Energy deficiency syndromes (TV4102, Lecture 33 Notes)

Discuss protein-energy malnutrition

- Protein and energy are present in the diet in suboptimal quantities (incomplete starvation)

- Requirements for maintenance receive the highest priority, growth/reproduction take a lower priority, however, both can be drastically curtailed in order to increase the probability of the animal's survival

Discuss the aetiology of protein-energy malnutrition

- Body stores of lipid and protein must be catabolised to meet all the animal's energy requirements, may be accompanied by the incomplete oxidation of NEFAs and ketone formation (rare)

- Loss of muscle mass and power with lethargy, weakness and recumbency

List clinical signs of protein-energy malnutrition

- One or more heavily pregnant, recumbent cows

- Others in the mob in poor body condition, may be weak or slightly ataxic

- Lumbar processes and ribs readily palpable

- Animals are bright and alert, with normal appetites

- Rumen contractions are often mildly decreased

- Palpation of the abdomen or rectal palpation usually reveals one or more large calves

- Submandibular oedema (hypoproteinemia)

- May be mild to moderate ketonuria

Discuss treatment of protein-energy malnutrition

- Increase the ME and CP content of thediet

- Additional oral treatment with propylene glycol

- Good nursing

- Consider aborting or elective caesarean (prognosis is poor and surviving animals are of little value)

- Prognosis is much poorer if animal is recumbent and unable to stand (should be assessed by using lifting devices)

Discuss pregnancy toxaemia

- Form of hepatic lipidosis

- Commonly very fat beef cows during last two months of gestation

- Net energy deficit in the diet with massive mobilisation of fat from body reserves causing hypoglycaemia, hyperketonaemia and severe fatty infiltration of the liver

List clinical signs of pregnancy toxaemia

- Heavily pregnant, very fat cow/heifer

- Dullness, anorexia, rapid respiration and deterioration of body condition

- Little rumen activity, and faeces are hard, dry and coated in mucus

- Terminal stages, faeces may be foetid and yellowish-coloured, or there may be bloody diarrhoea

- Severe ketonuria

- May be aggressive, have a stumbling or high-stepping gait and difficulty rising

- Death within 3-10 days after becoming recumbent

Discuss diagnosis of pregnancy toxaemia

- Recumbent animals serum [βOHB] are usually much higher than in cases of primary ketosis

- Liver enzymes are commonly elevated

- Packed cell volume (PCV) and serum [Ca] may be decreased

- Most consistent finding is a grossly enlarged, yellow fatty liver

Discuss management of pregnancy toxaemia

- Very poor prognosis if the animal is recumbent

- Intravenous 50% glucose solutions, followed by propylene glycol orally, and the provision of high-quality feed stuffs and concentrates

- Intramuscular anabolic steroid injections (off-label use)

- Emergency caesarean operation could be considered

- Prevention is by providing adequate dietary energy (80-90MJ/day) during late gestation

Discuss fatty liver/fat cow syndrome

- Form of hepatic lipidosis

- Overfeeding animals during the latter part of lactation and the dry period (rare in AUS), significant problem in 'carry-over' (hold-over) cows

List clinical signs of fatty liver/fat cow syndrome

Very heavily conditioned cow around calving is depressed and off her feed, failing to respond to treatment of;

- Peri-parturient hypocalcaemia

- RFM or metritis

- Inappetence

- Severe ketosis

- Diarrhoea

- Displaced abomasum

- Mastitis

+ prominent ketonuria

Discuss treatment of fat cow syndrome

- Twice daily 40% dextrose IV

- Alternate day SC administration of 200 IU protamine zinc insulin

- Daily tube feeding with 5 kg gruel (e.g. lucerne pellets mixed in water)

- Antibiotic therapy as required

- Oral propylene glycol

- Corticosteroid injections

Discuss ketosis/acetonaemia

- High-yielding, lactating dairy cows

- Associated with an inadequate supply of energy to sustain the high milk yield of early lactation

- Between 2 weeks and 2 months after calving

- Present with weight loss, reduced milk yield, hypoglycaemia and presence of ketone bodies in all body tissues/fluids

Compare and contrast primary and secondary ketosis

Primary ketosis - during early lactation in high-yielding cows where the cow cannot consume enough energy to supply her glucose requirements for lactogenesis.

Secondary ketosis - results from any disease that causes a reduction in appetite/food intake during early lactation (e.g. metritis, displaced abomasum or lameness).

Compare and contrast clinical and subclinical ketosis

Clinical ketosis - ketosis with obvious clinical signs, wasting or nervous form.

Subclinical ketosis - ketonuria and ketonaemia in cows that have no outward clinical signs, but may have profound effects on the animals' health, productivity and future fertility.

Describe the aetiology of ketosis

- Early lactation when energy demand for milk production exceed gluconeogenic propionate production in the rumen

- Energy deficit leads to the mobilisation of fat stores, primarily as NEFAs

- When blood glucose is low (due to insufficient ruminal propionate production, pregnancy drain or illness) oxaloacetate levels drop impairing the TCA cycle

- Acetyl-CoA from NEFA oxidation cannot be fully processed and is converted into ketone bodies like acetoacetate and beta hydroxybutyrate

- Excess NEFAs are re-esterified into triglycerides and stored in the liver, contributing to fatty liver syndrome

List the clinical signs of wasting ketosis

- Loss of appetite, and refusal to eat concentrate feeds

- Rapid loss of condition and sudden drop in milk yield (over 2-4 days)

- HR may be slightly lower

- Rumen contractions less frequent, weak, and often incomplete

- Faeces are often dark and form, with a 'waxy' (shiny) appearance

- Smell of ketones on the breath of affected cows

- Urine has a strong positive reaction for ketones with Ketostix® or Multistix® test strip

List the clinical signs of nervous ketosis

- Repeatedly licking at self or sucking on inanimate objects, depraved appetites, and chewing movements accompanied by excessive salivation and teeth grinding

- Hyperaesthetic to touch and sound

- Muscle tremors and a 'staggery' gait

- Sometimes circling or aimless wandering

- May appear blind or head press

- Signs of aggression

Discuss treatment of ketosis

- Dextrose (500 mL of 40-50% solution IV) results in a transient hyperglycaemia

- Gluconeogenic substrate or glucose precursors (e.g. propylene glycol) orally

- Glucocorticoid therapy (e.g. 40 mg dexamethasone, 5 mg flumethasone) stimulates gluconeogenesis

- Vitamin B12, essential for the metabolism of propionate

- Energy supplementation (e.g. propylene glycol, molasses) from 1 week before calving onwards