72
Q

how can you diagnose giardiasis?

A

fecal examination and detecting cysts or trophozoites

73
Q

what do giardia trophozoites prevent when the affect the intestinal lining?

A

absorption of fat, leading to diarrhea of a fatty nature

74
Q

how long can giardia cysts persist in the environment?

A

several months in cold water

75
Q

how may trophozoites are released from a cyst?

A

2

76
Q

where does giardia typically infect in the body?

A

small intestine

77
Q

how do trophozoites multiply?

A

longitduinal binary fission

78
Q

when does encystation occur?

A

as the parasites transit toward the colon

79
Q

why is person-to-person transmission of giardia possible?

A

cysts are infectious when passed in the stool or shortly afterward

80
Q

when trophozoites attach to the intestinal wall with their sucking disks, what do they cause?

A
  • malabsorption
  • inflammation
  • hyperplasia
81
Q

50% of infected indivduals are ____

A

asymptomatic

82
Q

symptoms of giardiasis

A
  • fatty diarrhea
  • gas
  • abdominal cramps
  • nausea
  • vomiting
    dehydration
83
Q

in children with giardiasis, malnutrtion may result in what?

A

delayed physical and mental growth

84
Q

what age group is most likely to be infected with giardia?

A

ages 1-4

85
Q

what are the two crypto species most common in humans? Which is zoonotic

A
  • C. hominis

- C. parvum (zoonotic)

86
Q

distribution of Crytposporidium

A

world wide

87
Q

T/F

cryptosporidium has a transplacental route of contamination

A

false

fecal oral contamination, possibly even respiratory secretions

88
Q

is the cryptosporidium oocyst environmentally labile or resistant?

A

resistant

89
Q

what are large risk factors for c. hominis?

A

daycare and swimming

90
Q

how can one acquire C parvum zoonotically?

A

from neonatal calves

91
Q

how does cryptosporidiosis occur?

A
  • the protozoa colonizes microvilli on the apical surface of the epithelial cells, predominantly in the small intestine
92
Q

symptoms of cryptosporidiosis

A
  • watery diarrhea
  • dehydration
  • cramps
  • weight loss
  • nausea
    • occasionally may see resp. symptoms
93
Q

when might one consider cryptosporidiosis zoonotic?

A

in immunocompromised individuals, like those with AIDS

94
Q

T/F in healthy individuals, crypto is generally self-limiting and symptoms resolve after ~10 days

A

true

95
Q

how has water been treated to prevent crypto infection?

A

with UV treatments

96
Q

where are most people getting infected with cryptosporidium

A

recreational water parks

97
Q

what is the pathogenesis of both giardia and cryptosporidium

A
  1. interaction between Crypto/Giardia and the apical surface of the epithelial cells of the GI wall results in a localized activation of signalling cascades, culminating in barrier disruption and polymerization of actin filaments in the region with host-parasite interaction
  2. several molecules result in cellular damage, enhancing fluid secretion from the crypts and supporting diarrhea due to active secretion and malabsorption, which can lead to cell death
  3. essentially, they come in, and penetrate or bloc the cell, which gets your immune system involved. The activation of the immune system can disrupt the barrier through cell death, and other forms of disruption
98
Q

which parasite is responsible for human coccidosis?

A

cyclospora spp.

99
Q

cyclospora distribution

A

worldwide, but most tropical and subtropical

100
Q

prevalence of cyclospora in

  • endemic areas.
  • developed countries
A
  • 2-18% in endemic areas

- 0.1-0.5% in developed countries

101
Q

T/F

cyclospora oocysts are not initially infective, thus fecal-oral transmission cannot occur.

A

true

102
Q

when does Cyclospora sporulation occur?

A
  • after days or weeks at 22C-32C
103
Q

what can serve as the vehicle for cyclospora sporulated oocyst transmission

A

fresh produce and water

104
Q

Where do Cyclospora oocysts excyst in the host?

A

GI tracted, thus freeing sporozoites which invade the epithelial cells of the Small Intestine.

105
Q

what symptoms are seen with human coccidiosis?

A
  • watery diarrhea
  • dehydration
  • cramps
  • weight loss
  • nausea
    • occasionally may see resp. symptoms
106
Q

Cyclospora is ____ in healthy individuals and ____ in immune-compromised individuals

A
  • self-limiting

- chronic

107
Q

What is the route of infection for Entamoeba histolytica?

A

fecal-oral contamination

108
Q

infective stage of Entamoeba histolytica

A

the cyst

109
Q

motile feeding stage of entamoeba histolytica

A

trophozoite

110
Q

distribution of Entamoeba histolytica

A

worldwide, but mostly tropical and subtropical areas

111
Q

what can lead to increased risk of E. histolytica infections

A

poor sanitation / contaminated water

112
Q

prevalence of E. histolytica

  • globally
  • US
A
  • 10-15%

- 1-2%

113
Q

Is one more likely to get E. histolytica in a crowded or low-density area?

A

crowded

114
Q

which stage of E. histolytica are you more likely to find in feces?

A

cysts

115
Q

Where does E. histolytica generally stay in the host?

where can it migrate to if it leaves that location?

A
  • the gut

- can go to the bloodstream –> liver –> lungs or brain

116
Q

T/F

an individual may be an asymptomatic carrier of Entamoeba histolytica

A

true

117
Q

Entamoeba histolytica

intestinal amebiasis symptoms

A
  • related to tissue destruction in LI
  • -> abdominal pain
  • -> cramping
  • -> colitis
  • -> bloody diarrhea
  • -> necrosis in intestine (flask-shaped lesions)
118
Q

entamoeba histolytica

extraintestinal amebiasis symptoms

A
  • invasion into deeper mucosa & peritoneal cavity (liver, heart, & brain may be affected)
  • systemic fever
  • rigors
  • abcess formation and enlargement of liver from filtering trophozoites, hepatomegaly
119
Q

Intestinal Protozoa

A
  • Giardia
  • Cryptosporidium
  • Cyclospora
  • Entamoeba histolytica
120
Q

blood and tissue protozoa

A
  • plasmodium (4 spp.)
  • Trypanosoma cruzi
  • Trypanosoma brucei spp.
  • Leishmania spp.
  • Toxoplasma
  • Babesia spp.