Small Ruminant Medicine - Weaner Ill Thrift

What target percent bodyweight should a ewe be prior to joining?

75% mature bodyweight prior to joining

What target bodyweight should a lamb be for weaning?

15kg (do not wean when 8-10kg) at 12-14 weeks of age

What target percent bodyweight should a lamb be to survive first winter or dryspell?

45% mature bodyweight (25kg)

What is the mature bodyweight of a sheep?

55kg (BCS 3)

How would you investigate weaner ill thrift?

1. History
2. Examine the environment
3. Examine the mob and individual animals
4. Use of anciliary aids/further diagnostics
5. Data analysis of records
6. Post mortem examination

What is the weaner ill thrift equation?

WLT = inadequate/suboptimal nutrition +/- parasitism +/- intercurrent disease

What are the some causes of weaner ill thrift?

1. Malnutrition
2. GIT parasitisim → coccidiosis → diarrhoea
3. Yersiniosis → diarrhoea
4. Trace element deficiencies
5. Eperythrozoonosis → breaksdown RBCs

What is the prime cause of weaner ill thrift?

Inadequate nutrition → doesn’t reach optimal bodyweight before first winter

What is an accepted weaner mortality rate?

5% as you expect 95% of weaners to survive

What is the normal weaning survival rate?

95% but can go down to 20% mortality and 80% survival rate due to weaner ill thrift

What is ‘imprint feeding’?

Preconditioning weaners to eat supplements +/- good quality hay to ensure adequate nutrition if there is not enough green pasture

Describe the aetiological agent of coccidiosis and what clinical signs does it present with in lambs?

Eimeria spp. → characteristic little white plaques in the intestines

Many agents cause diarrhoea and need differential diagnosis. List the agents that cause diarrhoea in weaner lambs.

* Coccidiosis
* Yersiniosis
* Salmonellosis
* Parasites

What is the pathogenesis of eperythrozoonosis?

Mechanical transmission via vector or contaminated needle/knives → protoza breaks down RBCs → anaemia, anoxia and maybe jaundice → forms a ‘tail’ in the mob and can cause death

List conditions that are considered Kelpie diseases

* Eperythrozoonosis
* White muscle disease (Se deficiency)

What are the causes of Se deficiency?

* Deficient in soils all around Australia
* Clover dominant pastures are low in Se
* Superphosphate application can worsen Se uptake

What is the function of Se?

* Antioxidants which protect integrity of the cell membranes
* Important for optimum immune function

What are the clinical presentations of Se deficiency?

1. White Muscle Disease → bilateral symmetrical lesions → looks chopped up, affected muscles appear pale with possible white plaque areas of calcification, appear flabby
2. Selenium Response Ill Thrift → poor weight gain/growth, diarrhoea, dry open fleeces, death

How can you treat Se deficiency?

1. Parental injection → short or long acting available
2. Oral drenches with sodium selenate but must be done regularly at every 6-8 weeks

What causes Co deficiency?

‘Coastal Disease’

* Coastal calcareous sands
* High rainfall granite soils
* Lush spring growth
* Limited reserves in young growing lambs

What is the function of Co?

* Essential for vitamin B12
* B12 used for energy and protein metabolism
* Important for immune system

What are the clinical signs of Co deficiency?

**White Liver Disease**

* Pale swollen liver

**Sub-clinical Signs**

* Reduced growth rates and wool growth after weaning

**Clinical Signs**

* Anorexia
* Loss of body weight, growth retardation
* ll-thrift
* Watery discharge from eye
* Reduced wool growth and quality
* Photosensitisation (scaly ears)
* ↑ Susceptibility for internal parasites
* Anaemia (normocytic, normochromic) (late sign of deficiency and rare) in pregnant ewes
* Reduced marking percentage

How would you diagnose trace element deficiencies?

1. Blood concentrations
2. Liver concentrations (usually more reliable but take both if Cu deficiency)

What causes copper deficiency?

1. Soil Factors → sandy coastal and some peat soils, high in Mo = less Cu absorption, alkaline soils
2. Pasture Factors → grasses have much more less Cu than clovers, new or wet pastures with less root development
3. Animal Factors → sheep and goats need a lot less than cattle, poor transfer to foetus and in milk, high Mo = less Cu absorption in the rumen

What is the difference between primary and secondary Cu deficiency?

**Primary Copper Deficiency**: insufficient dietary levels are unable to provide adequate copper

**Secondary Copper Deficiency (More Common)**: ruminal absorption inhibited by high levels of Mo, Fe, S or Mn

What is the function of Cu?

* Essential for at least ten metallo-enzymes
* Required for body, bone and wool growth
* Development of nervous system
* Maintenance of myelin sheath around nerve fibres
* Key component of immune system
* Role in iron metabolism and red blood cell maturation
* Fleece and skin pigmentation → deficiency leads to banding

What are the clinical presentations of Cu deficiency?

1. Increased lamb survival
2. Enzootic ataxia (swayback) → hypomyelinogenesis of the motor neurons in the CNS
3. Bone Fragility → spontaneous fracture of bones
4. Fleece Derangement → loss of crimp, banding of wool
5. Illthrift and/or Anamia (rare)

Why are sheep and goats more susceptible to copper toxicity rather than copper deficiency?

* Sheep and goats has a much lower Cu requirement than cattle
* Farmer usually cause toxicity due to excess supplementation

Describe what causes acute and chronic Cu toxicity?

Acute → usually after Cu treatment

Chronic → excessive Cu accumalation stored in the liver over prolonged period of time