Midterm Flashcards

(93 cards)

1
Q

What is a pathogen?

A

parasite that induces a disease (abnormal condition) meaning fitness reduction. Falling into disuse

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2
Q

What are some traits of microparasites?

A
  • small/unicellular
  • short generation time
  • simple life cycle (one host)
  • high parasite load
  • reproduces in host
  • short infection time (could be chronic also)
  • strong host immunity
  • passive transmission
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3
Q

What are some traits of macroparasites?

A
  • large/multicellular
  • long generation time
  • complex life cycles (multiple stages/hosts)
  • often reproduces outside of host
  • low parasite load
  • long duration of infection
  • active transmission
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4
Q

What are the types of macroparasites?

A
  • parasitoids
  • kleptoparasites
  • brood parasites
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5
Q

What is a parasitoid?

A

parasites that have a free living stage, typically insects. Larvae will infect hosts and kill upon emergence

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6
Q

What is a kleptoparasite?

A

stealing food from another

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7
Q

What is a brood parasite?

A

special form of kleptoparasitism. Exploit the social structure of the host group

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8
Q

About how much of life is parasitic?

A

~40% of arthropods
~ 30% of all eukaryotes
~ 20% fungi
~1% plants/mammals/reptiles
~5% bacteria (but unknown)

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9
Q

What is the most common parasite?

A

The nematode.
- 4/5 animals on earth is a nematode
- 60% of nematode species are parasitic
- 50% of nematode species have at least one nematode that lives in it

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10
Q

What are the largest parasites?

A
  • longest - whale tapeworms (up to 30m)
  • largest ectoparasite - lampreys (1m)
  • largest human - broad tapeworm (10-15m)
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11
Q

What is the progressive hypothesis?

A

viruses are mobile genetic elements that have evolved the added ability to escape from the cellular genome
ex: retro-transposons

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12
Q

What is the regressive hypothesis?

A

viruses are degenerate cellular parasites that have eliminated all but essential features

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13
Q

What is the virus first hypothesis?

A

viruses originated independent of cells at the beginning of cellular life

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14
Q

What did parasites evolve from?

A

All parasites evolve from non-parasitic ancestors

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15
Q

What are the ingredients for making a parasite?

A
  1. Frequent interactions between two organisms
  2. Large size difference between the two organisms (usually)
  3. Persistence preadaptation (can stay on host for extended period of time)
  4. Exploitation preadaptation (can extract resources from host)
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16
Q

What are the persistence preadaptations?

A
  • phoresy
  • environmental buffering
  • refuge
  • predator exploitation
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17
Q

What is phoresy?

A

using larger organisms for dispersal. Important for terrestrial parasites

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18
Q

What is environmental buffering?

A

using host-to-be to avoid environmental variance

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19
Q

What is an example of environmental buffering?

A

inland water copepod species either parasitize or diapause to help with environmental instability when marine copepod do neither

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20
Q

What is refuge preadaptation?

A

using host-to-be to escape predation

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21
Q

What is predator exploitation?

A

prey able to survive within and exploit predator

no other preadaptation lead to parasitism without this!!

likely how we got eukaryotes

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22
Q

What are four ways yellow fever has influenced human history?

A
  1. promoted African slave trade because it ravaged the new world and West Africans were resistant
  2. Aided the Haitian revolution because they were resistant and French troops were not
  3. When the French were defeated in Haiti, Napoleon surrendered to western empire and sold Louisiana for cheap (Louisiana purchase)
  4. The Panama canal was delayed 25 years because yellow fever caused 80,000 deaths leading to catastrophic financial collapse
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23
Q

What are some of the ways parasites shape our world?

A
  • drive evolution and maintenance of sex
  • shape reproductive behaviors and traits
  • shape offspring number and size
  • induce host migrations
  • drive population dynamics
  • structure host communities
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24
Q

What are the life history stages of parasites?

A
  1. find host
  2. infect host
  3. grow/differentiate/multiply
  4. reproduce
  5. transmit
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25
How does the size of the parasite impact dispersal ability?
They are generally small which limits their ability to disperse/find hosts
26
What is passive transport?
tend to be sit-and-wait parasites through host feces or spray and pray transported through aerosols - high failure probability - selects for: high fecundity, small size, and environmental resilience
27
What is active transport?
tend to seek out new hosts (typically parasitoids and ectoparasites) - low probability of failure - selects for: large size, low fecundity, and environmental vulnerability
28
Ectoparasites
much attach to host (parasite form generally remains unchanged)
29
endoparasites
must enter host (parasite form generally shifts in life cycle)
30
What are the morphological shifts of malaria?
1. Sporozoites - tranmission/infective morph 2. Merozoites - replicative morph 3. Gametocytes - reproductive morph - creates male and female morphs
31
What is the growth/differentiation/multiplication stage associated with
host disease/reduction in host fitness
32
What are the types of direct transmission?
horizontal transmission vertical transmission
33
What are the types of indirect transmission?
1. complex transmission (upward, downward, or paratenic) 2. Vector transmission (circulative or mechanical) 3. Fomite transmission
34
What is complex transmission?
multiple different species hosts. One definitive and one or more intermediate hosts
35
What is upward incorporation?
Common predator eats the original definitive host, that predator then becomes the host since it is usually larger and has more resources. Original host is kept as a means to infect host 2 (predator)
35
What is downward incorporation?
Host 2 is added from a lower trophic level. Parasite accidentally enters host two and remains there because it increases the probability of transmission to host 1.
36
What is paratenic transmission?
no parasite development occurs in the intermediate host but it could still act as an optional/substitute host as a means to infect the target species.
37
What is an accidental host?
When there is no Itransmission beyond paratenic host
38
What is vector transmission?
disease transmitted by biological or mechanical agent
39
What is a circulative vector?
special case of complex transmission where vector is permanent stage of transmission. The parasite circulates in the vector developing and reproducing ex: mosquitoes
40
What is a mechanical vector?
biological or non-biological If biological there is no infection of the vector
41
What is fomite transmission?
Inanimate object transmits the pathogen
42
What is an obligate parasite?
A parasite that has lost its ability to live without a host
43
Which kind of parasite has more common evolutionary reversal?
Ectoparasites
44
Why do obligate parasites become specialized?
1. evolutionary arms race leads to specificity 2. specificity leads to more efficient host utilization
45
What are parasite specialists?
Have few sympatric congeners. Tend to exploit large, abundant, long-lived, and broad ranged hosts
46
What are parasite generalists?
Have many sympatric congeners. Tend to exploit small, low-density, short-lived, narrow range hosts
47
What is host specificity?
number of hosts used at a given life stage
48
How is host specificity measured?
1. host number 2. Rhodes index 3. Specificity index
49
What are some limitations with host number?
suffers from geographical, temporal, and host sampling bias. Ignores infection severity
50
What does Si mean (Rhodes index)
1 = high specificity 0 = generalist
51
What does Std indicated (specificity index)
as Std increases, parasite specificity decreases
52
What are emerging infectious diseases associated with?
Environmental disruption 1. change in host/vector range (closer contact between species) 2. Alter novel host or vector physiology through anthropogenic activities 3. Alter pathogen via direct selection (ex: antibiotic resistance)
53
What are types of prophylactic behavior?
- spatial avoidance - temporal avoidance - migration (spatiotemporal) - prey avoidance - individual avoidance - selfish herd - anticipatory defense
54
What is spatial avoidance?
avoiding localities associated with parasites
55
What is temporal avoidance?
avoiding host activity when parasites are active ex: ants curb foraging during the day and wet season to avoid parasitoids
56
What is prey avoidance?
eating less profitable prey item to avoid parasitism ex: when food tastes/smells bad
57
What is selfish herd?
reducing parasitism risk by spreading it to your neighbors *assumes host density does not impact parasite transmission*
58
What are anticipatory defenses?
when infection risk increases, hosts reduce parasitism by increasing investment in immunity ex: when larvae are crowded, they become darker indicating an increased immune response
59
What are the types of social immunity behvaior?
- allogrooming - social exclusion - hygienic behavior - social apoptosis
60
What are antimicrobial peptides (AMPs)?
have antifugal/antibacterial properties and are secreted by skin/exoskeleton as chemical barrier.
61
What is the peritrophic membrane (PM)?
a chitin and protein sieve that protects against food borne illness.
62
What are mucosal membranes?
cover the gastrointestinal, respiratory, reproductive and urinary tracts secrete mucin glycoproteins in large quantities
63
What are leucocytes?
internal innate immunity. defends via phagocytosis (macrophages/neutrophils)
64
How do leucocytes recognize pathogens?
toll and toll-like receptors recognize specific pathogen associated molecular patterns (PAMPs)
65
What are natural killer cells?
Recognizes target cells via opsonization and destroys them by releaseing perforins, small granzymes, and lysozymes
66
What is interferon?
antiviral released by infected cells to warn neighbors to shut down protein production
67
What is RNA interference (RNAi)?
antiviral host enzymes dice up viral dsRNA keeping it from replicating
68
What is the complement system?
small circulating proteins that - activate inflamation - opsonize microbes to facilitate phagocytosis - lysis of pathogen cell membranes
69
What happens during the inflammatory response?
mast cells release histamine and increase vessel permeability. Also basophils and eosinophils macrophages arrive for cleanup dendritic cells arrive to gather information for adaptive immune response
70
What is a dendritic cell?
phagocytizes pathogen, presents antigens over cell surface, enters lymph system and searches for antigen match on helper T-cells
71
What are helper T-cells?
coordinate the adaptive immune response by activating B-cells and cytotoxic T cells
72
How are antibodies used?
Bind to virus' surface and block its ability to bind to host cell bind to antigens promoting phagocytosis activates complement system
73
What is an antigen?
any substance that elicits a response from immune cells. What cells recognize on foreign ones
74
What is a provirus?
When the virus genome is integrated into host cell DNA. A form of latency.
75
What is immune cell distruption?
A form of evasion where the parasite actively inhibits the cells that hunt them. ex: disruption of MHC presentation by tuberculosis
76
What are immune effectors?
soluble compounds that effect an immune response. parasites can: degrade effectors reduce efficacy catabolize effectors
77
What is host resistance?
minimizing pathogen load
78
What is host tolerance?
minimizing pathogen virulence
79
What is the Hamilton Zuk hypothesis?
negative frequency-dependent selection between host and parasite is why sexual reproduction is maintained and allows for genetic variation to be maintained in a host population
80
What is the difference between pathogenesis and pathogenicity?
pathogenesis - mechanisms by which disease develops, progresses, and persists or is resolved pathogenicity - the degree to which a biological agent can cause disease
81
What are the ways parasites cause disease?
1. use of host nutrients 2. host tissue alteration 3. pathogen induced collateral damage 4. virulence factors 5. immunopathology (host induced collateral damage)
82
What are the virulence factors?
- adhesion factors - colonization factors - invasion factors - immune evasion factors - toxins
83
What are adhesion factors/adhesins?
commonly found in bacteria. molecules that promote adhesion to internal tissues. can be general (fimbriae and pili) or specific ex: biofilms
84
What are endotoxins?
compounds associated with gram (-) bacterial outer envelope. The main component is liposaccharides (LPS). it is a fever inducing toxin (pyrogen)
85
What are exotoxins?
proteins secreted from parasites; can damage tissues or interfere with cell function far from point of release. ex: cytotoxins, neurotoxins, enterotoxins, cardiotoxins,, virulence plasmid
86
What is coincidental virulence?
parasite accidentally finds itself in a host with whom it has no co-evolutionary history. may result in a highly virulent host response type of non-adaptive virulence
87
What is short-sighted virulence virulence?
virulence is an inadvertent consequence of mutation and selection within the host; enhanced by parasite competition within the host non adaptive ex: invading tissues with no benefit - polio in brain
88
What is the avirulent hypothesis/conventional wisdom hypothesis?
parasite and host co-evolution will eventually result in benign relationship
89
What is the trade-off hypothesis?
virulence (a) evolves to optimize parasite fitness (R0) due to a trade-off between transmission rates (B) and host survival
90
Basic reproductive number (R0)?
number of new infections caused by original infection in a wholly susceptible population. (parasite fitness)
91
R0 = BN/(u + a + v)
makes the trad-off curve between transmission and host survival. Those factors shape parasite fitness B = transmission rate N = host population size U = background host morality v = recovery rate a = virulence
92
What factors influence host immune phenotype/disease susceptibility?
host genetics environment host life history