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Module 18: Ruminant Production > Ill Thrift in Lambs > Flashcards

Ill Thrift in Lambs Flashcards

1
Q

what are lamb diseases in preweaning period

A

nematodirosis

coccidiosis

parasitic gastroenteritis

ruminal acidosis

pulpy kidney

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2
Q

what are lamb diseases in post weaning period

A

parasitic gastroenteritis

pneumonia

ruminal acidosis

pulpy kidney

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3
Q

why is lamb growth important

A

Reduce housing pressure

Increase grass for ewes

Environmental pressure

Reduce feed costs

Reduce worm/fluke issues

Reduce losses (pneumonia/pulpy kidney)

Lamb price at market

Price at slaughter

Meat quality

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4
Q

what are pre weaning target growth rates

A

300g/day

hill: 240g/day

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5
Q

what are possible pre weaning growth rates in pre weaning

A

500g/day

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6
Q

what gives max growth rate in pre weaning period

A

single male with milky mother

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7
Q

what is target post weaning growth rate

A

200g/day

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8
Q

what is possible growth rate in post weaning period

A

350g/day

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9
Q

what gives max growth in post weaning period

A

clover and grass at optimal sward height in rotational paddock system

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10
Q

what influence the birth weight

A

genetics of dam and sire

ewe nutrition during preg

Weighing all lambs at birth can be useful but not all farms have the capacity

But even 10-20% of lambs will help give variation between years

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11
Q

what influences 8 week weight

A

20kg

ewe management

ewe performance (selection?)

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12
Q

what influences weaning weight

A
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13
Q

what influences fortnightly post weaning

A

nutrition (appropriate/deficiencies)

presence of disease

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14
Q

what influences good milk production

A
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15
Q

what should the DMI be for lambs

A

2.5-3.5% BW

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16
Q

what should ewe milk yield be

A

1L/lamb early lactation

down to less than 500ml/lamb later in lactation

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17
Q

what can delay weaning

A

good grass: enough for lambs as well as ewes

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18
Q

what weight can help with selection of ewes and is an important indicator for later productivity of lambs

A

8 week weight

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19
Q

how do you compare pre and post weaning DLWG

A

If it decreases - some decrease is expected in the short term but it should not be excessive or prolonged

If it increases – was weaning too late? Meaning that the ewes were competing with the lambs for the best grazing

Or are there trace element deficiencies that are masked before weaning

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20
Q

what should lambs ideally weigh at weaning

A

over 25kg

min 16kg

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21
Q

what DLWG shoud lambs be weaned at

A

<200g/day

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22
Q

what are potential problems with inadequate nutrition

A

poor milk production (maternal undernutrition, maternal disease, maternal genetics)

excessive stocking rates

poor quality pasture

inadequate grass length (ideal 5-8cm)

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23
Q

how much trough space do lambs need

A

30cm/lamb

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24
Q

how much lying space do lambs need

A

0.9m^2

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25
Q

what is the role of protein, CHO after weaning

A

protein: frame

CHO: fat

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26
Q

what % of grass is utilized in paddock, small field and set stocking

A

paddock: 80%

small field: 65%

set stocking: 50%

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27
Q

what are inhibitors of growth

A

Parasitic gastroenteritis

Mineral deficiencies

Liver fluke

Lameness

Nematodirosis

Coccidiosis

Pneumonia

Orf

Navel ill

Joint ill

Poor nutrition

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28
Q

when does coccidiosis occur

A

spring/summer

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29
Q

what are the coccidiosis species

A

Eimeria crandalis

Eimeria ovinoidalis

Eimeria bakuensis

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30
Q

why is coccidiosis difficult to diagnose

A

Coccidiosis and Nematodirosis have similar timing and clinical signs, so can be difficult to differentiate in lambs with diarrhoea

Concurrent infection of pathogenic Eimeria and Nematodirus battus is possible and the clinical signs are more severe than for either disease alone

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31
Q

what are the risk factors for coccidiosis

A

3-8 weeks old

Post weaning in naive animals

Youngest lambs

Indoors; wet, dirty conditions

Short grass

Areas that lambs congregate

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32
Q

what is the PPP of coccidiosis

A

2-3 weeks

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33
Q

how long can sporulated oocysts survive

A

over 1 year

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34
Q

how are coccidiosis oocytes destroyed

A

UV

heat

dessication

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35
Q

what are clinical signs in acute disease of coccidiosis

A

Diarrhea, dark, mucoid, +/- blood tinged

Dehydration (normally cause of death)

Death

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36
Q

what is the clinical signs of chronic coccidiosis disease

A

Chronic ill thrift/poor growth rates

Chronic, subclinical infection OR permanent GIT damage after acute infection

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37
Q

how is coccidiosis diagnosed

A

History of intestine lamb management

Clinical signs

  • Often coincide with start of oocyst shedding unless heavy infections, in which case signs can be seen earlier

Fecal oocyte count

PM

Response to treatment

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38
Q

how does fecal oocyst count diagnose coccidiosis

A

Fecal oocyst count >10-50,000

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39
Q

how can coccidiosis be diagnosed on PM

A

Hemorrhagic small intestines +/- cecum and colon

Histology or SI smear

Merozoites in smears from gut walls of freshly dead animals

Histopathology of guts from freshly dead animals

Samples have to be taken within 20mins of death because of the rapid autolysis of the intestinal mucosa

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40
Q

how is coccidiosis treated generally

A

Symptomatic treatment

Dehydration is most common cause of death

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41
Q

how is acute coccidiosis treated

A

Fluid therapy

Oral in most cases unless valuable lamb

Nutritional support may be needed if there is prolonged diarrhea and anorexia

Coccidiocidals

  • Need to dose during the pre-patent period with both if possible, 14 days after moving to high risk pasture
  • Diclazuril (Vecoxan) twice
    • Diclazuril is thought to only treat the later stages of the Eimeria spp, so needs to be repeated
  • Toltrazuril (Baycox) once
    • Treats all stages of infection, so only needs to be given once
    • Has more prolonged impact on DLWG and oocyst shedding in lambs

Anti inflammatories

Can help reduce the impact of the infection on the GIT

Reduce exposure

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42
Q

how is coccidiosis prevented

A

Avoidance is highly recommended and pharmaceutical products should only be used where they are unavoidable

Muck out sheds regularly

Avoid dampness in sheds

Rotate grazing

Keep later born lambs in different sheds/ on different pasture

Reducing stocking densities to reduce contamination

Maintaining good pasture height to avoid grazing too close to the ground

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43
Q

how pharamceuticals can be used to prevent coccidiosis

A

In feed treatment with the coccidiostatic, decoquinate, can be used in ewes prior to and after parturition.

Or it can be used for lambs, although because it is a coccidiostat, it is necessary to use it for a minimum of 28 days, otherwise development of the cocci stages will recommence and disease will only have been delayed

The coccidiocidal drenches used to treat lambs can also be used pre-emptively to prevent disease if the timing of exposure is known (e.g. when lambs were moved to a contaminated pasture)

44
Q

what pharmaceuticals are used to treat coccidiosis

A
45
Q

what does cobalt defiency in lambs cause

A

Epiphora

Poor growth rates

Unkempt fleece

Diarrhea

Anemia

Hepatic encephalopathy — associated with fatty liver (ovine white liver disease)

(Weak lambs)

46
Q

what does selenium defiency in lambs cause

A

poor growth rates

poor fertility in ewes, neonatal disease

can be toxic

47
Q

what does copper defiency cause in pregnant ewes

A

Reduced milk production

High perinatal lamb mortality

  • Weaker lambs with reduced vigour that are slower to get up and suckle colostrum —> higher mortality rates
48
Q

what is the function of cobalt

A

Incorporated into vit B12 by microflora in ruminoreticulum, released from microflora in abomasum and absorbed in small intestine

Gluconeogenesis from propionic acid (in liver)

Lack of utilization of propionic acid results in reduced appetite, hence clinical inappetance and ill thrift

49
Q

what are risk factors for cobalt deficiency

A

Varies between years

Soil type, iron-rich, alkaline, and manganese-rich soils

Soil impaction

Fast growing pasture

  • Improved pasture
  • Spring/summer

Well drained soils/dry pasture — summer

Low pasture clover content

50
Q

how is cobalt deficiency diagnosed

A
  1. clinical signs, grazing history and geographic location
  2. dose response trial
  3. serum vit b12
  4. liver vit b12
  5. soil cobalt
  6. pasture cobalt
  7. raised blood/urine MMA (methylmalonic acid)
51
Q

how is cobalt deficiency treated

A

Clinical disease associated with deficiencies requires injectable vitamin B12 in the first instance, to promote increased appetite in the lambs

Then other sources of supplementation can be provided

52
Q

how is cobalt deficiency prevented (6)

A
  1. cobalt salts (Co sulphate)
  2. anthelmintic, Co, Se drenches
  3. free access minerals
  4. intraruminal boluses (short or long term)
  5. minerals in compound feed
  6. pasture dressing in late spring (liquid or solid)
53
Q

what does selenium deficiency in adult sheep

A

reduced fertility, ewes and rams = fewer ewes in lamb

54
Q

what does selenium deficiency cause in pregnant ewes

A

causes weak lambs, white muscle disease

55
Q

what does selenium deficiency cause in growing lambs

A
  1. ill thrift
  2. impaired immune function
56
Q

what is the function of selenium (2)

A
  1. protects cell against reactive oxygen metabolites (ROM)
  2. complimentary role with vitamin E
57
Q

where are the most reactive oxygen metabolites (ROM)

A

skeletal, respiratory and cardiac muscles

white blood cells

58
Q

what are the risk factors of selenium deficiency (5)

A
  1. low soil content – large areas of UK
  2. fast grass growth (spring)
  3. under supply of other anti oxidants, as vitamin E
  4. high dietary oxidants (spring grass, root crops)
  5. generation of oxidants (exercise, infection, toxemia)
59
Q

how is selenium diagnosed (5)

A
  1. clinical signs, flock history/location, exclusion of other causes
  2. soil, pasture or animal testing
  3. serum glutathione peroxidase (GSHPx)
  4. serum and liver selenium ($$)
  5. WMD: creatinine kinase and post mortem
60
Q

how is selenium deficiency treated

A

care overdosing can be toxic

  1. injections
  2. oral supplementation
61
Q

what are selenium injections used to treat deficiency

A

Injection with selenium salts +/- vitamin E (1-3 months) — more expensive

Controlled release injections (9-12 months) — reduced risk of toxicity

62
Q

how is selenium deficiency treated with oral supplementation

A

Oral selenium salts

Intraruminal boluses (short or long term, often multiple elements)

Top dressing pasture (12-24 months)

Minerals in compound feed

Free access blocks/buckets/powders

63
Q

how is vitamin E deficiency diagnosed

A

plasma a-tocopherol

<1umol/L — high risk of WMD without Se deficiency

<2umol/L — high risk of WMD if Se also deficient

64
Q

what type of forages are high in vitamin E

A

green pastures

low in root crops

decline when forages are dried and stored for long periods

65
Q

how is vitamin E deficiency treated

A

injection with Se or oral supplementation

66
Q

what are the signs of acute selenium toxicity

A

Toxic to cardiovascular system

Dyspnea

Recumbency

Diarrhea

Death

67
Q

what are the signs of chronic selenium toxicity

A

seleniferous plants

Non-specific

Dullness

Ill-thrift

Anemia

Brittle hooves (sloughing in extreme cases)

68
Q

what does iodine deficiency cause in adult sheep

A

Perinatal lamb mortality (can be high)

+/- goitre

Scant wool

Poor thermoregulation

Poor lamb vigour

69
Q

what are the risk factors of iodine deficiency

A

Pasture or forage crops high in thiocyanate goitrogens

Late pregnancy

70
Q

how is iodine deficiency diagnosed

A

Post mortem — thyroid weight:body weight

  • >0.4g thyroid:1kg BW

Plasma inorganic iodine (PII)

  • Contemporary iodine intake
  • Good estimate of sufficiency, less for deficiency
71
Q

how is iodine deficiency treated

A

Intramuscular injection of iodized oil pre-mating

Sustained release ruminal boluses — I, Se, Co

Oral dosing

  • 280mg potassium iodide 8 and 4 weeks before lambing
72
Q

how is iodine deficiency treated with oral supplementation

A

Reduced IgG uptake by neonatal lamb

Beware of multiple supplements used:

  • Concentrate feed minerals
  • Intraruminal boluses
  • Oral drenches
73
Q

what does copper deficiency in lambs cause

A

sway back

ill thrift (not consistent)

lamb osteoporosis + fractures

tendon abnormalities – stiffness

depigmentation

steely wool

anemia

74
Q

what are the risk factors for swayback

A

Severe copper deficiency in mid- to late pregnancy

Mild winters — less supplementary feeding

Improved pasture (raised pH can make Mo more available)

Spring (higher Mo levels)

Soil (+ iron) intake in wet conditions (reduces SI copper absorption)

Breed

Scottish Blackface

High fibre diets

75
Q

what are the clinical signs of swayback

A

Swayback is either noted immediately after birth, with the congenital form, or at 2-4months of age after a stressful event

Hindlimb weakness results in a swaying, stumbling gait, along with other signs of neurological deficiency, secondary to demyelination of the nerve fibres

76
Q

what are the two forms of swayback

A

congenital

delayed form (enzootic ataxia)

77
Q

what are the clinical signs of congenital swayback

A

Small, weak lambs

Fine head tremors

Less severe — bright, poor coordination, weakness in hindlimb

Fine boned, dull coated

78
Q

what are the clinical signs of delayed form of swayback

A

Normal at birth, from 2-4 months of age

Hindlimb weakness results in a swaying, stumbling gait, along with other signs of neurological deficiency, secondary to demyelination of the nerve fibres

79
Q

how is copper deficiency diagnosed

A

Clinical signs and flock/local history

Histopathology brain/spinal cord

Plasma or serum (10-20% lower) copper

liver copper (3 samples)

response to supplementation (care)

80
Q

how is copper deficiency treated

A

congenital – hopeless

delayed may respond to supplementation

81
Q

how can copper deficiency be prevented through injections

A

Lasts 2-4 months

Good mid pregnancy swayback prevention

Overdosing = severe toxicity

82
Q

how can copper deficiency be prevented using oral supplements

A
  1. oral copper salt drenches
  2. boluses
  3. concentrate feed with minerals
  4. blocks/buckets/powders
  5. pasture top dressing
83
Q

how are oral copper salt drenches used

A

4-8 weeks pre-lambing

Risk of toxicity limits dose

84
Q

how are oral copper boluses used

A

Gelatine with copper oxide wire/needles

  • The copper oxide wires have lower toxicity risk in deficient animals than other more quickly absorbed methods
  • They are absorbed over 3 – 4 weeks and top up liver copper stores, wires stay in the abomasum during this time and dissolve in the low pH
  • Not susceptible to molybdenum or Sulphur interference in the rumen, but they are susceptible to reduced absorption due to iron absorption with soil ingestion in wet conditions

Multi trace element boluses

  • Multi-element boluses may not provide enough Cu in peak requirement times on deficient farms
85
Q

how are concentrate feed minerals used to prevent copper deficiency

A

Include molybdenum to reduce available copper

86
Q

how are blocks/buckets/powders used to prevent Cu deficiency

A

Copper levels low to avoid toxicity

87
Q

how is pasture top dressing used to prevent Cu deficiency

A

Top-dressed pasture cannot be grazed by stock for 3 weeks after dressing, or after heavy rain

Unweaned lambs have very efficient Cu absorption so should not be grazed on recently top-dressed pasture

88
Q

what breeds are especially sensitive to Cu toxicity

A

texel, suffolk, north ronaldsay

89
Q

what are risk factors for copper toxicity

A

Multiple supplements (remember concentrates)

Unweaned lambs

Breed

90
Q

what is seen on PM with Cu toxicity

A

Orange carcass

Gun-metal black kidneys

Black urine

91
Q

what does acute Cu toxicity look like

A

Within 24 hours

Severe gastroenteritis

Colic signs and diarrhea

Collapse and death

92
Q

what does chronic Cu toxicity look like

A

Acute hemolytic crisis

Jaundice

Anorexia

Diarrhea

93
Q

how does chronic Cu toxicity occur

A

Results from low levels of over-supplementation over a long period, the liver stores (in lysosomal cells) the excess copper, then when it reaches capacity the copper is released into the circulation all at once and a haemolytic crisis and jaundice results, it is often seen as sudden death

94
Q

when is Cu toxicity typically seen

A

Cu toxicity can occur after housing because sheep are not longer exposed to the iron in the soil which interferes with Cu uptake, and are likely to be fed concentrates

95
Q

how does liver fluke affect growth rate before weaning

A

poor ewe body condition –> low lamb birth weights + low milk production

96
Q

how does liver fluke affect growth rate after weaning

A

sudden death

liver damage

97
Q

how does lameness affect poor growth rates before weaning

A

poor ewe condition –> low birth weight + poor milk production

98
Q

how does lameness affect poor growth rates before and after weaning

A

lame lambs ==> poor growth rates

99
Q

what are some other diseases that can cause poor growth

A
  1. dental disease
  2. resp disease
  3. ectoparasites
  4. neuro diseases
  5. plochter – bog asphodel
  6. ruminal acidosis
100
Q

what ectoparasites can cause poor growth

A

Blowfly strike

Sheep soap (Psoroptes ovis)

Chewing lice (Bovicola ovis)

Sucking lice (Linognathus spp)

101
Q

what neuro diseases can cause poor growth

A

CCN

Louping ill

Meningitis

Coenurosis (GID)

Sarcocystosis

Chronic lead poisoning

102
Q

what are diseases that affect individuals

A

pneumonia

dental problems

103
Q

what are diseases that affect small #s

A

blowfly strike

neonatal diseases

104
Q

what are diseases that affect large #s

A

nutrition

TE deficiencies

liver fluke

sheep scab

haemonchus

105
Q

how do you tell the longevity of the growth problem

A

well grown but thin = recent problem

small frame and thin = long term

small frame but well fleshed = historical, potentially resolved

Module 18: Ruminant Production (25 decks)

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