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Small Ruminants Medicine and Production > Lecture 7 and 8 > Flashcards

Lecture 7 and 8 Flashcards

1
Q

What is the most common cause of ill thrift in wearers

A

Malnutrition, either on it own or associated with parasitic diseases and/or trace element deficiencies

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2
Q

Common causes of weaner ill-thrift

A
  • Malnutrition
  • Gastro-intestinal parasitism
  • Trace element and vitamin deficiencies
  • Yersioniosis, coccidiosis
  • Eperythrozoonosis
  • Fleece-rot and fly strike, dermatophilosis
  • Scabby mouth
  • Pneumonia
  • Arthritis, foot disease
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3
Q

What is ewe flock management

A
  • TIme and period of joining, parasitism of ewe and lambs before weaning, ewe nutrition before and during lactation -> influences health of weaners in following months
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4
Q

What are the key points with weaner management

A
  • Set clearly defined production targets
  • Short compact joining period
  • ‘Imprint’ fedding lambs before weaning
  • Wean merino lmbs 12-14 weeks after start of lambing
    • Don’t wean before D30
    • For maximal survival, lambs should be 15kg or heavier at weaning
    • Wean lambs 6-10 weeks before the ewes are next joined
  • Wean abruptly; do not progressively reduce the amount of milk, the big, strong lambs that are ready for weaning will continue to recieve milk where as the smaller lambs with starve
  • Ensure that lambs are taking solid food before weaning
  • At weaning time
    • Drench with effective anthelmintic
    • Wean lambs onto specially prepared paddock -> high quality low worm pasture
  • Fly control
  • Monitor body weight of weaners
  • Monitor faecal egg count
  • Move weaners to second low risk paddock after autumn break
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5
Q

Why is it important that weaners are over 20kg

A

If they are under, they have less than 1kg of fat reserves. Dietary energy deficiencies will therefore result in mobilisation of body protein stores for energy production -> leads to rapid weight loss, weakness and higher susceptibility for incurrent disease

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6
Q

What are the growth targets

A
  • 45% of mature weight when pastures dry off
  • Maintain slow growth over summer
  • Reach 75-80% of mature weight by 15-17 months of age
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7
Q

What are the important trace elements and vitamins

A
  • Se, Co, Cu, Vit E
  • Deficiencies generally limited to specific areas and are seasonal
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8
Q

What are some intercurrent diseases

A
  • Weaning = stressful event
  • Weaners are immunological inexperienced
  • Other predisposing factors
  • High prevalence of worms, fleece-rot, dermatophilosis, flystrike, pneumonia and arthritis may occur if no effective preventative measures are takes
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9
Q

What are the preventative measures for ill-thrift

A
  • Cfr key points weaner management
  • Establish target growth rates and body weights from birth to first joining
  • Have a good worm control program
  • Treat any trace element deficiencies
  • Monitor for other diseases that occur from time to time
  • Draft off the tail of weaner mob
  • Understand seasonal variation in feed availability on the farm and plan supplementary feeding in advance
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10
Q

What is Yersinoniosis

A
  • Bacteria are present in many apparently normal sheep as well as in many domestic and wild animals and birds
  • Primarly a disease of weaners
  • Disease usually inly occurs with ther eis prior damage to the gut wall and the animals is stressed
  • Outbreaks usually seen in winter and early spring
  • Faecal-oral route of infection
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11
Q

Treatment for Yersinoniosis

A
  • Antibiotics
  • Isolate sick animals
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12
Q

How to prevent yersioniosis

A
  • Prevent any stress affecting weaner sheep
  • Provide good nutrition to weaner sheeo
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13
Q

What causes coccidiosis

A

Eimeria spp

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14
Q

Epidemiology of coccidiosis

A
  • Coccidia are normally present in healthy sheep of all ages
  • No signs of disease if no concurrent disease or stress factors and level of pasture contamination with occcidia oocysts is low - lambs developing immunity to coccidiosis
  • Coccidia oocysts can survive for montsh under warm, moist conditions
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15
Q

What are the clinical sigsn of coccidiosis

A
  • Usually in lambs or goat kids just prior or after weaning
  • Most outbreaks occur under intensive husbandry systems under warm and moist conditions
  • Diarrhoea, loss of appetite, abdominal pain, dehydration, unthriftiness and weightloss, anaemia and sometimes death
  • Morbidity between 20 and 60%
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16
Q

Pathology of coccidiosis

A
  • In clinical coccidiosis, usually 2 or more Eimeria spp presnt in gut
  • Most pathogenic species invade ileum, caecum and colon rather than jejenum
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17
Q

What is the diagnosis of coccidiosis

A
  • Flock history
  • Clinical signs
  • Post-mortem
  • Faecal oocyst count
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18
Q

How to treat coccidiosis

A
  • Move animals away from contaminated pastures to ‘clean’ pastures at normal stocking rates
  • Chemotherapy
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19
Q

How to prevent coccidiosis

A
  • Prevent ingestion of large numbers of oocysts by susceptible animals -> good hygine
  • Control concurrent diseases and other stress facots
  • If overcrowding cannot be avoided, continuous preventative medication may help
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20
Q

What causes Eperythrozoonosis

A

Mycoplasma ovis

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21
Q

What is Eperythrozoonosis

A
  • Primary disease of weaner sheep; merino sheep are most susceptible; goats can be infected
  • High flock prevalence in the medium to high rainfall areas of Southern Australia after extensive tain
  • Bacteria adhere to and damage rbc in sheep -> anaemia and jaundice
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22
Q

Explain the transmission of Eperythrozoonosis

A
  • Mechanically between animals by the transfer of infected red blood cells
  • Primarily biting and/or blood sucking insects
  • Can also be spread during or after amrking time by contaminated vaccination needles, knifes or where flies move from wounds on one animal to the next
  • No transplacental or intra-uterine transmission
  • Carrier animals are source of infection for next year lamb drop
  • Stressed sheep appear more susceptible
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23
Q

What are the clinical signs of Eperythrozoonosis

A
  • Severity CS - level of infection
  • Can be contributing component of ‘ill thrift’ problem
  • Fever during acute infection period
  • Anaemia - weakness, sheep lag behind the mob when driven, respiratory distress, may collapse
  • Jaundice
  • May contribute to the development of ‘tail’ of the mob which often occurs when moving a mob of weaner sheep
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24
Q

PM of animals with Eperythrozoonosis

A
  • Splenomegaly
  • Pale or jaundice carcass
  • Possible haemoglobinuria
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25
Q

How to diagnose Eperythrozoonosis

A
  • History, clinical signs, PM
  • Blood spear - Romanovosky stain
  • Blood profile
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26
Q

Treatment and control of Eperythrozoonosis

A
  • Avoid handling stock for 4-6 weeks
  • Most sheep recover spontaneously when other stresses are kept to a minimum
  • Antibiotic treathems
  • Good hygine at marking, mulesling and shearing
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27
Q

When do most cases of selenium deficiency occur

A
  • Spring on clover dominant pastures; superphosphate application may make worsen selenium uptake by plants
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28
Q

What does Se cross

A

Placenta

29
Q

What % of flock can be affected by selenium deficiency

A

10%

30
Q

What does Se and Vitamin E act as

A
  • Antioxidants to protect the integrity of the cell membrane
    • Se and Vit E compementary but different systems
    • Selenium acts principally intracellular as a component of the enzume glutathione peroxidase
    • Vit E acts within the cell membrane, preventing the formation of lipid peroxides from polyunsaturated fatty acids
      • Vit E - stored in liver - deficiencies may occur if sheep have not grazed any dry feed for several montsh
        *
31
Q

Why is Se and vit E so important

A

Optimal function of the immune system

32
Q

What are the clinical signs of selenium deficiency

A
  • White muscle disease in lambs
  • Poor lamb growth
    • Ranging from subclinical signs of reduced weight gain and wool production to clinical signs of poor growth and increased mortality
  • Infertile ewes
    • Increased early embryonic death
    • Increased number of dry ewes at marking
    • Uncommon in australia
  • Reduced humoral and cell mediated immunity
  • Altered iodine metabolism
33
Q

What causes white muscle disease

A

Se and/or Vit E deficiency -> non-inflammatory degeneration or necrosis of the skeletal and cardiac muscles

34
Q

What it congenital WMD

A

Still born or die suddenly within a few days of birth

35
Q

What is delayed WMD

A
  • Occurs in rapidly growing lambs, growing lambs and goat kids most common at 3-6 weeks of age, sometmes as late as 3months of age
  • Clinical symptoms
    • Sudden death from heart failure
    • Respiratory distress
    • Weakness, stiffness, arched back, recumbency
    • Clinical disease is precipitated by exercise or stressors
36
Q

What is seen post-mortem with white muscle disease

A
  • Bilateral symmetrical lesions - affected muscles appear pale with possible with plaque areas of calcification
  • Histoathology - hyaline degeneration folloed by coagulation necrosis and variable level of mineralisation
    *
37
Q

What is the clinical pathology of WMD

A
  • Elevated plasma creatine kinase levels
  • Elevated aspartateaminotransferase
  • Vit E/ selenium/ glutathione peroxidase
38
Q

What is the selenium deficiency diagnosis

A
  • Blood selenium concentrations
    • 3-5 samples
  • Liver selenium concentration
    • 3-5 samples
  • Pastures
39
Q

Treatment and prevention of selenium deficiency

A
  • Always follow manufacture’s recommendations! small safety margin for selenium! Do not cmbine supplementation methods
  • Prevention - supplement ewes pre-lambing with selenium and/or selenium and vitamin E
  • Most treated stock recover - if confirmed deficiency - treat all animals in mob
  • Parental or oral supplementation
40
Q

Parental supplmentation of selenium deficiencies

A
  • Long-acting - slow release - SC in neck
    • 1mg Se/kg LW
    • Treat ewes 4 weeks before mating
    • If ewes were not treated and lambs are selenium deficient - treat lambs at marking time
  • Short-acting - smaller safety margins
    • Often included with clostridial vaccines
    • Protect lambs at marking time
41
Q

Expalin oral drenches with selenium deficiencies

A
  • 0.1mg Se/kg LW - cheap and safe - short term
  • Usually in form of sodium selenate often mixed with anthelmitic drenches
  • Treat ewes 4 weeks before mating, and 4 weeks before lambing
  • Treat lambs at marking
    *
42
Q

What is acute seleniumm poisoning

A
  • verdose of Selenium - small safety margin with Se treatments
  • Clinical signs
    • Respiratory distress and/or sudden death 1-7 days after treatment
  • Treatment
    • None
    • Nursing
  • Prevention
    • Follow manufactures guidelesin when giving selenium supplements
43
Q

What is Cobact deficiency know as and what is it

A
  • Costal sickness - Co deficiency is more likey on costal calcareous sands, high rainfall granite soils, may be exacerbated by liming, especially in lush seasons
44
Q

What is Co essential for

A
  • Synthesis of vit B12 by rumen microbes
    • Synonymous with insufficient synthesis of B12
    • B12 absorbed in small intestine
    • GI parasites may cntribute to B12 deficiency
      *
45
Q

Where are B12 reserves stored

A
  • Plasma and in the liver
46
Q

Who are most susceptible to Co deficiency

A

Lambs

  • Vit B12 is readly transferred across the placenta and colostrum is concentrated source of B12
47
Q

What is B12 important for

A
  • Energy and protein metabolism
  • Immune system
    *
48
Q

What are the 2 distinct forms of Vit B12

A
  • Methy; cobalamin is coenzyme for methionine synthesis
  • Adenosyl cobalamin is co-enzyme for proprionate metabolism
49
Q

What is Co deficiency linked to

A
  • Impairs lipid metabolism, evident as ovine white liver syndrome
  • Co deficency has also been linked to phalaris staggers
50
Q

What are the subclinical signs of cobalt deficiency

A

Reduced growth rates and wool growth after weaning

51
Q

What are the clinical signs of Co deficiency

A
  • Anorexia
  • Loss of body weight, growth retardation
  • Ill thrift
  • Watery discharge from eye
  • Reduced wool growth
  • Photosensitisation
  • Increased susceptibility for internal parasites
  • Anaemia
  • In pregnant ewes - reduced marking %
52
Q

What are the clinical signs of white liver disease

A
  • Lambs 2 -6 months of age
  • Severe ill-thrift
  • Hepatopathy
  • Depresssion
  • Ocular discharge
  • Photosensitisation
  • High morbidity with mortality rates 10-15%
53
Q

What is seen on a PM with White liver disease

A

Liver is pale and very swollen

54
Q

How to diagnose cobalt deficiency

A
  • Serum vit B12 concentrations
    • 10 samples
  • Liver vit B12 concentration
    • 3-5 samples
  • Pastures with cobalt concentrations
  • Controlled response trials
55
Q

Treatment and prevention of cobalt deficiencies

A
  • Vit B12 injections
    • Long acting
      • 3mg of microencapsulated vitamin B12 once at docking time
    • Short acting
      • 2mg of water soluble vit B12 at marking time, repeat every 4-6 weeks
  • Cobalt pellets - slow release
    • Not to stock < 3 months
    • Weaners
    • Ewes - ensure adequate vitamin B12 in colostrum asn adequate foetal liver reserves
  • Oral dosing
    • 7mg cobalt sulphate weekly
    • Impractical
  • Topdressing
    • Expensive
56
Q
A
57
Q

Explain copper deficiency

A
  • Animals become deficient before pants
  • Primary
    • Pasture avaliability
    • Avaliability of copper in pasture
  • Secondary
    • Presence of copper antagonists such as molybdenum, sulfur, zinc, iron, calcium and cadmium - decreases copper absorption
    • Formation of copper thiomolybdates complexes n rumen
    • Fertilisers can decrease copper absorption
58
Q

How does copper deficiency occur

A
  • When inadequate amounts of copper are absorbed from the gut over a period of weeks or months, and liver stores are exhaused
59
Q

What is the function of copper

A
  • Essential part of at least 10 metallo-enzymes
    • Copper is required for body, bone and wool growth, development of nervous systems and maintenance of myelin sheath around nerve fibres, key component of immune system, plays role in iron metabolism ans red blood cell maturation, fellece skin and pigmentation
60
Q

What are the subclinical signs of copper deficiency

A
  • Reduced growth rates and wool production
61
Q

What are the clinical signs of copper deficiency

A
  • Wool abnormalities
    • Steely wool
    • In black sheep- loss of wool colour, white bands in the staple
  • Nerve disorders - enzoonotic ataxia
    • Hypomyelinogenesis of CNS
    • Lambs are unable to stand or have incoordination of hind limbs
    • Signs are present at birth or develop in first weeks after birth
  • Bone disorders
    • Osteoporosis - thin fragile bones, more bone fragements
  • Ill thrift
    • If very severe deficiency
62
Q

Copper deficiency diagnosis

A
  • Liver copper concentrations
    • 4-8 samples
  • Serum copper concentrations/plasma caeruloplasmin
    • 7-10 samples
  • Response to treatment
63
Q

Treatment/prevention of copper deficiency

A
  • Only treat sheep with copper when copper deficiency is confirmed
  • Oral drenches
    • Copper sulphate or copper oxide
    • Not pratical
  • Copper oxide capsules
    • 5g CuO
    • Release copper over a period of months
  • Topdress pastures
    • 5-10kg of copper sulphate per ha
    • Do not graze pasture for at least 4 weeks following application
  • Copper injections
    • 0.5-1.0 mg/kg LW
    • Copper calcium edetate - minimal local reactions
    • Copper glycinate injections- depot formulation - slow release of copper into circulation
  • If copper in pasture is low
    • Top-dress pasture annually
    • Copper oxide capsule in early winter until pasture level are sufficient
  • If copper in pasture is adequate, but copper deficiency results from high molybdenum levels
    • Copper glycinate injections in winter
64
Q

Clinical signs of acute copper toxicity

A
  • Abdominal pain, diarrhoea
  • Red-brown coloured urine
  • Death may occur within 1-2 days; those that survive develop jaundice
65
Q

Cliical signs of chronic copper toxicity

A
  • Depressed, sheep go off feed
  • Red brown coloured urine
  • Severe jaundice
  • Death usually occurs within 1-2 days of showing signs, those that survive remain poor dooers
66
Q

How to diagnose copper toxicity

A
  • History, CS
  • Post-mortem -lver and kidney samples
67
Q

Treatment for copper toxicity

A
  • Reduce possible stress factors
  • Ammonium tetrathiomolybdenum - 1.68 mg/kg IV, 3 times over 5 day period
  • Licks containing molybdenum -> reduce further copper absorption
68
Q

Prevention of copper toxicity

A
  • Remove cause of chronic copper poisoning
  • Top-dress pasture with molybdenizde superphosphate

Small Ruminants Medicine and Production (6 decks)

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