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Module 18 Wk2 Flashcards

1
Q

(The mechanics of ewe obstetrics)

Why is lambing time care important?

A
  • ewe losses
  • lamb losses, scanning
  • ewe welfare
  • lamb welfare
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2
Q

What are the pros of outdoor lambing?

A
  • usually more hygienic
  • ewes more relaxed
  • less mis-mothering
  • less labour - 1 shepherd to 600-1000
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3
Q

What are the cons of outdoor lambing?

A
  • harder to catch ewes and lambs
  • predation/crows
  • risk of hypothermia
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4
Q

What are the pros of indoor lambing?

A
  • Easier to handle ewes and lambs
  • Close monitoring 24hrs per day
  • Nutrition easier to manage
  • Less reliant on weather
  • Less hypothermia
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5
Q

What are the cons of indoor lambing?

A
  • Increased risk of infectious disease
  • Poor ventilation = more pneumonia
  • Ewes can lie on lambs
  • More labour: 1 shepherd to 250–300 ewes
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6
Q

What are the main signs you are looking for with dystocia?

A
  • obvious malpresentation
  • discomfort
  • unproductive straining
  • discolouration of the birth fluids
  • parts of lambs protruding
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7
Q

How can you minimse damage to the ewe when intervening at lambing?

A
  • lube
  • don’t rush
  • gentle manipulation
  • avoid excessive treaction
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8
Q

What situations would you treat dystocia by foeatal manipulation and manual extraction?

A
  • correctable malpresentation
  • tangled/multiple lambs
  • No foetomaterna disproportion
  • No severe deformities
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9
Q

What sitauations would you treat dystocia via a foetotomy?

A

not reaaly feasible in sheep but rotton lambs

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10
Q

What sitauations would you treat dystocia via a caudal epidural, manual manipulation?

A
  • ewe appears painful
  • significant manipuation required
  • dead lamb with only slight disproportion
  • episiotomy needed
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11
Q

If there is no progress with lmabing within 15mins what should you do?

A

caesar

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12
Q

What other reasons other than no progression would you opt for caesaring the sheep?

A
  • foetomaternal disproportion
  • prosterior presentaion plus large lamb or small pelvis
  • vag prolapse
  • severe deformaties
  • unresponsive ringwomb
  • unresponsive uterine torsion
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13
Q

What are the causes of dystocia?

A
  • abnormal foetal placement
  • foeto-maternal disproportion
  • maternal structural.functional factors
  • deformaties
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14
Q

What is the relative fetomaternal disproportion as a result of?

A

From the ewe having a small pelvis

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15
Q

What age of sheel is relative foetaomaternal disproportion commonly seen in?

A

ewe lambs - lambing at 12months

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16
Q

What is uterine inertia?

A

Failure of the UTERUS to contract with normal strength, duration, and intervals during childbirth

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17
Q

Who is uterine internia common in?

A

Older ewes

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18
Q

What could cause uterine inertia?

A
  • lack of energy
  • lack of Ca
  • over-stretching of uterus
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19
Q

What is ringwomb?

A

Cervix less than 5cm dilated 2 hours into 2nd stage of labour

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20
Q

What are the possible causes of ring womb?

A
  • prematurity/abortion
  • distrubance in 1st stage of labout
  • malpresentation
  • Ca deficiencyy
  • inflammation/scarring from prolapse/historical injuries
  • exogenous oestrogens (fungal in feed)
  • poor initiation of parturition by lamb
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21
Q

How do you treat ringwomb?

A
  • Ca injection
  • attempt manual dilation but risk trauma
  • Hormonal
  • caesar
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22
Q

What are examples of infections that can cause structural issues/deformaties in lambs?

A

schmallenburg or Blue-tongue virral disease

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23
Q

Describe how you would manually extract a lamb?

A
  • gently and steady
  • LUBE
  • Angle of lamb
  • clear airways
  • check for any more lambs
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24
Q

What drugs should you use before performing a sheep caesar?

A
  • Ab cover
  • Anti-inflammatory
  • Local ana
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25
Q

What drug and ehy should you used after sheep caesar?

A

oxytocin - shrinks the uterus and encourage milk let down

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26
Q

What should be involved in caesarean section aftercare?

A
  • colostrum to lambs
  • ensure ewe can stand
  • ask far er to check for vag discharges and retained foetal mem and monitor for wound swelling
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27
Q

when should sheep caesar sutures come out?

A

2-3weeks

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28
Q

How can you prevent dystocia via selection?

A
  • Cull ewes after difficult lambings
  • dont keep daughters fro breeding
  • select rams for easy lambing traits ie no too big
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29
Q

How can you prevent dystocia via nutrition?

A
  • BCS = 2.5-3.5
  • dont under or over feed in last tri
  • feed at the same time
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30
Q

What are the key risk factors that contribute to vaginal prolapses in sheep?

A
  • BCS
  • Low blood Ca
  • Breed predisposition
  • short tail docking
  • lack of exercise
  • multiple foetuses
  • older ewes
  • Lameness
  • Bulky feed
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31
Q

Why should you lift the vaginal prolapse of sheep?

A

to allow urination and to check for lambing

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32
Q

What medication can you use when treating a vaginal prolapse in sheep?

A
  • Caudal epidural
  • Abs and NSAIDs
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33
Q

What dosage of lidocaine and xylazine should you use for caudal epi in vag prolapse sheep?

A
  • lignocaine = 1-2ml
  • xylazine = 0.25ml
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34
Q

Describe after mediating how to perform a vaginal prolapse replacementt

A
  • wash prolapse with dilute disinfectant
  • replace gently - use lube and flat parts of your hands
  • apply buhners suture
  • mark for culling
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35
Q

Describe the aftercare of a vaginal prlapse in sheep?

A
  • Close monitoring for lambing to open sutures
  • Monitor for excessive straining
  • Potentially cont anti-inflam
  • Warn cervix may not open fully
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36
Q

How can you prevent vaginal prolapses in sheep via nutrition?

A
  • scan ewes to enable targeted feeding
  • target BCS 2.5-3.5
  • Maintain blood Ca
  • avoid root crops in late preg
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37
Q

Why is effective housing important for prevention of vag prolapses in sheep?

A

So the obtain sufficient exercise

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38
Q

What can be sequelae to a vaginal prolapse?

A
  • abortion
  • urinary retention
  • infection/necrosis of vaginal wall
  • incomplete cervical dilation
  • evisceration through a tear
  • death to lambs
  • death to ewe
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39
Q

What is metritis?

A

Severe infection of the uterus

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40
Q

What are the key risk factors of metritis?

A
  • causative agents
  • unhygienic lambing
  • dead lambs
  • some abortive agents
  • uterine prolapses
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41
Q

What are signs of metritis?

A
  • signs of toxaemia = depression, inappetence and congested MM
  • Red/brown/purulent and smelly vulval discharge
  • vulval swelling
  • angry lambs as milk production decreased and unwilling to stand
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42
Q

How do you go about treating metritis?

A
  • oral or IV fluids
  • Systemic, broad spec Abs
  • NSAIDs
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43
Q

What are concurrent diseases that make metritis treatment response poor?

A
  • retained foetus or membranes
  • mastitis
  • vaginal rupture and peritonitis
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44
Q

What are the signs of mastitis in ewes?

A
  • abnormal gait
  • sick ewe = inappetence, isolation, depressed
  • Udder can be hot or cold, swollen +/- hard and discoloured
  • hungry lambs
  • watery, clotted or blood tinged milk
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45
Q

What are predisposing factors for mastitis?

A
  • Mostly within first 3 weeks of lactation
  • Inadequate nutrition - Hungry lambs
  • Orf
  • Teat trauma
  • Poor hygiene
  • Cold winds
  • Poor conformation
  • Young ewes
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46
Q

What are common causative agents of mastitis?

A
  • mannheimia haemolytica
  • staphylococcus aureus
  • coagulase-negative staphylococcus spp.
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47
Q

Describe the Cx of subclinical mastitis

A

leads to reduced milk yield and so slower lamb growth rates. It is more common as ewes get older, and in ewes of 4 years or more the effect of sub-clinical mastitis is more marked, with lambs growing more slowly and often needing supplementary feed.

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48
Q

Describe the Cx of acute mastitis

A

Ewes with acute mastitis are noticed because they do not come to the trough to eat, stand away from the flock, appear lame because of a painful udder and often refuse to let their lambs suckle. The affected udder can be hot, swollen and painful, or cold and discoloured. Milk might be watery or pussy or contain blood

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49
Q

Describe the Cx of chronic mastitis

A

Chronic mastitis can be detected as lumps, or masses, in the udder that feel different from normal udder tissue. The masses are abscesses caused by bacteria or fibrosis; they can be any size or shape. They can rupture and reform, so may not be present every time the udder is palpated.

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50
Q

Describe the Cx of gangerous mastitis?

A

The udder is often cold, hard, purple to black in colour and ewes are systemically unwell and often die of toxaemia. For those that survive, recovery is slow and they remain in poor body condition for a prolonged period. The udder never returns to function.

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51
Q

How to treat acute mastitis?

A
  • Clean and milk out
  • Abs - LA amocicillian and tilmicosin
  • Anti-inflam
  • Fedd the lambs
  • if gangrenous = IV/Oral fluids or kill it
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52
Q

How can you prvent mastitis?

A
  • Nutrition and control of BCS
  • Good hygiene
  • Orf prevention
  • cull/select ewes
  • prevent cold exposure
  • feed lambs when milk low
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53
Q

what ewes is pre-pubic tendon ruptures more common in?

A

Ilder multigravid ewes in late pregnancy

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54
Q

What clinical signs does pre-pubin tendon ruoture present with?

A
  • swelling of lower left abdomen just cranial to pubis
  • difficulty moving/feeding
  • extensive ventral oeadma
  • ventral displacement of uterus
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55
Q

(Flock Metabolic and Nutritional conditions)

What body condition score should ewes be when weaning takes place?

A

2-2.5

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56
Q

What body condition score should ewes be when tupping happens?

A

2.5-3.5

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57
Q

T/F stress in the first 21 days post fertilisation may cause early embryonic loss

A

true

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58
Q

What is the BCS allowed to drop by in the second trimester?

A

half = 2-3

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59
Q

How much foeatal growth takes place in the third trimester?

A

75%

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60
Q

How should you group ewes in last trimester?

A

According to energy need

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61
Q

How can you monitor the nutritional status of the ewe?

A
  • BCS
  • WEighing
  • Metabolic profiles
  • Lamb birth weight
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62
Q

What is the energy maintenance for a newe?

A

8-11MJ

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63
Q

What is the energy requirement for a ewe in late preg?

A

19MJ

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64
Q

What is the energy requirement of a ewe peak lactation?

A

30MJ

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65
Q

What are periparturient diseases in sheep?

A
  • Abortion
  • Pregnancy toxaemia
  • Hypocalcaemia
  • Hypomagnesemia
  • (Listeriosis)
  • (Septicaemia)
  • (Johne’s, OPA and all the other usual suspects)
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66
Q

How is preg toxaemia (twin lamb) caused?

A

Inadequate energy uptake coupled with excessive energy drain
- Ruman size decreases due to increasing uterine size which reduced feed intake
- energy demand is increased tho due to increasing lamb size

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67
Q

What is the primary disease of preg toxaemia?

A

hypoglycaemic encephalopathy

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68
Q

What are the later compounds of pregnancy toxaemia?

A

hyperketonemia

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69
Q

What is the clinical presentation of pregnancy toxaemia?

A
  • Inappetence
  • dull, weak and lethargic
  • Neuro signs ie blindness, head tilt, head pressing, tremor, convulsions, depression, recumbence.
  • diarrhoea
  • death
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70
Q

How do you treat twin lamb?

A
  • glucose
  • glucogenic precursors
  • fluids
  • Ca?
  • appetite stimulants
  • treat dx
  • remove lambs
  • insulin
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71
Q

What ewes are at risk of pregnancy toxaemia?

A

Any ewe with an energy intake/requirement mismatch

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72
Q

What are common results (subclinical disease) of preg toxaemia?

A
  • decrease in lamb birthweight
  • decrease is lamb viability
  • decrease in mothering ability
  • decrease in colostrum quality
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73
Q

How can you prevent preg toxaemia?

A
  • Group ewes according to feed requirements
  • good quality roughage
  • concentrate
  • control concurrent dx
  • scan ewes and use raddle marks
  • regular condiction scoring
  • metabolic profiling
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74
Q

How do ewes end up with hypocalcaemia?

A

Demand exceeds supply
- increase in demand for foetal bone
- decrease in availability

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75
Q

What are early clinical signs of hypocalcaemia?

A
  • staggering gait
  • weakness
  • tremor
  • sluggish PLR
  • tachycardic
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76
Q

What are the late clinical signs of hypocalcaemia?

A
  • tachypnoea
  • recumbancy
  • death
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77
Q

How do you treat hypocalcaemia?

A
  • 50ml 40% Ca borofluconate IV
  • Mg?
  • avoid stress in late gestation
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78
Q

What are the clinical signs of hypomagnesaemia?

A
  • Mostly sudden death
  • Anxiety, hyperaesthesia/tachycardia
  • Unsteady gait, staggering
  • Apparent blindness
  • Nystagmus
  • Recumbency (+ paddling)
  • Opisthotonus
  • Hypersalivation (frothing at mouth)
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79
Q

How do you diagnose hypoglycaemia?

A
  • Clinical signs and history- otherwise the ewe will die
  • Pre-treatment bloods to confirm diagnosis if there is a treatment failure
  • Anterior or posterior chamber Mg 2+ level as part of a PM (this is easy)
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80
Q

How do you go about treating hypomagnesaemia?

A
  • 50 ml 25% MgSO4, SC multiple sites (skin necrosis: not IV)
  • Also CBG, IV or SC
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81
Q

How do you prevent hypomagnesaemia?

A

Mg supplementation via

  • rumen bolus
  • in concentrates
  • Mg licks/’buckets’ (variable intake)
  • top dressing pastures with calcined magnesite
  • Drinking water
  • Do not use potash fertilisers in spring
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82
Q

(Introduction to ruminant parasites and their pathology)

What is the 3-word statement associated with control of parasites in ruminants?

A

Test dont guess

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83
Q

Why is parasitology important in farm management?

A

It plays a key role in controlling diseases, improving animal health, and ensuring economic productivity.

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84
Q

How does grassland management impact parasitology?

A

Proper pasture rotation and grazing management help reduce parasite burdens.

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85
Q

What role does ecology play in farm management?

A

It helps understand parasite life cycles and transmission dynamics in different environments.

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86
Q

What are the three main types of helminths in ruminants?

A

Nematodes, Trematodes and Cestodes

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87
Q

What type of helminth are roundworms?

A

nematodes

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88
Q

what type of helminth are flukes

A

Trematodes

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89
Q

What type of helminth are tapeworms?

A

cestodes

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90
Q

What are the two major groups of arthropods that parasitize ruminants?

A
  • insects and arachnids
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91
Q

Give two examples of parasitic insects in ruminants

A

Lice and flies

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92
Q

Give two examples of parasitic arachnids in ruminants

A

ticks and mites

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93
Q

What parasite is responsible for causing cryptosporidiosis?

A

Cryptosporidia

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94
Q

What parasite causes babesiosis in ruminants

A

babesia

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95
Q

Which parasite causes theileriosis in rumininats

A

Theileria

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96
Q

What protozoan parasite is assocaited with abortion in cattle

A

Neosporin

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97
Q

Which protozoan parasite is linked to repro failure and fetal abnormalities

A

toxoplasma

98
Q

(Nematodes in cattle)
Describe the lifecycle of gur and lungworms in cattle?

A
  • The parasitic stage is in the animal and reasonable constant
  • Free-livong stage where the envroment influences behaviour so can be very variable
99
Q

What is Parasitic Gastroenteritis (PGE)?

A

A disease caused by gutworms, affecting cattle, particularly young stock.
Leads to reduced growth rates, poor performance, and clinical illness in severe cases

100
Q

Key Gutworms Causing PGE in Cattle

A

Ostertagia ostertagi (abomasal parasite)

Cooperia spp. (small intestinal parasite)

101
Q

Describe the abomasal Damage by O. ostertagi?

A

Reduced hydrochloric acid (HCl) secretion
Increased gastrin secretion
Failure to convert pepsinogen to pepsin
Increased blood pepsinogen levels

102
Q

What does reduced HCL secretion lead too?

A

Increased abomasal pH

103
Q

What does increased gastrin secretion lead too?

A

Higher blood gastrin level

104
Q

What does failure to convert pwpsinogen to pesin lead too?

A

Poor digestionW

105
Q

What does increased blood pesisnigen levels lead too?

A

Indicator of ostertagia infection

106
Q

What are the symptoms of clinical paratism?

A

Diarrhoea and ill thrift

107
Q

When does clinical parasitism effect yearlings?

108
Q

What does subclinical parasitic PGE cause?

A

Poor/uneven growth without obvious clinical signs?

109
Q

How long does immunity take with cooperia?

A

One full grazling season

110
Q

How long does immunity take to build up agains ostertagia?

A

two full grazing seasons

111
Q

What are the effects of immunity on worm biology?

A
  • decreased egg production
  • stunted egg growth
  • expulsion of adult worms
  • limited establishment of new larvae
112
Q

What are factors effecting larval development and spread

A
  • invertabrates
  • dung = stock movement, footwear, harrowing
  • weather = rain and water dispersion
113
Q

Describe PGE larvae survival on pasture

A
  • Most disappear within 12months
  • some survive up to 24 months
114
Q

What can act as a reservior for PGE larvae?

A

soil babes

115
Q

What happens to infective ostertagiosis larve when ingested in late summer/autumn?

A

They become dormant in the stomach

116
Q

Are inhibited larve able to cause any damage or immune response?

A

No, they are metabolically inactive

117
Q

When do the inhibited ostertagious larvae resume development?

A

late winter leading to severe disease if many mature at same time

118
Q

Why are weaned dairy calves at a high risk of exposure to PGE?

A

becuase of the seasonal larval contamination

119
Q

Why are beef suckler calves less exposed to PGE in their first season?

A

Due to low pasture contamination but greater risk in second season

120
Q

Describe the pros and cons of faecal egg count as a stratagy for helminth control

A

Pros - easy and cheap, indicated pasture contamination and heps assess wormer effectiveness
Cons - does NOT indicate actual worm burden or clinical disease

121
Q

What should integratd parasite control system include?

A
  1. grazing management
  2. appropriate use of wormers
  3. resistant/resilient stock
  4. vaccination
  5. monitoring stock
122
Q

How can you manage grazing to reduce larval challange?

A
  • newly sown grass fields
  • grass re-growth after silage/hay
  • mixing livestock grazing
  • multispecies swards
  • rotational grazing
  • deferred grazing
123
Q

What colour are Group 1 - benzimidazoles in cattle ?

124
Q

What are examples of benzimadazoles?

A

Albendazole, Fenbendazole.

125
Q

What colour are group 2 - levamisole anthelmintics forcattle?

126
Q

What colour are group 3 - macrocytic lactones anthelmintics for cattle?

127
Q

How is targeted selective treatment (TST) used for PGE control?

A
  • Monitors Daily Live Weight Gain (DLWG).
  • Reduces anthelmintic use while maintaining performance.
128
Q

At what daily live weight gain should you treat for PGE?

A

Treat if DLWG <0.75kg/day.

129
Q

Why is housing treatment important for parasite control?

A
  • Eliminates gutworms acquired during grazing.
  • Prevents Type II Ostertagiosis.
  • Reduces pneumonia risk.
  • Stops pasture contamination in spring.
130
Q

What is the main lungworm species affecting cattle?

131
Q

What is the main lungworm species affecting cattle and what doe sit cause?

A

Dictyocaulus viviparus.

Causes parasitic bronchitis (“Husk/Hoose”).

132
Q

What are the clinical signs of lungworm in young cattle?

A

Coughing, respiratory distress, possible death.

133
Q

What are the clinical signs of lungworm in dairy cattle?

A

Sudden drop in milk yield, depression.

134
Q

What are subclinical signs of lungworm in cattle?

A

Poor performance

135
Q

What are the main sources of lungworm larvae?

A
  • Overwintered larvae on pasture.
  • Carrier animals (5% of lungs in Feb/March contain worms).
  • Inhibited larvae that reactivate in spring.
136
Q

How does lungworm immunity work?

A
  • First-line defence (Prevents larvae from reaching lungs – lasts ~6 months).
  • Second-line defence (Destroys larvae in lungs – lasts >24 months).
137
Q

How is lungworm vaccination done?

A

Two doses, 4 weeks apart.

138
Q

When should you start vaccinating for lungworm in cattle?

A

8 weeks old in healthy calves

139
Q

Whne should you turn out after second dose?

A

at least two weeks after

140
Q

What should you avoid use of until 2 weeks after second dose of lungworm vaccination?

A

anthelmintics

141
Q

What are common causes of lungworm treatment failure in the individual animal?

A

Secondary infections.
Irreversible lung damage.
Reinfection syndrome.

142
Q

What are common causes of lungworm treatment failure interms of group disease?

A

At pasture: IBR, other respiratory infections.
After housing: Bovine Respiratory Disease (BRD) complex.

143
Q

What are the three main strategies for lungworm control?

A
  • Anthelmintics (e.g., ivermectin-based treatments).
  • Vaccination (pre-turnout immunization).
  • Grazing management (reduce larval exposure).
144
Q

(nematodes in sheep)

What are the shared characteristics of Sheep GI nematodes?

A
  • Direct life cycle
  • Require warm and moist conditions for environmental stages
  • Cause similar clinical signs (weight loss, diarrhoea)
  • Resistance is species-specific and anthelmintic class-specific
145
Q

What are the key differences between sheep GI nematodes?

A

Climatic preferences – Slight variations in climatic conditions mean some species are dominant at different times of the year.
Anatomical location – GI nematodes affect different parts of the gastrointestinal system:
Clinical presentation – Some GI nematodes cause anaemia (H. contortus), while others cause diarrhoea and weight loss (T. circumcincta).
Life cycle differences – Some species, like N. battus, have different hatching patterns or life cycles.

146
Q

Why are GI nematodes important in sheep farming?

A
  • Animal welfare impact
  • Productivity losses – Reduced growth and feed intake.
  • Financial impact
  • Environmental – Overuse of anthelmintics can lead to resistance, which impacts long-term farm sustainability.
147
Q

What are the clinical signs of Parasitic Gastroenteritis (PGE) in sheep and why?

A
  • Reduced weight gain
  • Poor body condition
  • Diarrhoea
  • Dehydration
  • Death
148
Q

What are the causes of PGE clinical signs in sheep?

A
  • anorexia
  • GIT inflammation due to immune response
  • Mucosal damage
  • malabsorption
149
Q

What factors influence the severity of GI nematode infections in sheep?

A
  • Species of nematode – Some cause more severe disease
  • Worm burden – Higher infection levels result in greater clinical disease.
  • Host immunity – Younger sheep and stressed animals are more susceptible.
  • Morbidity rates – Typically high in affected flocks.
  • Mortality risk – Can be high in untreated cases, particularly in lambs.
150
Q

What are the differential diagnoses for GI nematode infections in sheep?

A

Coccidiosis
Nematodirosis
Trace element deficiencies – Cobalt and selenium deficiencies c
Dietary issues – Lush pasture, poor nutrition

151
Q

How are GI nematode infections diagnosed in sheep?

A

Clinical signs
Faecal Worm Egg Count (FWEC)
Post-mortem examination
Pepsinogen test – Elevated in some GI nematode infections
FAMACHA scoring – Assesses anaemia levels in Haemonchus contortus infections.

152
Q

How does the Faecal Worm Egg Count (FWEC) help in diagnosis?

A

Estimates pasture contamination
Detects infection patterns
Identifies Nematodirus battus

153
Q

What are the limitations of faecal worm egg count?

A

Cannot differentiate Trichostrongylus species.
Egg counts do not always correlate with clinical severity.

154
Q

What are the main classes of anthelmintics used to treat GI nematodes in sheep?

A

Broad-spectrum:

  • Benzimidazoles (White drenches)
  • Levamisole (Yellow drenches)
  • Macrocyclic lactones (Clear drenches)

Narrow-spectrum:
- Closantel, Nitroxynil – Target Haemonchus contortus.

155
Q

What is hypobiosis in GI nematodes, and why is it important?

A

Hypobiosis – The arrested development of larvae inside the host when conditions are unfavorable (e.g., winter).

Importance:

  • Allows worms to survive until optimal conditions return.
  • Leads to Peri-Parturient Rise (PPR), where larvae re-emerge in pregnant ewes, contaminating pasture.
156
Q

What strategies can help manage anthelmintic resistance in sheep?

A

Refugia-based control – Leaving a proportion of untreated worms to maintain susceptible populations.

Avoid “Dose and Move” strategy – Can accelerate resistance development.

Targeted Selective Treatment (TST) – Treat only high-burden animals based on FWEC and body condition.

Quarantine protocols – Prevent introducing resistant worms from newly purchased stock.

157
Q

What are the causes of peri-parturient rise (PPR)?

A
  • Development of hypobiotic larvae into laying adults
  • Increased susceptibility to further infection from pasture
  • Increase in fecundity (egg shedding) of adult female worms
158
Q

Why does immunity reduce in peri-parturient ewes?

A

Likely due to physiological changes associated with pregnancy, including redistribution of nutrition to fetal development and milk production.

159
Q

Why is understanding the lifecycle of GIN important?

A
  • Helps understand the annual cycle of infection
  • Recognizes climatic conditions that impact infections
  • Evaluates effects of recent pasture management
160
Q

How does diagnosis of GIN help?

A

Identifies seasonal infection patterns
Aids in treatment timing
Monitors pasture contamination

161
Q

What are the primary control strategies for GIN?

A

Grazing management (rotation, safe pasture)
Timing of treatments to match lifecycle and resistance management

162
Q

How is resistance managed in GIN?

A

Timing of post-treatment testing
Maintaining effective refugia

163
Q

How can anthelmintic resistance be reduced?

A

Avoid “dose and move”, especially onto clean pasture
Increase dosing intervals
Leave a proportion of animals untreated
Use quarantine measures to prevent introduction of resistant worms

164
Q

How can lambs’ exposure to GIN be reduced?

A
  • Improve immunity via nutrition and selective breeding for resistance
  • Use of clean/safe grazing
  • Anthelmintic treatments
165
Q

What are the different anthelmintic treatment approaches for lambs?

A
  • Regular routine treatments (every 3-4 weeks)
  • Therapeutic treatments (FWEC-guided)
  • Targeted selective treatments (treat only high-risk individuals)
  • Reducing pasture contamination through strategic deworming
166
Q

What factors contribute to immunity in lambs?

A

Some exposure to GIN is necessary for immune development
Barbervax vaccine: Effective but not self-boosting
IgA testing to monitor immune response

167
Q

How do lambs respond to GIN infection?

A

Resistance: Low burdens and egg output
Resilience: High growth rates despite GIN infection

168
Q

What tests can detect anthelmintic resistance?

A

In vivo tests
- Faecal Egg Count Reduction Test (FECRT)
- Drench test
In vitro tests

169
Q

What factors must be considered in resistance testing?

A

Prolonged activity of the anthelmintic used
Prepatent period (PPP) of the worm species

170
Q

What is the location, clinical signs, sequelae and time of year for teladorsagia circumcincta

A
  • location = abomasum
  • Cx = scour, loss of appetite
  • Sequelae = hypoproteinemia
  • Time = summer
171
Q

What is the location, clinical signs, sequelae and time of year for trichostrongylus spp

A
  • Location = prox small intestines
  • Cx = dark scour, anorexia, poor growth and chronic ill-thrift
  • Sequelae = protein leakage, electrolyte imbalances
  • Time = late summer/autumn/winter
172
Q

What is the location, clinical signs, sequelae and time of year for Haemonchus contortus

A
  • Location = abomasum
  • Cx = acute watery scour, dehydration, rapid weight loss, death
  • Time = spring +/- autumn
173
Q

(Anthelmintic Resistance)

What is the most common gastrointestinal parasite of sheep in the UK?

A

T. circimcincta

174
Q

What is the most important gastrointestinal parasite of sheep worldwide?

A

H.contortus

175
Q

How do benimidazoles work?

A

They bind to B-tubulin

176
Q

How does levamisole work?

A

It is a nicotinic acetylcholine receptor agonist

177
Q

How do ML work?

A

Via glutamate-gated choline receptor agonists

178
Q

What is resistance?

A

A heritable reduction in the sensitivity of a parasite population in the action of a drug

179
Q

How does resistance arise?

A

Anthelmintic resistance arises when repeated or improper use of dewormers allows resistant worms to survive and reproduce, leading to a population that no longer responds to treatment. Factors include frequent use of the same drug, under-dosing, and lack of refugia (untreated worm populations).

180
Q

How are parasites highly adaptable?

A

The populations are large and genetically diverse with frequent mutations that spread rapidly

181
Q

How can you use FECRT to measure resistnace?

A

FEC before and after treatment

182
Q

Post - treatment when should you test for 2-:V, 1-BZ and 4-Ad and 3-ML?

A

7 days post treatment for 2-LV, 14 days for 1-BZ and 4-AD, 14+ days for 3-ML

183
Q

How else can you measure resistance?

A

Expose parasites to different anthelmintics and measure response

184
Q

How do helminths reduce sensitivity to anthelmintic drugs?

A

By changing the target binding site, preventing the drug from acting effectively.

185
Q

How do helminths reduce the amount of drug they absorb?

A

By modifying their tegument, cuticle, or amphids to limit drug uptake.

186
Q

How do helminths remove anthelmintics from their bodies?

A

By increasing the expression of ABC transporters (e.g., P-glycoproteins) to pump the drug out.

187
Q

Why is it difficult to identify genes responsible for anthelmintic resistance?

A

Helminth genomes are large, complex, and highly diverse, making it hard to pinpoint relevant mutations.

188
Q

What are the genome sizes of common helminths?

A

H. contortus: 300 Mb

T. circumcincta: 600 Mb

F. hepatica: 1.3 Gb

189
Q

What challenge does high genetic differentiation pose in resistance studies?

A

here are thousands to millions of genetic differences between populations, making it difficult to identify which mutations cause resistance.

190
Q

Why should we reduce reliance on anthelmintics?

A

To slow resistance development, prevent residues in meat/milk, and reduce environmental toxicity.

191
Q

What are some alternative methods to control helminths? Are these alternatives widely available?

A

Selective breeding for resistant sheep, vaccines, and grazing management strategies.

No, anthelmintics remain essential for treating clinical cases.

192
Q

How can you prevent introducing resistant worms to a flock?

A

Use effective quarantine protocols before introducing new animals.

193
Q

Why is it important to test for anthelmintic resistance?

A

To ensure treatments are still effective and to avoid using ineffective drugs.

194
Q

What are common mistakes in administering anthelmintics?

A

Underdosing, poor technique, using expired products, and improper storage.

195
Q

Why should you avoid routine whole-flock treatments?

A

It accelerates resistance development by removing susceptible worms.

196
Q

What factors should influence your choice of anthelmintic?

A

Target parasite species, resistance status, and effectiveness.

197
Q

What is refugia, and why is it important?

A

A population of susceptible worms in the environment that helps maintain drug effectiveness.

198
Q

How can farmers reduce reliance on anthelmintics?

A

By adopting grazing strategies, genetic selection, and targeted treatments.

199
Q

What is the “Gold Standard” quarantine treatment?

A

Use of both newest compounds (4-AD & 5-SI).

200
Q

What is the “Silver Standard” quarantine treatment?

A

One new compound plus Moxidectin (3-ML).

201
Q

What are the key steps in quarantine treatment?

A

Yard new sheep for 24-48 hours.
Treat with recommended products.
Isolate on contaminated pasture for 3 weeks.

202
Q

What other parasite should be considered in quarantine?

A

Sheep scab (requires injectable Moxidectin or OP dip).

203
Q

What is the most common cause of anthelmintic failure?

A

Resistance.

204
Q

How does underdosing contribute to resistance?

A

Sublethal doses allow resistant worms to survive and reproduce.

205
Q

What are common reasons for underdosing?

A

Incorrect weight estimation, poor technique, and faulty equipment.

206
Q

What storage mistakes can make anthelmintics ineffective?

A

Exposure to heat/light, expired products, and mixing with other substances.

207
Q

How does misdiagnosis contribute to anthelmintic failure?

A

The wrong drug may be used, failing to target the correct parasite.

208
Q

What is the difference between whole-flock treatment and TST?

A

Whole-flock treatment treats all animals, while TST targets only those in need.

209
Q

What percentage of animals typically harbor most worms?

A

80% of worms are found in 20-30% of the hosts.

210
Q

How can TST be implemented in the UK?

A

By using automated weigh pens to track growth rates.

211
Q

What are the benefits of TST?

A

Reduces drug use, slows resistance, and maintains refugia.

212
Q

What are the most common anthelmintics used in cattle?

A

MLs (Macrocyclic Lactones).

213
Q

Why is resistance a growing concern in cattle?

A

Overuse of long-acting anthelmintics with limited alternatives.

214
Q

What is a major concern with eprinomectin?

A

It has zero milk withdrawal, leading to frequent use.

215
Q

(Ectoparasites of Ruminants)

what is the generation time for lice?

216
Q

What is the generation time for mange mites?

217
Q

how long can lice survive off the host?

218
Q

How long can mites survive off the host?

A

up to 3 weeks

219
Q

what are the two categories of lice you see in cattle

A

Biting/chewing and sucking

220
Q

where do sucking lice locate?

A

head and neck of the cattle

221
Q

where di biting lice loacate?

A

withers and back

222
Q

where are common sites for mange on cattle?

A

body
heel/tail

223
Q

What is chorioptic mange in cattle?

A

Classically discrete lesions in the skin folds on either side of the tail head with little inflammation

224
Q

When would chorioptic mange lesions be more extensive?

A

Lesions can be more extensive in that region with more marked dermatitis and self-inflicted traumatic damage to the skin

225
Q

What are risk factors for severe bovine chorioptic mange?

A
  • Housed
  • Stanchion
  • Straw bedding
  • Poor condition
226
Q

Why are belgian blues and charollais at risk of suffering psoroptic mange?

A

light coloured skin is a risk factor

227
Q

Describe a psoroptic mange lesion?

A

Inflamed with exudate, hypersensitivity and mites at periphery

228
Q

Describe sarcoptic mange lesion

A

Thick crusts, hyperkeratosis, intensely pruritic and self trauma

229
Q

How do you diagnose ectoparasites?

A
  • visual
  • sample
  • skin scrapes for mange mites
230
Q

What is the impact of sheep scab?

A
  • welfare of diseased animals
  • rapid loss of condition in ewes
  • poor lamb crop
  • poor growth rates in fattening lambs
  • hide damage
  • reduced wool clip
  • deaths
231
Q

Is scab notafiable in scotland

A

apparently yes lol

232
Q

How is sheep scab directly transmitted?

A
  • markets and shows
  • brought in animalss
  • at boundaries with other flocks
  • on shared grazing
233
Q

How is sheep scab indirectly transmitted?

A
  • In transit
  • At markets
  • On fences
  • Shearing equipment
234
Q

How do you control sheep scab?

A
  • ectoparasiticides ie dips and injectables
  • movement control
  • biosecuiritybiosecurity
235
Q

What is the dip that treats and controls lice in sheep?

236
Q

What are the three miscellaneous ectoparasites of sheep?

A
  • sheep kep
  • midges
  • nasal bot
237
Q

What are risk factors for blow strike in sheep?

A
  • diarrhoea and feacal staining of wool
  • late shearing - no dagging
238
Q

How do you control blowfly?

A

Ectoparasiticides
* Sprays (persistency)
* Dips
Traps
Carcass disposal
Dagging/Shearing
Worming

239
Q

What are ticks vectors of in cattle?

A

babesiosis

240
Q

What are ticks vectors of in sheep?

A

tick borne fever, louping Ill, tick pyaemia, Q fever

241
Q

What is the dip used to control ticks in sheep?

BVMS 3 (23 decks)

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