Ill Thrift In Lambs (Sh6)

Front 1

What are common causes of ill thrift in weaned lambs? (6)

Back 1

1) Poor nutrition

2) Parasitic gastroenteritis

3) Cobalt deficiency

4) Selenium deficiency

5) Liver fluke

6) Other, due to infectious and management problems:

*Respiratory dz

*Lameness

*Sheep scab

*Coccidiosis

*Border dz

Front 2

What should the basic hx of ill thrift lambs include? (7)

Back 2

1) Farming system and feed management throughout the year

2) Times of lambing and weaning

3) Lambing percentage and spread

4) Worming regime and anthelmintics used

5) Previous trace element problems and supplements used

6) Observations of scouring, coughing, lameness, or skin dz

7) Weather conditions

Front 3

What is an indicator of a long going problem?

Back 3

The more uneven the groups become

Front 4

What should be the target for daily FCE?

Back 4

250g/day

Front 5

What observations should be noted during examination of the flock? (5)

Back 5

1) Pasture and feed availability over the whole farm

2) Variation in size and weight within the group

3) Body condition scores across the group

4) Size variations within the group

5) Lameness, coughing, scouring, ocular dz, and pruritis

Front 6

What is a practical diagnostic tool from an economic perspective?

Back 6

Ill thrifty lambs are of low financial value, so the humane destruction and PMI of 1 or 2 of the worst affected animals can be useful.

*If inconclusive, then fecal samples should be collected for worm egg counts, coccidia oocyst counts, and/or identification of fluke eggs. Serum and blood samples should be taken for vitamin B12 and glutathione peroxidase assays.

Front 7

Cobalt Deficiency

1) What are the clinical signs?

2) What are the animal requirements? (Why is cobalt required?)

3) How is it diagnosed?

4) Describe short term vs long term supplementation options

Back 7

1) Lambs: empty, pot bellied, and depressed. Watery, ocular discharge with low-grade conjunctivitis often present.
Severely affected animals: pale and anemic. Fatty infiltration of the liver (lack of VitB12).
Lambs to cobalt deficient ewes: high perinatal mortality rates and susceptibility to infection.
2) Cobalt is required for the manufacture of vitamin B12. Vitamin B12 is required in the liver for teh utilization of rumen-derived propionic acid in energy production and metabolism of certain S-amino acids for optimum growth and wool production. Growing animals have higher requirements than adults. Sheep have higher requirement than cattle and deer.
3) Causes are multifactorial (need to consider soils and pasture cobalt-uptake is lowest when pasture growth is rapid, mature pasture). Good method: dose response trial. Blood vitamin B12 indicates immediate dietary cobalt intake. Liver vitamin B12 indicates limited continuous body storage. Can measure Methylmalonic acid (MMA) which accumulates in the plasma of cobalt deficient (due to reduced vitB12 co-enzyme activity).
4) Short term: oral drenching of weaned lambs with cobalt sulphate (not practical, last for 7d), foliar spraying with cobalt sulphate (last 6w), or vitamin B12 injections (last 1-4w; expensive).
*Long term: Intraruminal cobalt bullets (risk of poor efficacy and care of administration) or pasture top-dressing with cobalt sulphate (not currently cost effective).

Front 8

Selenium and Vitamin E Deficiencies

1) What are their roles in the body?

2) What 4 factors are related to the occurrence of clinical dz caused by anti-oxidant deficiencies?

3) What are the clinical signs? (5)

4) How can it be diagnosed?

5) How can selenium deficiency be treated?

6) How can VitE deficiency be treated?

-END ILL THRIFT IN LAMB-

Back 8

1) Act as cellular anti-oxidants; failure of protection leads to membrane damage and tissue necrosis.

2)*Selenium status

*Supply of other dietary anti-oxidants (primarily VitE)

*Supply of dietary oxidants. The main ones are PUFA which are found in high levels in young, rapidly growing pastures

*Generation of oxidants (e.g. via exercise at turnout, infection, toxins)

3) Nutritional muscular dystrophy, ill-thrift, fertility, impaired immune function, and retained fetal membranes.

4) *Diagnosis of WMD via CK or AST. PM.

*Soil and pasture levels of selenium.

*Selenium levels in blood and liver.

*Glutathione peroxidase (GSHPx) levels in blood.

*VitE levels in blood.

5) Direct methods: oral compounds (oral sodium selenate or intra-ruminal boluses) or injectable compounds (short-term vs long-term supplementatin) or inclusion in compound feeds or free-access minerals or medication of water supply. Indirect methods: application of selenium fertilizers to pasture.

6) Supplementation via selenium combinations or Tocovite tablets. Consider supplementation of the dam's diet with selenium and VitE in late pregnancy to ensure good supplies to the newborn lamb/calf.

Front 9

Incisor loss (Broken mouth)

1) Why is this a problem?

2) What is the aetiology?

3) What does it result in?

4) How can it be prevented/controlled?

Back 9

1) Unable to bite short pasture

2) Repeated bouts of acute gingivitis leads to recession of gingival margin and damage to periodontal ligament (bacterial involvement).

3) Malnutrition, poor production, and weight loss on marginal grazing and hill pastures.

4) Via mgmt (drafting to lowground pastures).

Shortening incisor teeth (not effective).

Front 10

Excessive Incisor Tooth Wear

1) What is the aetiology?

2) What are the ddx?

Back 10

1) Soil ingestion or enamel defects in permanent incisors (Ca, Cu, parasites, trauma).

2) Caries. Malocclusion. Dentigerous (odontogenic) cysts. Osteomyelitis of the mandible. Actinomycosis. Mandibular fracture. Cellulitis. Tumor.

Front 11

Cheek Tooth Problems

1)Define

2) What is the aetiology?

3) What are the clinical signs?

4) What are the ddx?

5) How can it be prevented/controlled?

Back 11

1) Excessive wear leads to poor mastication. Tooth loss/malalignment/malocclusion. Major cause of poor condition in older sheep.

2) Excessive wear-sheep's age and diet. Tooth loss preceded by gingivitis and periodontitis similar to incisor teeth.

3) Swelling of cheek-impaction of food or overgrown/displaced teeth. Short jerky jaw mvmts w/mouth slightly open. Quidding. May raise head while masticating. May have fibrous feed from side of mouth.

*Palpate dental arcade through cheek (sharp irregular ridges, lost cheek teeth). Gag and torch. May have tooth root infection w/bone changes.

4) Weight loss and poor BCS (nutrition, mgmt). Food impaction in the cheek (actinobacillosis, diptheresis). Swelling of the mandible (osteomyelitis or tumor).

5) No prevention measures. Consider concentrate feeding for weight loss (careful of ruminal acidosis/overfeeding). Restoration of BCS to allow sale.

Front 12

Abomasal Emptying Defect

1) What are the clinical signs? (8)

2) What are the ddx?

Back 12

1) Gradual weight loss. Abdominal distension-lower right. Poor appetite, febrile, dull, apathetic. Firm pelleted feces, dehydration. Rumen sounds often increased. No fluid thrill. Raised rumen chloride. Confirmed at necropsy.

2) Scrapie (other signs). Peritonitis and adenocarcinoma (fluid). Rumen distension-poor cheek teeth, vagal indigestion (papple).

Front 13

Chronic Inflammatory Bowel Dz

1) What is the common presentation?

2) What are the clinical signs?

3) What are the diagnostic tests?

4) How can it be treated?

Back 13

1) Unresponsive, ill thrift, reduce appetite, and soft feces. Less than or 3y.

2) Dull, anorexic, pasty feces (no blood or mucus), rumen hypomotility, abdominal size reduced. May have dehydration and pallor.

3) Hypoalbuminemia. Neutrophilia. PM-histopathology (lymphocytic-plasmacytic, granulomatous, or eosinophilic).

4) Long-term IM corticosteroid tx (temp effect). Supportive tx. Guarded prognosis if lack of rapid response.