KETOSIS

  • It is characterized as multifactorial disorder of energy balance in ruminants.
  • Itcommonly appears inearly lactation or late pregnancy.
  • Manifested as ketonemia, ketonuria, ketolactia, hypoglycemia, poor liver glycogen content with β- oxidation of fatty acids.
  • Ketone bodies involved are BHBA, Acetone & Isopropanol.
  • It gets precipitated with fever, metritis, mastitis, peritonitis and abomasal displacements during peri-parturient period.

Etiology

  • Blood glucose level is maintained via gluconeogenesis.
  • Very little dietary carbohydrates absorbed as hexose sugar.
  • In rumen carbohydrates are fermented to short chain fatty acids i.e. Acetate, Propionate & Butyrate.
  • Propionate is major glucose precursor and liver is primary glucose producing organ.
  • These propionates and aminoacids (from protein source) are essential for gluconeogenesis, milk lactose &milk protein synthesis.
  • Acetates transported to mammary gland metabolized to long chain fatty acids and secretes as milk fat.
  • Hormones playing role in energy metabolism of ruminants are Insulin , Glucagon &Somatotrophin (most important for milk production)

Primary ketosis

  • Cows in good to excessive body condition commonly affected.
  • Cows with high lactational potential being fed good-quality rations but are in a negative energy balance.
  • Greater proportion of cases remains as subclinical with increased levels of circulating ketone bodies without overt clinical signs.
  • A less proportion of cases appear as clinical ketosis.

Secondary ketosis

  • Concurrent diseases / affections decreasing feed intake in peri-parturient periods of high yielders.
  • The common affections are :
    • Abomasal displacement
    • Traumatic reticulitis
    • Metritis& mastitis
    • Fever
    • Inclined weather

Starvation ketosis

  • Occurs in cattle in poor body condition and fed with poor-quality feedstuffs.
  • There is a deficiency of propionate and protein from the diet and a limited capacity of gluconeogenesis from body reserves.
  • Affected cattle recover with correct feeding.

Epidemiology

  • Commonly Seen in high yielders and intensive farming system. (complete housing)
  • Early lactation period of 3rd or 4th
  • Depends on management &nutritional status of herd.
  • Re-occurrence may appear in same lactation.
  • Median time is 10-28 days post calving, but cows of any age and any lacational stage are also affected.
  • Fattiness at calving due to long dry period predisposes to ketosis.
  • Milk fever, retained placenta, lameness, hypomagnesaemia, mastitis & metritis cause secondary ketosis.

Clinical findings

  • Wasting form (more common)
    • Gradual decrease in appetite& milk yield over a period of 2-4 days.
    • First refuse to eat grains, then silage. May continue to eat hay.
    • Depraved appetite with rapid loss of body wt.
    • Woody appearance due to wasting.
    • Loss of cutaneous elasticity due to loss of s/c fat.
    • Firm & dry feces.
    • Moderately depressed, disinclined to move & eat.
    • Normal temperature, resp, pulse.
    • Normal frequency but decreased amplitude of ruminal motility.
    • Characteristic aromatic odour of ketone from breath.
    • Sharp drop in SNF content of milk.
    • Occasional nervous sign with transient bouts of staggering.
    • Partial blindness.
  • Nervous form
    • Bizarre and begin quite suddenly.
    • Syndrome is delerium rather than frenzy.
    • Walking in circle.
    • Straddling, crossing of legs.
    • Head pressing, leaning into stanchion.
    • Apparent blindness, aim less movement.
    • Wandering, vigorous licking of skin and in animate object.
    • Chewing movement with salivation.
    • Depraved appetite.
    • Bellowing on pinching or when stroked.
    • In coordinated gait with moderate tremor &tetany.
    • Short periods of nervous sign lasting 1-2 hrs, reoccur frequently at 8-12 hrs interval.
  • Differential diagnosis
    • Wasting form
      • Traumatic reticulitis
        • Pain on palpation of hypogastric area.
        • Absence of ruminal motility.
        • Leukocytosis
      • Abomasal displacement
        • sudden anorexia at calving,
        • reduced abdominal size.
        • Small pasty feces.
        • Abomasal sound over lower left abdomen.
        • No response to treatment against ketosis
      • Secondary ketosis from mastitis, metritis
        • Mild fever.
        • Increased heart rate.
        • Leucocytosis
        • Moderateketonuria
      • Vagus indigestion
        • Secondary ketosis with stasis of alimentary tract.
        • Abdominal distention.
        • Moderate bloat.
        • Papple shaped abdomen
    • Nervous form
      • Listeriosis
      • Rabies
      • Lactation tetany.
      • Acute lead poisoning.
      • Poisoning with Clavicepspaspali

Treatment

  • Replacement Therapy
    • Intravenous injection of 50% dextrose 500ml- 2ltrs.
    • Relapses without repeated treatment.
    • s/c should be avoided.
    • i/p 20% dextrose à presence of risk.
    • Fructose more efficient than dextrose but cause reaction with muscle tremor, collapse
  • Oral hyper glycemic agent
    • Propylene glycol orglycerine @ 225g twice a day for 2 days.
    • Followed by 110g once daily for 2-3 days orally.
    • Parenteral glucose with feeding glycerol depresses the fat content of milk.
    • Propylene glycol – absorbed directly from rumen à increases mitochondrial citrate concentration à decreases ketogenesis.
    • Sodium propionate @ 110-225g once daily for 3 days.
    • Calcium lactate / sodium lactate @ 1kg initially followed by 500g daily for 7 days.
    • Ammonium lactate @ 200g daily for 5 days.
  • Steroidal Therapy
    • Glucocorticoid administration à hyper glycaemia within 24 hrs by repartitioning of body glucose rather than gluconeogenesis.
    • 10mg of dexamethasone i/m à hyper glycaemia in cow for 4- 6 days.
    • Triamcinolone: 10- 20 mg -- i/m – on alternate day. (vet log)- 6mg/ml – 5ml
    • Isoflupredone (isoflud)- cattle 12-20mg – i/m. (5ml, 10ml @ 2mg/ml.)
    • Prednisolone –cattle 5-10ml –i/m– every 3rd (10mg/ml– 10ml ampule
    • Trenbolone: 60-120mg trenbolone acetate single injection
    • Nandrolone: 200mg once, repeat after 21 days.

  • Insulin Therapy
    • Cases unresponsive to glucose and steroid therapy require insulin therapy.
    • Facilitates transport of glucose into cells.
    • Cattle: 200-300 I/U may repeat after 24-48 hrs.