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Sem 1: Parasite and pathogen ecology > Week 9 > Flashcards

Week 9 Flashcards

1
Q

What are specialist pathogens or parasites?

A

Can only infect a narrow host range

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2
Q

What are generalist pathogens or parasites?

A

Can infect a wide host range

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3
Q

What are the downsides of specialism?

A

Specialists rarely evolve to specialise on one resource without loosing effciency on another

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4
Q

What are the advantages of specialists?

A

Better establishment of a host
Higher parasitemia (proxy for intensity in blood parasites)
Higher prevalence

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5
Q

What are the advantages of generalist?

A

Match or exceed prevalence of a specialist
Maybe better insurance against host extinction (more reservoirs and opportunistic jumping)

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6
Q

What are STD (inverse bottom power for TD)?

A

This measures the taxonomic distinctness of all host species a parasite makes use of
Measures as the mean number of step back up a phylogeny to get to a taxon common to two species

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7
Q

How specialist are most parasites?

A

Most parasites have a high frequency in few hosts with few having low frequency in many hosts

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8
Q

What are the 2 filters for evolution of parasite specificity?

A

Ecological filter and Physiological filter

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9
Q

What is the ecological filter?

A

Niche and shared habitats affect the likelihood of an encounter between a potential host and parasite species

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10
Q

What is the physiological filter?

A

Determine the suitability of the host, if a parasite encounters a host, can it establish an infection and transmit further. Phylogenetically close hosts are physiologically similar so may have a similar physiological filter and attract the same parasites

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11
Q

What are biogeographical factors impacting number of hosts?

A

Parasites with larger distrubution have a larger range of possible hosts (though a small set of those may be suitable)

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12
Q

What are the two outcomes for a wide ranger parasite species?

A

Widely distributed parasites may be highly specialised
Or they could evolve towards generalism to make most of the resources

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13
Q

What determines which outcome a parasite species becomes?

A

Depends on gene flow between localities of both host and parasitess
Opportunism may also come into play

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14
Q

What is spatial heterigeneity?

A

The locally differentiated host populations may be more diffucult for parasite to adapt any specific population

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15
Q

How might parasites evolve spatial heterigeneity?

A

Either broad host range and generalist however each location could also develop differing degress of specificity via local adaptation

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16
Q

How can host phylogeny impact host range?

A

Common ancestry shapes phtsiological traits
Parasite may not be able to establish an infection it has never evolved the necessary traits
Species rich taxonomic groups may have more parasites simply because of morphological similarity

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17
Q

How can transmission impact host range?

A

More frequent transmission with the same host species could lead to specialisation

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18
Q

How can transmission mode come into play?

A

Direct transmission are more likely to be specific
Vectors make use of a vector show intermediate levels of specificity

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19
Q

How did direct transmission amogst helminths impact host range?

A

Amongst all known species two thirds that undergo direct transmission infect a single host species and non are known to be able to infect hosts

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20
Q

How did vector transmission amogst helminths impact host range?

A

Intermediate hosrs are transmitted tropically are less specific with half restricted to a single definitive host and a quarter able to infect hosts of different orders

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21
Q

How can larger hosts impact host ranges?

A

Larger hosts can be thought of as larger islands in biogeographical theory - more resources and niches
This sometime means that larger hosts harboring a greater parasite richness

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22
Q

What is parasite evasion?

A

To avoid host immune system meaning they can stay in and maximise use of their host

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23
Q

What is parasite manipulation?

A

When the parasites change the host phenotype

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24
Q

What are the pre-infection defences of the host?

A

Reducing exposure and Anticipatory defences e.g secretions and barriers

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25
What are immunoglobulins?
Proteins that bind to foreign binds marking them as foreign to the rest of the immune system
26
What are compliments?
A complex cascade which ends in the formation of the Membrane Attack Complex (MAC) which forms pores in cell walls and causes parasites to lyse
27
What is passive evasion?
Where no parasite-borne molecules are secreted
28
What are the passive evasion mechanisms that may be employed?
Hiding and host mimicry Antigen variation Antigenic shift Quiescence Encapsulation
29
How do schistomiasis hide from the immune system?
Schistosomes have a tegument
30
How does the tegument help the schistosomes (type of trematodes) hide from the immune system?
The tegument utalises surface molecules that share glycosylation patterns with their host hemocytes
31
What causes sleeping sickness?
African trypanosomes (type of protozoan)
32
What makes sleeping sickness chronic?
Despite continuous exposure to immune attack trypanosomes can persist
33
Why can trypanosomes survive continous exposure?
Antigenic variation where the surface glycoproteins change their identity allowing for the protection from immune recognition
34
What is antigenic shift?
The hybridising of antigens from 2 viruses through mixing of RNA
35
What is antigenic drift?
Antigen change due to mutations over time
36
What is quiescence?
When pathogens lay dormant
37
Where is quiescence and capsule formation often seen?
In bacteria and viruses
38
Can parasites quiescence and form capsules?
Yes
39
What is bacteria capsule made from?
Polysaccharide
40
What does quiescence look like in viruses?
Reduced production of viral proteins
41
What is an example of viral quiescence?
Herpes has a life long latent infection in sensory neurons, flareing up when immune system is already stressed
42
What is the lifecycle of Toxoplasma?
In bird and rats, toxoplasma lives as tissue cysts then the bird or rat is eaten by a cat. This then gets poo'd out and then reconsumed by bird or rat. This can enter humans.
43
How many people have toxoplasma?
1/3 of all people but in parts of europe it is almost everyone
44
What happens to toxoplasma in the body?
Lives in most cell types In a cell it feeds and reproduces, when exactly 128 it rips open cell and infects new cells A cycst forms containing a few hundred and every now and again the cyst will break and a new infection will begin
45
What are the symptoms of taxoplasma?
Light flu Though asymptomatic when cyst forms
46
How does taxoplasma keep its populaiton in check?
Through the host immune system
47
Who is at risk from toxoplasma?
Only people with immune problems and fetuses
48
What is active interference?
The parasite produces molecules that directly interfere with host machinery
49
What are examples of active interference?
Interference with recognition Block the host regulatory network Distort essential cellular function eg apoptosis Impede actions of effectors
50
What family of viruses make decoy molecules?
Orthopoxviruses (smallpox, monkeypox, mouse pox and cow pox)
51
What immue function is prevented?
The type 1 interferon response involves a family or pro inflammatory cytokines that help control virus infections, they are secreted from infected cells
52
What do Orthopoxviruses do to prevent type 1 interferon response?
Secrete soluble proteins that bind to type 1 interferon proteins with high affinities to reduce antiviral action and prevent infected cells signalling to healthy cells
53
How schistosomiasis deactivate hemocyctes?
Mimic host production of immune cell inactivating hormones making hemocytes inactive and harmless
54
What is commonly used in bacteria to inject effectors?
Many bacteria have type 3 secretory (T3SS) systems which can inject effector molecules into host cells
55
How does Bordetella pertusis use T3SS to supress the immune system?
Inject effector molecules into host cells that stimulate anti-inflammatory interleukin-10 (IL-10) which then blocks neutrophil recruitment
56
What does IL-10 do?
An important negative regulator of immflamation (neutrophil response), T cell responses and dendritic cell maturation (antigen presentation and adaptive immunity coordination)
57
What do HIV, Hepatitis B and C do to reduce threat of IL-10?
Stimulate IL-10 production
58
What do Herpes and pox viruses do to reduce threat of IL-10?
Create their own version of IL-10
59
What do parasites do at start of infection?
Avoid recognition and block macrophages and neutrophiles
60
What do pathogens do in early induced response?
Block inflammation Interfere with signalling Avoid phagocytosis
61
What do pathogens do in adaptive immune response?
Block NK cells Induce apoptosis Interfere with receptors and signalling Interfere with antigen presentation

Sem 1: Parasite and pathogen ecology (11 decks)

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