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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
Q

What are immunoglobulins?

A

Proteins that bind to foreign binds marking them as foreign to the rest of the immune system

26
Q

What are compliments?

A

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
Q

What is passive evasion?

A

Where no parasite-borne molecules are secreted

28
Q

What are the passive evasion mechanisms that may be employed?

A

Hiding and host mimicry
Antigen variation
Antigenic shift
Quiescence
Encapsulation

29
Q

How do schistomiasis hide from the immune system?

A

Schistosomes have a tegument

30
Q

How does the tegument help the schistosomes (type of trematodes) hide from the immune system?

A

The tegument utalises surface molecules that share glycosylation patterns with their host hemocytes

31
Q

What causes sleeping sickness?

A

African trypanosomes (type of protozoan)

32
Q

What makes sleeping sickness chronic?

A

Despite continuous exposure to immune attack trypanosomes can persist

33
Q

Why can trypanosomes survive continous exposure?

A

Antigenic variation where the surface glycoproteins change their identity allowing for the protection from immune recognition

34
Q

What is antigenic shift?

A

The hybridising of antigens from 2 viruses through mixing of RNA

35
Q

What is antigenic drift?

A

Antigen change due to mutations over time

36
Q

What is quiescence?

A

When pathogens lay dormant

37
Q

Where is quiescence and capsule formation often seen?

A

In bacteria and viruses

38
Q

Can parasites quiescence and form capsules?

A

Yes

39
Q

What is bacteria capsule made from?

A

Polysaccharide

40
Q

What does quiescence look like in viruses?

A

Reduced production of viral proteins

41
Q

What is an example of viral quiescence?

A

Herpes has a life long latent infection in sensory neurons, flareing up when immune system is already stressed

42
Q

What is the lifecycle of Toxoplasma?

A

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
Q

How many people have toxoplasma?

A

1/3 of all people but in parts of europe it is almost everyone

44
Q

What happens to toxoplasma in the body?

A

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
Q

What are the symptoms of taxoplasma?

A

Light flu
Though asymptomatic when cyst forms

46
Q

How does taxoplasma keep its populaiton in check?

A

Through the host immune system

47
Q

Who is at risk from toxoplasma?

A

Only people with immune problems and fetuses

48
Q

What is active interference?

A

The parasite produces molecules that directly interfere with host machinery

49
Q

What are examples of active interference?

A

Interference with recognition
Block the host regulatory network
Distort essential cellular function eg apoptosis
Impede actions of effectors

50
Q

What family of viruses make decoy molecules?

A

Orthopoxviruses (smallpox, monkeypox, mouse pox and cow pox)

51
Q

What immue function is prevented?

A

The type 1 interferon response involves a family or pro inflammatory cytokines that help control virus infections, they are secreted from infected cells

52
Q

What do Orthopoxviruses do to prevent type 1 interferon response?

A

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
Q

How schistosomiasis deactivate hemocyctes?

A

Mimic host production of immune cell inactivating hormones making hemocytes inactive and harmless

54
Q

What is commonly used in bacteria to inject effectors?

A

Many bacteria have type 3 secretory (T3SS) systems which can inject effector molecules into host cells

55
Q

How does Bordetella pertusis use T3SS to supress the immune system?

A

Inject effector molecules into host cells that stimulate anti-inflammatory interleukin-10 (IL-10) which then blocks neutrophil recruitment

56
Q

What does IL-10 do?

A

An important negative regulator of immflamation (neutrophil response), T cell responses and dendritic cell maturation (antigen presentation and adaptive immunity coordination)

57
Q

What do HIV, Hepatitis B and C do to reduce threat of IL-10?

A

Stimulate IL-10 production

58
Q

What do Herpes and pox viruses do to reduce threat of IL-10?

A

Create their own version of IL-10

59
Q

What do parasites do at start of infection?

A

Avoid recognition and block macrophages and neutrophiles

60
Q

What do pathogens do in early induced response?

A

Block inflammation
Interfere with signalling
Avoid phagocytosis

61
Q

What do pathogens do in adaptive immune response?

A

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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