Practical Parasite Control in Farmed Animals Flashcards

1
Q

At what age are internal parasites most important?

A

Internal parasites are the most important production limiting disease in UK sheep systems

In beef and dairy calves (<18 months old) they are important.

In adult dairy cows they are rarely important except occasionally lungworm and liver fluke

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2
Q

What are the most common parasites in farmed species?

A
  1. GI Nematodes (Trichostronyles, Nematodirus battus, Haemonchus, Teladorsagia, Ostertagia, Cooperia
  2. Trematodes (Fasciola hepatica and Oesophagostomum)
  3. Coccidia (sheep and cattle)
  4. Lungworms (Cattle and sheep)
  5. Ectoparasites (Lice and Mites) – important but covered else where in the course
  6. Tapeworms (sheep)
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3
Q

What are the most clinically important GI nematodes?

A

GI Nematodes: Trichostronyles, Nematodirus battus, Haemonchus, Teladorsagia, Ostertagia, Cooperia

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4
Q

Name 2 trematodes

A

Fasciola hepatica and Oesophagostomum

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5
Q

What does trickle exposure do and to which parasites?

A

Sheep and Cattle develop immunity with TRICKLE exposure over time to all the following parasites (Trichostrongyles, Nematodirus battus, Teladorsagia, Ostertagia, Cooperia, Coccidia, Lungworm)

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6
Q

Sheep and Cattle develop immunity with TRICKLE exposure over time to some parasites.

Which parasites do sheep and cattle NEVER develop immunity to?

A

They NEVER develop immunity to the following Fasciola hepatica or Haemonchus contortus

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7
Q

What is trickle challenge?

A

A trickle or low infectious challenge over time allows immunity to develop without clinical signs of disease

However, a high, abrupt infectious challenge encountered over a short period of time exceeds the ‘threshold’ and causes clinical/sub-clinical disease – and can result in clinical disease

Avoiding all challenge means animals are naïve and susceptible to infection. Important to remember this when you are devising a parasite control plan for a client

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8
Q

What is the cycle of nematadirus in terms of seasons?

A

All the eggs passed the previous year require a period of cold over the winter to prime them to hatch all together over a short period of time the following spring when weather conditions are consistently over 10oC. Causing a high seasonal peak of infectious larvae on pasture in spring to infect lambs when they start to graze. Exact date depends on how far north you are (late April in Cornwall, June in Scotland). A warm spring means an earlier peak. This is predicted by climate modelling

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9
Q

What is the clinical disease of neamtadirus caused by?

A

Clinical disease is caused by the huge numbers of immature larvae attacking the gut wall causing dehydration and rapid death. This happens before they reach adulthood so often NO EGGS FOUND on faecal egg count during an outbreak of clinical disease.

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10
Q

Why do we see outbreaks of nematodirus in autumn now?

A

Winter before temperatures warm up – allowing edges to hatch, however we do now see outbreaks of Nematodirus in autumn as well – where we are getting eggs released onto pasture this year, hatching that year and seeing disease in the autumn

Weather is important to enable hatching

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11
Q

What drug is nematodirus still susceptible to?

A

Nematodirus is still susceptible to almost all of the anthelmintics so we commonly use BZ wormers to treat them which are almost useless to treat other infestations. Rare cases of BZ resistance have now been reported in Nematodirus so BZ’s may also be of little use for Nematodirus either in the future

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12
Q

What is shown here and what is the likely cause?

A

Lambs suffering from nematodirus

Dirty back end, tucking in flanks – can be quite painful! Open fleece related to dehydration you will see with these lambs

Can also result in sudden death

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13
Q

What age of lambs is most susceptible to coccidiosis?

What is the difference between first born lambs and the youngest lambs?

A

Lambs on intensive systems are at greatest risk = early lambing systems with high levels of contamination in buildings and on dirty pasture around creep feeders or water troughs. Lambs 3-12 wks old most at risk. Disease in older lambs is rare as they become immune after exposure to low numbers of oocysts.

Typically lambs born in the first half of the lambing period are only exposed to a low level of oocyst challenge and develop immunity. However, these early lambs do multiply up the oocysts in the shed or field whilst they develop immunity and the later born, youngest lambs then encounter a high challenge of infectious oocysts and suffer with clinical disease (scouring, dehydration) before they develop immunity.

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14
Q

How many strains of coccidiosis are pathogenic to sheep?

What does this mean?

A

Only 2 of the 11 Eimeria species in sheep are pathogenic so a high oocyst count is not necessarily proof of coccidiosis

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15
Q

How can you tell the difference between coccidia and neamtodirus infection?

A

Coccidia vs Nematodirus – ask where were the lambs grazing the previous year,. If grazing on land used previously – may be Nematodirus. If early lambs not appearing to have clinical disease but later lambs do – coccidiosis. Might need to treat both if cannot differentiate

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16
Q

What are the 2 main GI nematodes in lambs?

A

Teladorsagia & Trichostrongylus

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17
Q

When do Teladorsagia & Trichostrongylus larvae hatch?

A

Infectious larvae can only hatch when conditions are warm and wet enough so ewes lambing in March-May contaminate the pasture with eggs which hatch in time to infect their lambs when they start grazing.

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18
Q

How can disease from Teladorsagia & Trichostrongylus present?

A

Disease presents as either clinical or sub-clinical depending on the dose of infectious larvae ingested:

Clinical = scouring, weight loss, poor fleece quality, dull depressed, dehydrated, death!

Sub-clinical = slower weight gain (Daily Live Weight Gain (DLWG)), reduced feed conversion efficiency and reduced immunity to other infections e.g. mastitis

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19
Q

When do the levels of Teladorsagia and Trichostrongylus drop off and what time of year is important?

A

Lambing period is the most important factor in worm control as it determines if the susceptible lamb crop will overlap with a pathogenic level of infectious larvae. Level drops off in colder months. At lambing time, hypobiotic larvae with lambing and levels stress at this time – reduction in immunity, so they go and shed more eggs that they would previously

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20
Q

What is the problem with immunity to ewes around lambing time?

A

Ewes under nutritional stress around lambing lose some of the immunity they have acquired to the parasite allowing hypobiosed EL4 larvae to develop to adults and also new infections to become patent.

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21
Q

What is the seasonal peri-parturient egg count like throughout lambing, peak lactation?

What does this mean for the lambs born?

A
  • Ewes under nutritional stress around lambing lose some of the immunity they have acquired to the parasite allowing hypobiosed EL4 larvae to develop to adults and also new infections to become patent.
  • As ewes pass peak lactation and the nutritional stress declines they recover their immunity and kill off the parasites so their FEC falls
  • This seasonal (PeriParturient) egg count rise is crucial for the parasite as it contaminates the pasture for the lambs to become infected
  • Ewes under low stress (e.g. adult ewes in good BCS carrying 1 lamb) do not loose much immunity but ewes under high stress (Triplets, Low BCS, young (ewe lambs & shearlings)) are under greatest stress and will generate most of the pasture contamination
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22
Q

What causes parasitic gastroenteritis in cattle?

A

Ostertagiosis & Cooperiosis

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23
Q

What causes parasitic gastroenteritis in sheep?

A

Strongylosis & Haemonchosis

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24
Q

What is type 1 parasitic gastroenteritis and what causes it to occur?

A

Wet summers cause eggs to hatch and infect stock early and cause disease in the same season – clinical signs of scour, weight loss, low DLWG, poor feed conversion efficiency…. Very Very Very common

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25
Q

What is type 2 parasitic gastroenteritis and what causes it to occur?

A

Dry summers cause eggs to remain unhatched until autumn wet conditions at which point the infectious larvae enter hypobiosis inside the stock rather than completing development to adulthood. All the larvae emerge from hypobiosis at the same time in the spring in the gut of the animal causing severe disease, dehydration and death (Ostertagia) and anaemia (Haemonchus) – type 2 is quite rare but need to understand the epidemiology

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26
Q

What is the difference in sheep with regards to haemonchus contortus and other strongyles?

A

sheep do not become resistant in the same way as they do to other strongyles

Different to the other strongyle roundworms of sheep – blood sucker similar to the adult Liver Fluke so causes anaemia, weakness, weight loss and sub-mandibular oedema in chronic cases. Fertility, fecundity, milk yield may all be affected by the infection in the same way as any other debilitating disease

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27
Q

What can you use to treat haemonchus contortus in sheep?

A

Can also use Closantel to treat Haemonchus infections as well as the other BZ, LV & ML groups

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28
Q

What are the different types of disease caused by fasciola hepatica?

A

Different types of disease: PerAcute, Acute and Sub-acute

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29
Q

What is the difference between peracute, acute, sub-acute and chronic infections with fasciola hepatica?

A

PerAcute – Chronic is just the question of dose. The higher the infectious dose of parasite the more severe the damage and the more severe the clinical signs.

PerAcute / Acute – sudden death – diagnosis by post mortem exam (PME)

Sub-acute - rapid deterioration, dull, depressed, sometimes anaemia ….dead – diagnosis by serology/biochem and PME

Chronic – weight loss, anaemia, poor productivity, sometimes submandibular oedema only die after a long slow decline – diagnosis by FEC, coproantigenELISA

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30
Q

What is the cycle for fasciola hepatica – liver fluke?

A
  • Infected sheep drop fluke eggs onto pasture which then infect mud snails
  • The parasite develops in the snail and emerges to contaminate the grazing pasture for the next sheep
  • These first two stages can take 5 weeks to several months depending on the temperature and moisture.
  • Once a sheep has ingested the parasite it migrates from the gut to the liver and completes its development. Migration through the liver destroys liver tissue due to the immune reaction to foreign protein. The more parasites the more damage and the worse the clinical signs
  • In the bile ducts the adults suck blood and starts producing eggs that are passed in the faeces. This takes 10 – 12 weeks.
  • Sheep and cattle never become immune to fluke unlike they do to the roundworms so ewes and cows are as suceptable as lambs
  • But liver size means that for a given dose of fluke a smaller % of liver mass is affected in ewes and cows (bigger livers) compared with lambs
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31
Q

Once the sheep has ingested Fasciola hepatica, where does it migrate to and from?

What causes the immune reaction?

A

Once a sheep has ingested the parasite it migrates from the gut to the liver and completes its development. Migration through the liver destroys liver tissue due to the immune reaction to foreign protein. The more parasites the more damage and the worse the clinical signs

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32
Q

Which parasite can sheep and cattle not become immune to unlike roundworms, so are as susceptible to it as lambs?

A

Sheep and cattle never become immune to fasciola hepatica – liver fluke unlike they do to the roundworms so ewes and cows are as suceptable as lambs

33
Q

Name 6 flukicides

A

Oxyclozanide

Albendazole

Clorsulon (cattle only)

Nitroxynil

Closantel

Triclabendazole

34
Q

Which flukicides have their activity 10 - 14 weeks after ingestion?

(50-70% after 10-11 weeks and 80-99% after 12-14 weeks)

A

Oxyclozanide

Albendazole

Clorsulon (cattle only)

35
Q

Which flukicides have their activity 7 - 14 weeks after ingestion?

(50-90% after 7-9 weeks and 81-99% after 10-14 weeks)

A

Nitroxynil

Closantel

36
Q

Which is the only flukicide that has activity at different stages of fluke 2 weeks after ingestion?

A

Triclabendazole

37
Q

What is one of the most unpredictable parasites in cattle and sheep?

When are peak numbers?

A

Lungworm

One of the most unpredictable parasites, can cause disease at any time in the grazing season but peak numbers of cases in late summer early autumn.

38
Q

What are some clinical signs of lungworm in cattle and sheep?

A

Coughing after any exercise (very few things cause coughing in sheep or cattle) Can cause death very rapidly if large numbers are ingested in a matter of a few days in naïve cattle (unusually calves but occasionally adults is never previously exposed!)

39
Q

What is the best protection for lungworm in cattle and sheep?

A

Vaccination is best protection (the only parasite for which we have a vaccine in the UK), anthelmintic boluses can be effective. Responds well to early treatment.

40
Q

What are some treatment/preventions for lungworm?

A

‘Huskvac’ – vaccinate twice before risk of challenge

Pulse release bolus-possibility of developing immunity between doses – pulses every 2-3 weeks, issue with this is that lungworm has a short PPP so these releases may not be soon enough

Continuous release bolus – continuous protection and no immunity

41
Q

What are we trying to achieve with anti-parasitics on farms?

A
  • Good productivity / profitability i.e. fast growth, high milk yield, high fertility.
  • Good immunity where possible rather than relying on treatment
  • Sustainability = continued efficacy of anthelmintics = delay the development of resistance to the products within the parasite population
42
Q

How can we diagnose parasitic infection?

A
  • Direct Diagnosis
  • Clinical signs
  • Related outcomes
  • Prediction
43
Q

What are the different types of faecel egg count?

A

Floatation for gut worms

Sedimentation for fluke Baermann for Lungworm larvae

44
Q

What can you use for serology to test for parasitic infection?

What is the problem with serology?

A

Fluke (blood and milk)

Roundworms (milk)

Serology indicates previous exposure not necessarily current infection status as the antibodies remain in the animal for months – need to use your clinical judgment

45
Q

What is pre-patent disease and why does this differ for nematodirus?

A

Remember that for Nematodirus, acute and subacute Liver Fluke and Type2 PGE clinical disease is pre-patent so you can’t rely upon finding eggs or even antibodies to diagnose them

So nonspecific biochemical tests such as albumin, fibrinogen, GLDH and plasminogen are all important supportive evidence but not definitive means of diagnosing a problem

Post-mortem is always an important definitive option to go for if appropriate

46
Q

What are the thresholds for faecal egg counts?

A
  • Poor growth and feed conversion efficiency with a FEC >300/350epg
  • Obvious Clinical disease >500 epg
  • Deaths >900 epg
    *
47
Q

What is different for faecal egg counts for haemonchus contortus compared to other strongyles?

A
  • H.controtus is a very fecund worm and will produce many more eggs per adult than the other strongyles so if lambs are not scouring but have a very high egg count then think H.contortus
  • These can be spectated by APHA with a stain specific for H.controtus eggs to differentiate them from other strongyles
48
Q

What is monitoring DLGW?

A

Daily Live Weight Gain (DLWG) = growth rate.

DLWG is high pre-weaning because milk is so nutritious, it then slows down as the lamb matures and is eating grass

49
Q

How is targeted selective treatment an alternative approach to parasite control?

A

Use expected DLWG to work out at any give age of lamb which are underperforming and would potentially benefit from a treatment

50
Q

How is pooled (mob) faecal egg count an alternative approach to parasite control?

A

Use regular (weekly, fortnightly) FEC to track the rise in FEC and predict when a treatment is required

51
Q

What is your clinical responsbility as a vet with regards to parasite control?

A
  1. Your Patient
  2. Your Client
  3. The wider public interest (sheep/cattle industry)

You have to Balance Short term clinical need with Long term sustainability of the treatment efficacy

52
Q

What are some treatment considerations when prescribing an anti-parasitic?

A
  • Efficacy for that farm, the animals and the parasite (eg. Immature fluke and BZ+LV resistant nematodes)
  • Withdrawal period for the class of animal being treated. – always check the datasheet!!
  • Administration route and owner compliance.
  • Resistance and long term effects. Eg ML’s for Sheep Scab.
53
Q

What is the difference between persistent vs short acting products for parasite control?

A

Only a small number of persistent products

Moxidectin, Doromectin… (and Closantel for H.contortus only) – persistnet for up to 120 days?

Other products are short acting so re-infection can occur rapidly.

Resistance present to all anthelmintics and Flukicides in the UK but the status of individual farms varies hugely

54
Q

What are the different anthelmintic product classes?

A
  • BZ (Group 1) (white) >85% flocks have resistance – still good for Nematodirus on most farms (a few cases of resistance)
  • LV (Group 2) (Yellow) increasing resistance rapidly.
  • ML (Group 3) (Clear) Some resistance found in sheep and a few cattle units.
  • AD (group 4) Orange (‘Zolvix’ monepantel) no resistance yet, useful for extending the life of Group 1,2,3.
  • SI (group 5) Purple (‘Startect’) dual active product 50% ML abermectic 50% spiroindol – derquantel.
55
Q

What are the principles of prescribing parasite control?

A

Use as narrow spectrum product as possible to avoid unnecessary resistance selection in other (‘off-target’ species).

56
Q

Will you ise triclabendazole or Albendazole for Liver fluke in adult ewes in May?

A

ALBENDAZOLE – keeping the triclabendazole for when we have acute liver fluke emergencies type thing

57
Q

What is anthelmintic resistance and how does it come about?

A

The more often you treat the more selection events giving to the parasite

Only expose the minimum number of parasites to a selection event by targeting your treatments to only those animals that need it.

58
Q

Why should you discourage whole flock/group treatments?

A

Maintain an in-regugia population that is not exposed to treatment, this will dilute the eggs produced by AR worms. Whole flock or whole group treatments to be discouraged.

59
Q

How can you use non-chemical control to control parasites?

A

Avoid the parasite with rotational grazing

60
Q

What do we need to know before we can make a parasite control plan?

A

•Susceptibility of the animals on the farm:

–Age, time of year, grazing history, nutritional status, stocking density.

•Parasite status on the farm:

–Present or absent esp Haemonchus, Fasciola

–Anthelmintic resistance status to BZ, LV, ML, TBZ

•Risk assessment of the available pasture:

–Clean grazing (silage aftermaths, new leys)

–Prior weather conditions and forecast.

61
Q

What are some threats you can consider when making a parasite control plan?

A

List all the parasites of importance so you are sure you will not miss out something important.

Rank them in order of priority and chronology based on the flock or herd management to make the plan clear for the client.

62
Q

What is the most appropraite parasite control plan for nematodirus?

A

FEC’s not useful but strategic prophylactic treatment with a BZ based on the timing of the larvae peak is appropriate

63
Q

What is the most appropraite parasite control plan for Trichostrongyles and Telodorsagia?

A

Regular, routine FEC and DLWG monitoring and treatment only at a threshold epg is the most effective method (TST) to prevent disease and minimise resistance.

64
Q

How does anthelmintic resistance come about and how can we overcome it?

A

The more often you treat the more selection events giving to the parasite – idea of trying to reduce the selection pressure:

Only expose the minimum number of parasites to a selection event by targeting your treatments to only those animals that need it.

65
Q

Explain what each section of this graph means with regards to anthelmintic resistance

A

Doesn’t suddenly occur – a slow build up process

Have those genes occurring as a random mutation in parasite, then transfers resistance over time as they are selected for – things will increase selection pressure

In green zone – don’t notice too much difference in terms of anthelmintic effectiveness and no clinical difference

Over time – resistance builds up, go into orange area, where get greater level of resistance and starting to impact on efficacy of anthelmintics and may see subclinical disease –reduction in performance

Eventually selection pressures continue, go into red zone – resistance becomes obvious, greater than 50% resistance – notice clinically that seeing reduction in efficancy of anthelmintics and reports of drenches not working – end stage

Want to try and intervene at early on and idea is that we extend the life od the products and efficacy

66
Q

What kind of worm population do you want to maintain?

A

Maintain an in-regugia population that is not exposed to treatment, this will dilute the eggs produced by AR worms. Whole flock or whole group treatments to be discouraged. Where are the worms and what are we exposing

Over summer – have less of parasite burden in ewes compared to lamb on pasture

Winter – find in refugia population is greater in ewes compared to pasture, lambs have gone by this stage so don’t provide us with population anymore. Need to deice which animals to treat and when

67
Q

How can you test for anthelmintic resistance?

A

Huge problem!!! Important we try and reduce selection pressures to reduce AR

Easy to test for

  • FECRT on lambs with a high starting FEC (>500epg)
  • Individual samples
  • Drench accurately the three groups each with a different group
  • Resample at 7days (LV) and 10-14 days (BZ,ML)
  • Less than 95% reduction in FEC = resistance
  • Less than 50% reduction in FEC = obvious drench failure

BZ – 100% AR found, drench failure high

Drench failure seen across all groups

Small proportion that are resistant to all 3 of these products.

68
Q

What are 4 things that drives anthelmintic resistance?

A
  1. Buying in resistant worms. Buying in stock – essentially buying in other peoples history and their use of anthelmintics on their farm and potentially their problems as well!
  2. Under dosing individuals. Don’t worry about over-dosing, not much of an issue.
  3. Over treating the population
  4. Allowing resistant worms the chance to dominate, don’t want to give them reproductive advantage
69
Q

How can you prevent anthelmintic resistance with buying in resistant worms. Buying in stock – essentially buying in other peoples history and their use of anthelmintics on their farm and potentially their problems as well!?

A

Quarantine treatments for purchased stock (Combination of Monepantel & Moxidectin on quarantine). Put into environment where they will pick up parasites from that particular farm so they are the same level as the others on that farm

70
Q

How can you prevent anthelmintic resistance with under dosing indivduals - what can you change?

A

Don’t worry about over-dosing, not much of an issue.

Dose for the heaviest in the group and calibrate equipment so that it is accurately dosing

71
Q

When you have over treating the population as a driver and AR - how can you prevent this?

A

Minimise number of treatments (base treatment decisions on FEC, DLWG, TST)

72
Q

What are 6 ways you can prevent anthelmintic resistance?

A
  1. Quarantine treatments for purchased stock (Combination of Monepantel & Moxidectin on quarantine). Put into environment where they will pick up parasites from that particular farm so they are the same level as the others on that farm
  2. Dose for the heaviest in the group and calibrate equipment so that it is accurately dosing
  3. Minimise number of treatments (base treatment decisions on FEC, DLWG, TST)
  4. Administer the correct (narrow spectrum) product correctly!
  5. Dilute out any AR worms (in refugia population) – flock dosing of ewes at tupping will put big selection pressure on as all we are left with after dosing is resistant worms, which give resistant eggs which go on to contaminate the pasture for the following season
  6. Use non-chemical means of control (including clean grazing) -
73
Q

How can you avoid parasite burden with rotational grazing?

A

Lambing field, highly contaminated – we can then use other grazing lands to try and avoid this contamination, so at 3-4 weeks before lambs graze, remove from contaminated field to pre-weaning and then do the same again to post-weaning field

So basically avoiding the contamination!

Depending on if the farm ahs appropriate fields for them to do this

Can also then: Rest lambing field or cut for hay or silage or put lambs back onto it after the hay or silage aftermath

74
Q

How can you use different grazing crops as a method of non-chemical control?

A

Kale, Stubble turnips, Forage Rape can all be used to fatten lambs after weaning. Depending if it fits with clients system. Can be used to fatten lambs after weaning. Idea behind this in terms of reducing infectious burden in lambs I that on the grass, larvae can crawl out of grass easier compared to some of these forages – can help to reduce infection.

75
Q

How can you enhance the ability to fight infection as a non-chemical control method?

A

Provide extra protein and energy – by using reseeded, highly nutritious grasses and clovers (red or white clovers) – not possible on very harsh hill farms and also quite expensive to establish the crops and requires more skill to manage. Immune system is important – try and provide extra protein and energy through nutritious grasses and clovers – farm depend, cost associated with it and can be more diffiuclt to manage sometimes.

Use crops with anthelmintic chemical properties such as high tannins – e.g. chicory and sainfoin – similar difficulties with management and establishment

Reduce reliance on grazed Dry Matter i.e. provide creep – this is an expensive option! Need a high lamb price to justify it – more intensive system and much higher cost option – means we are going to have to finish the lambs quickly and high lamb price to justify it!

76
Q

What do we need to know before we can make a parasite control plan?

A

•Susceptibility of the animals on the farm:

–Age, time of year, grazing history, nutritional status, stocking density.

•Understanding the parasite status on the farm:

–Present or absent esp Haemonchus, Fasciola

–Anthelmintic resistance status to BZ, LV, ML, TBZ

–Are they a problem on this farm?

–Test for whether they are an issue on this particular farm

•Risk assessment of the available pasture:

–Clean grazing (silage aftermaths, new leys) – is this an option?

–Prior weather conditions and forecast – can predict the parasite problems ahead, influence when risk periods occur for different parasites

77
Q

What monitoring is available for parasite control monitoring?

A

FEC (sedimentation, floatation)

Larval count (lungworm) – Baermann

Antibody and coproantigen ELISA’s - primarily for fluke

How and when to monitor depends on the parasite:

Eg. GI nematodes – regular sampling of a group via a pooled faecal sample from first grazing until sale or immunity is established. Cheap, easy way to monitor where we are at

78
Q

What are some considerations when prescribing an anti-parasitic?

A

–Efficacy for that farm, the animals and the parasite (e.g. Immature fluke and BZ+LV resistant nematodes)

–Withdrawal period for the class of animal being treated, when will they be slaughtered??. – always check the datasheet!!

–Administration route and owner compliance.

–Resistance and long term effects. Eg ML’s for Sheep Scab.