Cattle - Endocrine/Metabolic Dz Flashcards
What two other names is hepatic lipidosis in post-partum dairy cattle know by?
Fat Cow Syndrome and Lipid Mobilisation Syndrome.
What cattle are at risk of developing Fat Cow Syndrome?
Postparturient dairy cows which were overconditioned in the during late lactation and the dry period.
Obese/well conditioned cows with a large amount of omental and subcutaneous fat.
List the clinical signs of Fat Cow Syndrome.
Depression, anorexia, weight loss, weakness –> recumbency.
Non-specific signs may include decreased ruminal motility and milk production.
Other signs related to concurrent conditions e.g. mastitis, metritis, parturient paresis and displaced abomasum.
How do you diagnose Fat Cow Syndrome in a cow?
- Liver enzymes: often a poor indicator of dz severity; most consistently elevated are OCT, TBili, AST.
- CBC: often leukocytosis with a left shift (non-specific).
- Increased NEFAs and decreased cholesterol and triglycerides.
- BSP excretion > 9mins –> guarded Px.
- U/S: may see increased echogenicity of liver, rounded margins.
- Liver biopsy: % hepatocytes containing fat vacuoles - mild 75%. Liver will float in distilled water when >34% (NB all high-producing, post-parturient dairy cows will have fatty infiltration).
Describe post-mortem findings in a cow with Fat Cow Syndrome.
- Generalised obesity if sick
How do ruminants differ from monogastric animals in their intake of dietary energy?
- Most of the energy is absorbed is VFAs not glucose.
- Glucose is still needed and must be produced by gluconeogenesis, 85% of which occurs in the liver.
List conditions in which negative energy balance occurs in cattle.
- Lactation.
- Foetal growth.
- Exercise.
- Decreased feed consumption.
- Environmental chilling.
- Disease.
Describe the changes in insulin, glucose and hormone sensitive lipase (HSL) that occur in cattle during periods of negative energy balance or prior to lactation.
- Blood glucose concentration decreases.
- Insulin:glucagon ratio drops.
- Glucose, insulin, catcholamine, growth hormone changes activate HSL production.
- HSLs convert tissue fat to FFAs/NEFAs and glycerol.
What happens to the glycerol and NEFAs produced by breakdown of fat in cattle in negative energy balance?
- Glycerol –> liver –> produce glucose OR combine with FFAs to make triglycerides (TGs).
- FFAs –> combine w glycerol to make TGs OR degrated through beta-oxidation –> acetyl CoA –> krebs cycle –> glucose.
- If there is not enough oxaloacetate for acetyl CoA to combine with to enter the krebs cycle, acetyl CoA is converted to ketone bodies.
- NB ketones reduce feed consumption and perpetuate negative energy balance.
How does hepatic lipidosis develop in cattle with negative energy balance?
- When liver is overwhelmed with NEFAs greater amounts of TGs are deposited within hepatocyte.
- TGs eventually leave liver as VLDLs (plasma-soluble complexes of phospholipid, cholesterol and apolipoprotein A).
- Hepatic lipidosis occurs when rate of hepatic TG formation excedes oxidation of FAs and formation and release of VLDLs into peripheral circulation.
What dietary factors can increase the risk of hepatic lipidosis in cattle?
- Cows on low-protein diet in the dry period.
- Depression in DM intake in the final week before calving.
- Limiting feeding take of over-conditioned cows immediately after calving.
Is hepatic lipidosis a reversible condition in cattle?
Yes, if the cause is removed and the energy balance becomes positive (or less negative).
Outline treatment of hepatic lipidosis in cattle.
- Mild to mod: as for traditional ketosis.
- Severe: eliminate negative energy balance and factors/dz causing it:
- Getting them eating is most imp; transfaunation may help.
- IV glucose or insulin –> induces an insulin:glucose than will dec HSL mobilisation of FAs and stim prod of VLDLs.
- Glucocorticoids IV/IM + glucose precursors orally e.g. propylene glycol, glycerol.
- Choline: precursor of lipoproteins may inc rate of VLDL prod (not IV –> neuromuscular blockate); no controlled studies.
- Nicotinic acid (niacin) may reduce lipolysis at the tissue level and the amount of fat presented to the liver.
What are the key pre- and post-parturient risk factors for development of hepatic lipidosis in dairy cattle?
- Pre-parturiet: obesity (BCS > 3/5), severe feed restriction, feeding excess energy, long calving interval.
- Post-partum: concurrent dz, anorexia or fasting, feed restriction, sudden feed changes.
Outline methods to prevent hepatic lipidosis in cattle.
- Prevent over-conditioning during the late lactation and dry periods.
- Tx peri-parturient dz early and aggressively.
- Adequate protein in dry period essential; good quality roughage (hay/silage).
- Commence feeding grain 2-4wks pre-partum to allow rumen to adapt to lactation diet; do not overfeed! Dm intake should be approx 2% BWt/day.
- Supplement dry cow ration w cobalt = precursor of vit B12 = co-factor in rate limiting step in conversion of propionate to succinyl CoA and thus glucose prod.
- Dry cow and lactating ration incl nicotinic acid to aid in dev of ketosis = primary risk factor for hepatic lipidosis.
- Monensisn in dry cow and early lactating ration may aid in prevention of ketosis.
Outline the signalment of cattle most at risk of Protein-Energy Malnutrition (PEM) and Pregnancy Toxaemia.
- Diseases of beef cattle on marginal diets.
- Growing, pregnant heifers are at greatest risk as energy requirement of growth are superimposed on other calorie requirements.
List risk factors for development of PEM and Pregnancy Toxaemia in beef cattle.
- Winter season e.g. snow cover.
- Unpalatable feed.
- Poor quality feed.
List clinical signs of PEM and Pregnancy Toxaemia in beef cattle.
- Weight loss/poor BCS.
- Weakness +/- inability to rise but still alert.
- Depression.
- Long hair coat.
- Body temp normal or hypothermic.
- +/- diarrhoea.
- Death usually occurs 7-14d after becoming recumbent.
Outline diagnostic test findings in beef cattle with PEM or Pregnancy Toxaemia.
- Demonstrating dec caloric intake + ruling out other chronic dz e.g. Johne’s, lymphoma, parasitism.
- +/- hypoCa, anaemia, dec serum insulin conc.
- Ketonuria is not typical in PEM.
- Necropsy: dec muscle mass, atrophy of fat; fatty liver if acute or small liver if more chronic.
Describe treatment of PEM and Pregnancy Toxaemia in beef cattle.
- Treatment is often unrewarding.
- IVF, improve energy balance, tx concurrent dz.
- IV glucose, forcefeed alfalfa gruel, propylene glycol.
Outline strategies for prevention of PEM and Pregnancy Toxaemia in beef cattle.
- Nutrient requirements inc greatly for beef cattle in third trimester of pregnancy.
- Have adequate body condition (5-7/9) entering third trimester and feed adequate amounts of good to excellent quality forage.
- As quality of forage dec, time spent in rumen inc, therefore maximum daily intake of feed dec, therefore feed good quality forage.
- Decreasing temperature inc energy needs e.g. 10 C –> 10% higher energy req, 0 C –> 20% higher energy req.
Ketosis occurs in ruminants during times of increased mobilisation of fat stores, usually just after parturition. List the three ketone bodies which are elevated in the blood of ruminants during ketosis.
- Acetone (Ac).
- Acetoacetic acid (AcAc).
- Beta-hydroxybutyric acid (BHB).
Define type I ketosis.
- Aka classic ‘primary’ or ‘spontaneous’ ketosis.
- Causes reduction in glucose in the blood and liver.
- Increased fat mobilisation culminating in elevated ketone body accum from a neg energy balance during early lactation.
- Becomes a dz condition when absorption and prod of ketone bodies exceed their use by the ruminant as an energy source –> elevated blood ketones, NEFAs and dec blood glucose.
Define type II ketosis.
- Involves high blood insulin conc and transient hyperglycaemia secondary to overconditioning and fatty infiltration of the liver.
Describe the aetiology of ketosis in dairy cattle.
- Processes that require glucose peak in late gestation and early lactation; daily glucose req inc 30% in late lactation and 25% w onset of lactation.
- Gluconeogensis must occur for cattle to meet glucose demands; substrate = propionic acid (FFA) which is prod in the rumen or by breakdown of body proteins.
- Alternate energy sources = ketone bodies or fat-derived NEFAs.
- High milk prod in early lactation exceeds ability of cow to ingest sufficient feed to meet this requirement for energy; milk prod peaks at 4wks post-calving, feed intake peaks at 7-8 wk post-calving.
- Cow mobilises body fat and protein stores for gluconeogenesis –> normal dairy cows have some degree of ketone body prod during this time, certain factors tip them over into subclinical or clinical ketosis.
List risk factors for development of subclinical or clinical ketosis in dairy cattle.
- Any dz that dec feed intake: mastitis, metritis, peritonitis, LDA most common; subclinical hypoCa, mild ruminal overload, laminitis, lameness, pyelonephritis and musculoskeletal calving inj less common.
- Poor quality/low energy feed.
- Ingestion of pre-formed ketones e.g. in ketogenic silage.
- Cobalt deficiency.
- Concentrates with low levels of lincomycin have been reported in herd outbreaks of ketosis.
List clinical signs of clinical ketosis in dairy cattle.
- Gradual loss of appetite and dec in milk production over several days.
- Rapid weight loss.
- Type I: typically 3-6wks post-partum.
- Type II: typically immediately post-partum.
- Normal TPR.
- Firm, dry faeces.
- Moderate depression.
- +/- reluctance to move.
- Ruminal atony if inappetent for several days.
- +/- pica.
- +/- odour of ketones on breath and in milk.
- +/- transient nervous signs e.g. staggering, blindness.
- +/- primary dz: mastitis, metritis, peritonitis, LDA (NB ketosis inc risk of LDA so may be primary or secondary).
List clinical signs of nervous ketosis in cattle.
- Acute onset of bizarre neuro signs lasting 1-2h and recurring at 8-10h intervals.
- Circling, proprioceptive deficits, head pressing, apparent blindness, wandering, excessive grooming, pica, ptyalism.
- +/- hyperaesthesia, bellowing, moderate tremors, tetany.
- +/- aggression towards people of inanimate objects.
- +/- ataxia when walking.
List clinicopathologic abnormalities in cattle with ketosis.
- Detection of ketone bodies in plasma, milk, urine.
- Blood glucose conc 20-40 mg/dL.
- Total blood ketones > 30 mg/dL.
- Total urine ketones > 84 mg/dL (better indicator than blood ketones).
- Total milk ketones > 10 mg/dL.
- Blood BHB > 3 mmol/L.
- AST, SDH elevated in severe cases.
- Plasma insulin elevated initially then depressed w anorexia.
- Subclinical ketosis: no Csx but low-normal blood glucose, blood ketones 10-30 mg/dL, milk ketones 2 mg/dL, BHB 1.2-2.9 mmol/L, blood NEFAs > 0.5 mEq/L.
What factors mainly influence the control of blood glucose in ruminants?
- Insulin.
- Favours cellular uptake of glucose, lipogenesis, glycogen synthesis.
- Decreases lipolysis and hepatic gluconeogenesis.
- Ruminants are relatively insulin resistant, but during early lactation low insulin conc are accomp by high tissue insulin sensitivity.
