Host-Parasite Interactions 1 & 2

Front 1

What is in the triad of host and parasite interactions? How are they relevant?

Back 1

Host - Species and innate immunity affects parasite infection outcome

Parasite - Direct (e.g. blood feeding) and indirect (e.g. Inflammatory response) effects

Environment - Determines parasite transmission, susceptibility/exposure to infection and life cycle stages in parasite

(All interlinked)

Front 2

What is the main feature in host-parasite interactions?

Back 2

Host will try to rid parasites with immune response (generally effective).

Parasite will try to evade immunity and complete life cycle.

Front 3

Name 3 parasites that elicit a strong immune response in the host, but can still complete its life cycle regardless.

Back 3

Faciola

Onchocerca

Dictyocaulus

Front 4

Name 3 parasites that are eliminated by the immune response.

Back 4

Dictyocaulus

Strongyloides

Babesia divergens

Front 5

Name 3 parasites that avoid host immune response.

Back 5

Toxoplasma

Trichenella

Hydatid cysts

(Leishmania)

Front 6

Name 3 parasites that persist by stimulating further immune response.

Back 6

Liver fluke

Trypanosoma

Thelazia

Front 7

What does the Medley-Kyriazakis model demonstrate?

Back 7

The use of resources by the host in immunity, taking away from resources that could be used for other bodily functions (e.g. growth, milk production etc.)

Front 8

What factors may effect whether a host initiates/maintains a strong immune response to parasites?

Back 8

Reproduction

Consequences of infection (e.g. Toxoplasma gondii higher priority than Teladorsagia)

Front 9

Is immunity optimised or maximised? Can it cause pathology?

Back 9

Optimised - yes

Front 10

Parasites are generally said to elicit concomitant immunity, what des this mean?

Back 10

Simultaneously immune and infected - (Low level) infection elicits immunity while infected, meaning the host is immune when infection is over.

Front 11

How do most parasites live in the environment?

Back 11

Free living OR ectothermic intermediate host

Front 12

What is the main factor determining development and mortality rates for a parasite in the environment? What does this mean for control?

Back 12

Temperature - Seasonal patterns observed which are important for control

Front 13

Other than temperature, what other climatic factors influence the development and mortality of parasites in the environment?

Back 13

Rainfall and humidity

Front 14

What is the temperature at which survival and development rate of parasite crosses over and is fairly high called? How can climate change effect this?

Back 14

Optimal zone - Climate change can push some parasites into, and some parasites out of their optimal zone as temperature increases.

Front 15

Aside from climate, what other factors have an influence on the parasite-environment relationship?

Back 15

Biotic interactions (natural enemies) e.g. Nematode-trapping fungi in dung.

Landscape (e.g. land use) - for example deep pools of water good for fluke transmission

Front 16

What is the most important factor to be considered with any host-environment interaction in the triad?

Back 16

The host's exposure to parasites that is governed

Front 17

At what point in the host's life are parasite burdens most common? What will this result in?

Back 17

Young animals - elicits immunity when older

Front 18

What must be taken into consideration in farming industries when looking at whether to give young animals sufficient exposure to parasites for immunity?

Back 18

Trade offs with production, for example the immunity generated against a parasite in a lamb may not be worth the potential for reduced growth prior to selling (may depend on impact infection has and resources used for animal - minor or major?)

Front 19

What options are available to farmers to minimise the impact parasitic infection has on cows (e.g. with Ostertagia ostertagi)?

Back 19

Option 1 - Treat to protect first season grazers, meaning second season grazers and all other cows are susceptible and must be treated for infection.

Option 2 - Expose first season grazers, giving second season grazers immunity and cows are resistant.

Front 20

Name an advantage and disadvantage of using slow release boluses which treats and protects against worms.

Back 20

Advantage - Kills infection, protects for up to 13 weeks

Disadvantage - Can provide too much protection, not allowing any exposure for immunity

Front 21

How can anthelmintic treatment be used in a way that allows exposure?

Back 21

Use pulse release bolus anthelmintics that does not keep releasing the drug, use in a way that allows occasional exposure. Therefore, the animal in protected and can also develop immunity.

Front 22

What methods can be used for diagnosis of worm burdens? Evaluate these.

Back 22

Faecal egg count - Tells burden at one point but not if increasing or decreasing in individuals. Must use at multiple points over time.

Plasma pepsinogen - Indicates abomasal damage over the season (Too high = Impact on growth / Too low = not enough exposure). Used to modify future exposure and treatment

Milk antibody-detection ELISA test - Gives exposure of susceptible animals (not immunity) e.g. Low titre = Not being exposed (unlikely), or exposed and susceptible/ High titre = Susceptible and exposed

Front 23

Give an example of a disease which is good to expose to young due to increased severity with age? Why?

Back 23

Babesia divergens - Colostral antibodies reduces impact and elicits immunity

Front 24

What must we consider when looking at reducing the force of diseases such as Babesia divergens on farms? Why?

Back 24

Reducing force of disease can increase clinical prevalence, this is because fewer young are exposed as the average age of first infection increases with the number of ticks carrying the disease decreasing. Therefore, more severe clinical disease is seen.

Front 25

Is vaccination effective?

Back 25

To an extent, but sterile immunity is rare - must be integrated with other methods.

Front 26

Give 4 examples of parasitic diseases that can be vaccinated against.

Back 26

Toxoplasma gondii (sheep)

Coccidiosis (poultry)

Taeniid tapeworms in intermediate host

Lungworm in cattle

Front 27

As drugs become increasingly resistant, what methods may be employed to reduce parasitic infection on farms?

Back 27

Breed resistant OR resilient sheep

Front 28

What is the problem when breeding cows/sheep by looking at performance?

Back 28

While those with a high performance might be resistant, it may be the case that they have just not been exposed.

Front 29

What can we conclude if a sheep/cow has been highly exposed but has a low faecal egg count? What are the problems in using this to breed as opposed to other options?

Back 29

Resistant - May be a problem where animal has strong immune response to minor infection (e.g. Teladorsagia) and uses resources on this that can stunt growth and production where not needed. Resilience might be more useful.

Front 30

Why might resistance work better than resilience on a group scale?

Back 30

Reduced FEC from resistant individuals, which reduces challenge for the group

Resilience causes tolerance to infection, which may help one individual but result in more eggs on pasture, so potentially more infection

Front 31

Why is it an advantage to have resistant ewes when reproducing?

Back 31

Immunity acquired in lambs

Peri-parturient eggs fewer, so less infection and less amplification of L3 through season

Front 32

What are the potential limitations of breeding for resilience?

Back 32

Challenge, hence selection, is variable and we may only be choosing high performing cows (worm monitoring needed)

Unknown if it can be transferred to new environment (where the challenge and exposure is greater)

Front 33

What flexible method can be used on farms instead of looking at specific resilience and resistance tactics?

Back 33

Use targets (targeted selective treatment) on a points system