Small ruminants 5 Flashcards
Weaner illthrift what is the aim for percentage, how many farm exceed this, why and cost
Aim for <4% weaner mortality per annum - GOOD BENCHMARK -> may takes years to get to this
- 40% of farms exceed this
- Illthrifty weaners ‘disappear’ so often under-estimated by farmer
- Mainly merino problem but some crossbreds too
- $90M + annual problem
Weaner illthrift how will this present
- There is a spectrum from illthrift to overt disease
○ From just don’t grow/live well
○ Regular outbreaks of disease, ongoing illthrift
○ Conception rates in the maiden ewe mob is very poor
Weaner illthrift diagnosis/recognition what are the 4 main steps within
1) know your targets/benchmarks to comapre against
2) check bodyweigth regularly
3) other suggestive clinical findings
4) other findings that suggest contributing problems
in terms of diagnosis/recognition of weaner illthrift what are the 4 main target to compare against and why important
1) . <4% mortality weaning - 12 months
§ Comparing the change in numbers when bringing in for different husbandry
2) Weight 45% of mature weight at end of spring - AT THIS WEIGHT WILL HAVE BODY FAT
§ Important to measure to indicate issues - liveweight
3) Grow > 1-1.5kg/month over summer (once hit 45% above)
§ Can have compensatory growth if have a time where growth is not as high
□ Stagnated in growth can be missed so monitoring every 6 weeks is better than every 6 months
® At this point there is a high risk period - need to identify and fix this
4) 75% of mature weight at end of 2nd summer
In terms of recognising weaner illthrift what is involved with checking body weight
- Weigh q 4-6 weeks: 40 tagged or random 80 untagged from mob and compare against targets
- Bodyweight targets just make sure a weaner’s need to accumulate fat and continue to grow are met
What are hte other suggestive clinical findings that suggest weaner illthrift
1) Healthy bone: fat in marrow (and thick cortices)
○ Weaner illthrift: serous atrophy of marrow (and thinned cortices)
§ Gelatinous bone marrow (serous atrophy)
§ Poor milk intake or low pasture intake - predisposes
2) Evidence of malnutrition: atrophied ruminal papillae
○ Don’t get turnover of feed that is needed
○ Haven’t been feed properly for weeks or just haven’t been eating
§ MOVE ONTO DIFFERENT PADDOCK -> increase nutrition, decrease competition
What are 3 other findings that suggest contributing problems to weaner illthrift
- WEC/TWC
- Trace mineral status
- Clinical/necropsy findings of other diseases (pneumonia, bacterial enteritis)
Weaner illthrift what is the major risk and 3 main causes
MAJOR death risk if low bodyweight and/or growth rate
- THEREFORE nutrition reduces mortality risk
1) malnutrition (macro-nutrients - energy and protein)
2) bone disorders - related to micro and macro nutrition
3) trace minerals - rule out others first
in terms of nutrition for weaners what is needed and how to monitor if getting nutrition
- Weaners need better energy and/or protein than adults
○ Need 12-16% crude protein (KNOW THIS) in diet - younger the more protein you need (will need this up to 1 year of age)
§ If eating green feed - WILL GET THIS
○ Use bodyweight monitoring to identify if nutrition OK
In terms of assessing pasture to determine if malnutrition could be a factor in weaner illthrift what looking at and what to do if issue present
1) Energy - good digestibility?
□ Start with 1.5kg/week cereal grain (introduce over 2-3 weeks - to avoid ruminal acidosis) - KNOW THIS
® HIGHLIGHTS importance of regular monitoring - anticipate problem able to change feed over the 2-3 weeks and not result in stagnated growth that would result if in danger and have to wait 2-3 weeks to get sufficient energy
2) Protein - any green present?
□ Supplement with lupins, beans, peas, lucerne etc 25% of grain or 0.5kg.week (minimal introduction period as lower risk of ruminal acidosis)
® EXPENSIVE - so don’t give at the rate would give the cereal grain
what are the principles with introducing new feed to weaners if malnutrition is an issue and what crops to consider
○ Feed 2-3 times/week once established, to let shy feeders get to grain too
○ Weaners may need imprinting to feeding equipment as well as feed
§ 50g per head offered 5-8 times should be sufficient
§ CAN EVEN continue to feed the supplementary feed AT LOW RATES passed weaning so when pasture quality decline just increase the supplementary feed (already adapted to the feed at this point)
○ Summer fodder crops can supply energy and, particularly, protein very well
○ Standing oat crops can be poor calcium sources: may worsen Ca-related bone problems
Bone disorders leading to weaner illthrift what are the 2 main ones, what causes them and what they result in
○ Osteoporosis - thinned cortices
§ Energy and protein young, calcium and phosphorus deficiency
§ Copper deficiency as well ○ Rickets - large deformed growth plates
§ undernourished (vitamin D deficiency - so no calcium and phosphorus)
□ SUNLIGHT - autumn born and going through winter
Bone disorders clinical signs/diagnosis
○ Deformed limbs ○ Pathological fractures ○ Lameness ○ Hunched posture ○ Reluctance to move ○ Hypocalcaemia ○ Enlarged epiphyses
Bone disorders what are the 3 main stages of bone development, what is needed at each stage and therefore what is the issue and how to fix
1) Growth of bone (pre-weaning)-> need energy, protein, Ca, Cu
§ ISSUE - osteoporosis
□ CAUSE -> Decreased with pre-weaning milk deficiency, poorer ewe nutrition, post: oat crops (low protein), grain feeding (need to give CaCO3 at 1.5% so Ca:P - 2:1), worms, low Cu, high Mo
2) Mineralise matrix ( about 12months) -> need Ca, P (vitamin D for to get access to this)
§ ISSUE - rickets
□ CAUSE -> low vitamin D (southern Australia - give vitamin D3 drench/injection to at risk mobs in autumn) or antagonists (carotenes in oat crops), low sunlight, low Ca
3) Enough healthy bone (later)
§ Strong bones - trabecular bone reserve for Ca source in pregnancy
§ ISSUE - dystocia, pregnancy toxaemia?
list some other conditions that are associated with weaner illthrift
- Pneumonia
- Mycoplasma vis
- Flystrike
- Septic arthritis
- Coccidiosis
- Bacterial enteritis
- Scabby mouth
- Lupinosis
What are trace mineral/vitamins and what needed for (specifics)
- 15 trace micro nutrients (mg/head/day)
- Central to metabolic systems
○ Enzyme structure and function - Cu, Se, Mo, Zn
○ Hormones - iodine
○ Vitamins - Co (B12)
○ Co-factors - Mn - Interactions exist in absorption and function
○ Eg Cu and Mo (COPPER ANATOGONIST), S, Fe
○ Se and S
in what farming systems are trace mineral/vitamin deficiencies more common and why
Deficiencies are more common in high input farm systems
- Antagonists in fertiliser (sulfur)
- More pasture growth = less soil ingestion
○ DON’T JUST MEASURE THE SOIL -> NEED TO MEASURE THE LEVELS WITHIN THE ANIMAL
what are the 3 main things that make you suspicious of a trace mineral deficiency
1) location
2) are there environmental risk factors
3) are there suggestive clinical signs
in terms of location for trace mineral deficiency where is Se, Co, Cu and I deficiency more often found
○ Selenium deficiency - west and hills of great dividing range, sanding coastal soils of Gippsland
○ Cobalt deficiency - coastal areas
○ Copper deficiency - South Gippsland and south western district
○ Iodine deficiency - great dividing range, moving central (granite stores area)- NOT IN COASTAL AREAS
what are the environmental risk factors for trace mineral deficiencies
○ Se, Cu, Co, I availability decrease by high rainfall (leaching (away into subsoil), abundant pasture, less soil ingestion)
§ Deficiency often develops in spring - As storage goes down -> transport within the blood decreases -> function starts to decrease eventually - months later
○ Deficiency often presents several months later when function is depleted - late summer into autumn
what are possible clinical signs of trace mineral deficiency and what to do about interpreting mild abnormal test results
○ There could be a spectrum of signs
§ Just illthrift/poor growth -> poor reproduction -> mild/vague clinical signs -> overt clinical disease
○ Interpreting mild or marginally abnormal test results
§ Hard to interpret significance
§ Consider doing response trial to evaluate economic efficacy
□ Treat half the weaners
□ Measure response: liveweight, wool reproduction
□ Compare value of extra production to total costs of treating all weaners
nutritional myopathy what is it caused by, what does each trace element do and when occurs/results in
Selenium or vitamin E deficiency
○ Similar mechanism -> stabilisation of cell membrane
§ Selenium mop up free radicals, vitamin E - direct stabiliser of cell membrane
□ Selenium deficiency occurs with lots of rainfall
□ Vitamin E abundant of green feed - therefore deficiency in DROUGHT
○ Pathophysiology - ALL results in muscle damage by oxygen free radicals
§ Oxidative load on muscles (high excretion)
§ High dietary PUFAS (high grain feeding, rancid feed, low roughage)
§ Low dietary selecium (grasses, grains, better uptake without sulphur)
Nutritional myopathy diagnosis
§ Signs of muscle damage
□ Increase serum CK (VERY HIGH), AST
□ Muscle necrosis, inflammation, fibrosis on histopathology - MUSCLE SAMPLE IMPORTANT
§ Low plasma Vit E (measure alpha-tocopherol)
§ Low plasma glutathione peroxidase (enzyme that selenium drives)
Nutritional myopathy clinical signs what are the severe and less severe and what demographics does this occur in
§ SEVERE - Acute (white muscle disease) in lambs pre-weaning
□ Sudden death (cardiac failure - take sample of heart muscle)
□ Respiratory distress
□ Acute lameness
§ LESS SEVERE - myopathy in older weaners
□ Lameness
□ Reluctance to move
□ Falling behind mob
Nutriional myopathy treatment
§ REMEMBER - excess selenium is TOXIC
□ Causes death with acute respiratory distress
□ Multiple se-containing treatments - drench, vaccine, long-acting, supplement
® Generally will not poison if had a drench a few weeks ago as doesn’t last long in the system
□ OR miscalculated dose
Coastal or white liver disease what caused by, clinical signs and diagnosis
cobalt/vitamin B12 deficiency ○ Clinical signs
§ Ill-thrift/poor growth rate
§ Weeping eyes
§ Photosensitisation (scaly ears)
§ Anaemia
§ White liver disease - fatty infiltration from deranged energy metabolism
○ Diagnosis
Decrease B12 (cobalamin) in plasma (sheep) or liver (cattle
