Discuss about the factors attributable to acetonaemia in buffalo alongwith its clinical findings, diagnosis, differential diagnosis and line of treatment.

Factors Attributable to Acetonaemia in Buffalo

Acetonaemia in buffaloes is a complex disorder influenced by a combination of nutritional, physiological, and management factors.

• Negative Energy Balance: This is the primary underlying cause. In early lactation (typically 10 days to 2 months post-calving), milk production rapidly increases, demanding substantial glucose for lactose synthesis. If the feed intake does not meet this high energy demand, the buffalo enters a state of negative energy balance.
• Nutritional Factors:
  • Low-Energy Diets: Insufficient intake of carbohydrates and energy-rich feeds, especially during the periparturient period.
  • Poor Quality Forage: Diets high in poor quality roughage or silage with a high content of butyric acid can predispose to ketosis. Butyrate is a ketogenic precursor.
  • Sudden Dietary Changes: Abrupt changes in feed type or quantity can disrupt rumen microbial activity and reduce feed intake.
  • Underfeeding/Anorexia: Any condition leading to reduced appetite, such as concurrent diseases (e.g., metritis, mastitis, lameness), stress, or unpalatable feed, decreases glucose precursor availability.
• Physiological Factors:
  • High Milk Yield: High-producing buffaloes have a greater demand for glucose, making them more susceptible.
  • Stage of Lactation: Most common within the first 2-8 weeks post-calving, coinciding with peak lactation.
  • Number of Lactations: Incidence is often higher in buffaloes during their 3rd to 5th lactations, though it can occur from 1st to 6th.
  • Over-fat or Thin at Calving: Buffaloes that are too fat (Body Condition Score > 3.5) at calving tend to have lower dry matter intake in early lactation. Conversely, overly thin animals lack sufficient body reserves.
  • Hepatic Insufficiency: Impaired liver function can reduce gluconeogenesis (glucose production from non-carbohydrate sources), which is vital in ruminants.
• Management Factors:
  • Lack of Exercise: Can decrease the utilization of ketone bodies by muscles.
  • Inclement Weather/Cold Stress: Increases energy requirements, exacerbating negative energy balance.
  • Overcrowding and Stress: These factors can lead to reduced feed intake.
  • Cobalt Deficiency: Cobalt is essential for rumen microbial synthesis of Vitamin B12, which is required for propionate (a major glucose precursor) utilization.

Clinical Findings

Clinical ketosis in buffaloes primarily manifests in two forms: the wasting form and, less commonly, the nervous form. Subclinical ketosis, characterized by biochemical changes without obvious clinical signs, is also prevalent.

1. Wasting/Digestive Form (Most Common)

• Selective Anorexia: Refusal to eat concentrate feeds, but often still consuming roughages.
• Marked Drop in Milk Production: A sudden and significant decrease (25-100%) in milk yield.
• Rapid Loss of Body Weight: Progressive emaciation, leading to a "woody" appearance and loss of skin elasticity.
• Moderate Depression and Lethargy: Dullness, disinclination to move, and decreased activity.
• Sweetish/Acetone Smell: A characteristic sweet, pungent odor in the breath, milk, and urine due to the excretion of acetone.
• Feces: Usually firm, dry, and often covered with mucus; ruminal motility is reduced and weak.
• Vital Parameters: Body temperature, pulse, and respiration rates are typically normal.

2. Nervous Form (Less Common)

• Exhibits more pronounced neurological signs, often observed in severe cases.
• Abnormal gait, circling, incoordination, and staggering.
• Hypersensitivity, licking of body continuously, head pressing, and grinding of teeth.
• Aggressiveness or apparent blindness.
• These signs can be intermittent, lasting a few hours.

3. Subclinical Ketosis

• Characterized by elevated ketone bodies in blood, milk, or urine without visible clinical signs.
• May cause a mild drop in milk yield.
• Can progress to clinical form or resolve spontaneously.

Diagnosis

Diagnosis relies on a combination of history, clinical signs, and laboratory tests.

1. History:

• Recent calving (2-8 weeks post-partum).
• High milk yield, underfeeding of carbohydrates, or sudden dietary changes.

2. Clinical Findings:

• Selective appetite, significant drop in milk production, emaciation, and the characteristic sweetish breath odor.

3. Laboratory Tests:

• Urine/Milk Ketone Tests (Field Tests): These are quick and cost-effective screening tools.
  • Rothera's Test: Detects acetoacetate and acetone in urine or milk using sodium nitroprusside reagent. A color change (purple) indicates positive. A positive result in milk is more significant for diagnosis as urine normally contains low levels of ketones.
  • Commercial Ketone Test Strips (e.g., Keto-Diastix, BHBCheck™): Convenient for rapid detection of ketone bodies (acetoacetate and beta-hydroxybutyrate) in urine, blood, or milk.
• Blood Analysis:
  • Hypoglycemia: Reduced plasma glucose concentrations (e.g., below 40 mg/dL; normal is 50-65 mg/dL).
  • Ketonemia: Elevated plasma or serum beta-hydroxybutyrate (BHB) levels (e.g., > 2.5 mmol/L for clinical ketosis, > 1.0 mmol/L for subclinical ketosis; normal is < 1.0 mmol/L).
  • Elevated NEFAs: Increased non-esterified fatty acids (NEFAs) in plasma (above 0.3 mmol/L) indicate fat mobilization.
  • Other changes: Elevated total bilirubin, decreased liver glycogen, changes in liver enzymes (AST, ALT).
• Response to Treatment: A good response to specific anti-ketotic treatment, especially glucose therapy, can support the diagnosis.

Differential Diagnosis

It is crucial to differentiate acetonaemia from other conditions presenting similar signs, especially those causing anorexia, weight loss, or reduced milk yield.

Condition	Distinguishing Features from Acetonaemia
Traumatic Reticuloperitonitis/Pericarditis	Fever, recurrent tympany, evidence of pain, X-ray reveals foreign body. No or transient response to ketosis treatment. Pericarditis may show chest pain, brisket edema, muffled heart sounds.
Displaced Abomasum (LDA/RDA)	Often presents with reduced appetite and milk drop. Auscultation and percussion over the left/right flank reveals a "ping" sound. Ketones may be present as a secondary complication.
Hypocalcaemia (Milk Fever)	Muscle weakness, recumbency, cold extremities. Some cows with hypocalcaemia may also develop secondary acetonaemia.
Metritis/Mastitis	Signs of uterine infection (discharge, fever) or mammary gland inflammation (swelling, heat, pain, abnormal milk). These can cause secondary ketosis due to reduced feed intake.
Indigestion/Ruminal Acidosis	General digestive upset, altered ruminal motility, changes in fecal consistency. History of dietary mismanagement.
Listeriosis	Nervous form of acetonaemia can resemble listeriosis, but listeriosis usually presents with fever.
Hypomagnesaemia (Grass Staggers)	Hyperexcitability, muscle tremors (especially eyelids), tetanic convulsions. Distinct neurological signs from ketosis.
Bovine Spongiform Encephalopathy (BSE)	Progressive apprehension, kicking. Blood glucose and ketone levels will be normal in BSE.
Rabies	Mania, ascending paralysis, always fatal.

Line of Treatment

The treatment of acetonaemia aims to restore normal blood glucose levels, promote complete oxidation of fatty acids, and increase the availability of dietary glucogenic precursors.

1. Immediate Glucose Restoration:

• Intravenous Glucose: Administration of 500 mL of 40-50% dextrose solution intravenously is the most common and immediate therapy. This provides a rapid, though transient, rise in blood glucose. It may need to be repeated.

2. Glucogenic Precursors (Oral):

• These compounds are metabolized to glucose in the liver, providing a sustained energy source.
  • Propylene Glycol: 200-400 mL daily orally for 3-5 days. It is preferred over propionate or glycerol as propionate can be fermented in the rumen causing digestive disturbances, and glycerol can be converted to ketogenic acids. Doses over 500 mL/day may be deleterious.
  • Sodium Propionate: 80-110 g orally daily for 5-6 days.
  • Glycerol/Glycerin: 110-220 g daily for 4 days.
  • Jaggery: Oral administration of jaggery is a traditional supportive therapy.

3. Corticosteroids:

• Dexamethasone, Betamethasone, Triamcinolone acetonide: These drugs increase blood glucose by promoting gluconeogenesis and decreasing tissue uptake of glucose. They also reduce milk production temporarily, diverting energy.
  • E.g., Dexamethasone @ 0.04 mg/kg IV daily for 2-3 days.
  • Often used in combination with glucose therapy for enhanced efficacy.

4. Insulin:

• Insulin Therapy: Glucose (20% @ 0.5g/kg IV) plus protamine zinc insulin (200-300 IU/animal) can be highly effective, especially in cases unresponsive to glucose or corticoid therapy. Insulin suppresses fat mobilization and promotes glucose uptake.

5. Supportive Treatments:

• Vitamin B Complex: Injectable liver extract with B complex (5-10 ml IM on alternative days) helps improve metabolic functions. Vitamin B12 is particularly important for propionate utilization.
• Mineral Mixture: Provision of mineral mixture comprising phosphorus and cobalt.
• Anabolic Steroids: Trenbolone acetate (60-120 mg single injection) can be effective.
• Dietary Adjustments:
  • Offer highly palatable, energy-dense feeds (e.g., ground maize, molassed feed) to encourage appetite.
  • Gradually increase concentrate feeding in early lactation.

6. Management and Prevention:

• Optimal Body Condition Score: Aim for a BCS of 3.0-3.5 at calving to avoid both over-fat and overly thin animals.
• Adequate Nutrition: Ensure a balanced, high-energy diet during the transition period and early lactation. Gradually increase grain rations pre-calving.
• Reduce Stress: Minimize overcrowding, provide adequate exercise, and protect from inclement weather.
• Regular Monitoring: Weekly testing of urine/milk samples for ketones up to two months post-calving in high-risk animals.
• Prophylactic Use of Glucogenic Precursors: Oral propylene glycol (e.g., 250 ml once daily for 5 days during the close-up dry stage) can effectively prevent subclinical ketosis in high-risk buffaloes.