a disturbance in the normal metabolic mechanisms resulting in a failure of homeostasis, and result from a breakdown in the animal's capacity to meet the demands of high production. 

negative energy balance

in early lactation

resulting in subclinical acetonaemia which has profound effects on cow health, productivity and future fertility. 

may have upto 20% fat in the liver in the immediate periperturient period

normal cow has less than 5%

If the negative energy balance is severe and prolonged, you can get more than 20%, which can interfere with liver function-> fatty cow syndrome

1. increase the amount of energy taken in from the diet: either increase the energy density of the diet or increase the DM intake 

1. mobilisation of body reserves ( body fat and protein)

Cows on knife's edge

propionate->oxaolacetate -> TCA cycle ->gluconeogenesis

Acetate and butyrate-> acetyl COA

Energy stable: fat deposition, energy via TCA cycle ( need oxaloacetate) 

Energy defecit: ketone bodies as no oxaloacetate present 

1. primary acetonaemia: may occur during early lactation, cant consume enough energy to supply her glucose requirement

2. secondary acetonaemia: secondary to diseases that suppress food intake

1. inadequate energy content of the ration ( Type 1) 

2. inadequate intake of the diet

3. secondary acetonaemia- followin primary disease ex. LDA

4. excessive intakes of ketogenic food: eg. silage with high levels of butyric acid

5. poor rumen function: sudden changes in diet, excessive concentrates ( SARA) 

6. poor utilisation of the diet

7. poor transition cow nutrition (Type II) 

occur within first month of calving

Two forms: 

1. Wasting form

2. Nervous form

most common form

loses BC over days or weeks

loss of appetite, drop in milk yield

dark faeces, firm with waxy appearance ( like a horse) 

TPR usually normal 

hypoglycaemic encephalopathy

jumpy to a frenzied dilirium

head pressing, circling, wandering, licking objects

signs are intermittent because the CSF glucose and blood glucose levels wax and wane 

1. History- high yielding, first month lactation

2. clinical signs- 

3. clinical biochem: hypoglycaemia, mobilisation of fat, ketone bodies

hypoglycaemia: low plasma glucose levels ( below 3mmol/l)

mobilisation of body fat: elevated NEFA levels, over 0.7

Ketone bodies: levels of beta hydroxybutyrate in the serum/plasma, Blood BHB over 3mmol/l, cowside test: rethera's reagent- milk or urine 

Restoration of blood glucose levels

- use 400ml of 40% IV- only lasts for 2-4 hours

- oral admin of glucose precursors such as propylene glycol or glycerine twice daily by drench

- glucocorticoid hormone therapy: dexamethasone, stimulate gluconeogenesis, reduces milk yield ( reducing energy requirements) 

- vitamin B12 is essential for propionate and thus some people drench with cobalt to promote b12 synthesis

- correct predisposing factors

- chloral hydrate: propionate fermentation

reduced milk yield

reduced milk quality ( depresses milk protein)

increased incidence of clinical disease

immunosuppression

reduced fertility

1. Diagnosis of clinical disease

2. loss of BCS

3. milk production records: reduced persistency

4. reduced fertility

5. metabolic profiles

extreme manifestation of NEB and fat mobilisation in early lactation. is due to excess BCS in fat dry cows prior to calving

This will result in a depressed DMI at calving, thus enter a state of severe NEB in early lactation-> fat deposited in liver in mass amounts, thus interferes with liver function

- fat dry cows >4, rapid BC loss in early lactation

- reduced appetite, anorexia

- reduced milk yields

- metabolic disease unresposive to conventional therapy

- high mortality rates

- about 34% fat -> severley affected 

1. History and clinical signs

2. Biochem

3. disorders of fat mobilisation

4. elevated liver enzymes and bilirubin

5. depression of the immune system, low WBC

6. massive fatty liver on PM 

prognosis very poor

symptomatic treatment to enhance energy metabolism and promote liver function

euthanasia may be the best option for the advanced cases 

1. correct dry cow management- cows 2.5-3-avoid excess fat, 

2. provision of suitable ration to cows in late dry periods- good forage to cows, diets that increase levels of insulin and thus levels of propionate production, by the feeding of high quality concentrate, dont overestimate energy contribution from forages available- ex. grazing at grass

3. Maximise dry matter intake in the late dry period 

4. good nutrition management- change gradually, group cows according to nutritional requirements , heifer management- enough space for everyone, ensure that atleast 40% of ration is dry matter  good quality forage 

5. optimum rumen health: do not overfeed concentrates

6. ensure cowcomfort

7. monitor nutritional status: BCS, feaces, metabolic profiles

8. sodium monensin- improve propionate production- alters microbial population in rumen to favour propionate production, increases feed conversion effeciency ( uk- slow releasing bolus) 

metabolic disease in lowground flocks in the last month of pregnancy

- version in suckler cattle-poor diet

- the rapid growth of the foetus in the last month results in a marked increased in glucose requirements of the gravid uterus 

- last month of gestation

- ewes carrying two or more lambs

- prolonged period of energy shortage ( inadequate forage, concentrates) 

- ewes in poor condition score, but may occur in overfat ewes

- older ewes

- stress makes it worse- bad weather, housing , handling

- isolation from flock, refusal to feed

- easy to catch, dull and depressed

- neurological signs, head pressing, star gazing

- progression to recumbancy

- high mortality rate

- affected ewes will frequently abort 

clinical signs and history

serum betahydroxybutyrate levels over 3.0

PM- fatty liver

presency of two or more foetuses in the ewe

Response to treatment poor

50-70% mortality rate

treat early: 

- 160ml oral electrolyte and glucose solution or 50ml propylene glycol orally 4 times daily

- 100 ml 40% glucose IV, as well as calcium if needed. 

- TLC

- induce parturition- if ewe is more thn 136 days pregnany, induction of parturition within 48 hours can be performed using 16mg dexamethasone

- euth or C section 

dependent on nutrition of the ewe, and provision of quality feed to ewes in late pregnancy