Ketosis in different farm animals

Bovine ketosis

Etiology

1. Nutritional or metabolic deficiency in high-yielding cows in early lactation results in negative energy balance.
2. Failure to provide sufficient glucose when the animals are subjected to heavier demands on their resource of glucose and glycogen than can be met by their digestive and metabolic activity.
3. Dysfunction of the adrenal gland. The stress of parturition, lactation (cattle) and stress of late pregnancy (in ewes), and stress of malnutrition leads to decreased ACTH activity.
4. Relative hypothyroidism.
5. Composition of ration – ensilage (high in butyric acid) is more ketogenic than hay.
6. The composition of ruminal flora influences the digestive process and thus changes in end products of digestion and their relative concentrations. Hence, there is a difference in ketogenicity between feeds. Eg. A high protein diet produces more butyric acid.
7. Factors that decrease energy supply, increase demand for glucose, and increase utilization of body fat will lead to ketosis.
8. Animals in 4 -10 weeks post-partum, peak milk yield, and decreased dry matter intake are prone to ketosis.
9. Starvation decreases propionic acid (relative) resulting in excessive utilization of fat.
10. From quantitative and qualitative estimations of ketone bodies in rumen liquor and body fluids, it appears that abnormal ruminal conditions may play an important part in the production of clinical ketosis.
11. Hepatic insufficiency – primary or secondary. Hypoglycemia results in mobilization of fat & its deposition in the liver – the perpetuation of hepatic insufficiency.

Ovine ketosis

• A disease of intensive farming system and relatively rare in grazing units.

Etiology

• Increased plasma cortisol due to environmental and nutritional stress, failure by the liver to metabolize the cortisol.

• Decline in the plane of nutrition during the last 2 months of pregnancy.

• Exposure to inclement weather

• Worm load Eg. Haemonchus contortus.

Types of ketosis

• Ketosis is of two types – Primary (Estate acetonemia) and secondary

Primary (estate acetonemia)

• Ketosis of heavily fed high producing cows
  • Inheritance maybe there
  • Tendency to reoccur in individual animals is probably due to variation in digestive capacity or metabolic efficiency
  • Excessive feeding of ensilage
  • Inadequate exercise
  • Over fatness at calving time
  • Inadequate energy intake during early lactation
  • Specific dietary deficiency of cobalt (essential for metabolizing propionic acid),
  • phosphorous and vitamin B12

Secondary ketosis

Caused by;

• Reduction in appetite
• Abomasal displacement
• Traumatic reticulitis
• Metritis
• Mastitis
• Fluorosis

Epidemiology

• Highly fatal may occur as an outbreak, mostly during the last month of pregnancy

• Ewes carrying more than 1 lamb are more susceptible

• Precipitating factor – fall in the plane of nutrition precipitated by sudden short periods of starvation up to 48 hours (by management), cold inclement weather.

• Occur in animals mainly housed during winter and occasionally in animals at pasture

• Death of animal is rare

• Morbidity variable and difficult to measure

• Economic losses due to individual ketosis

• Prevalence of subclinical ketosis – 10 % in undernourished cows

• Ketosis of pregnant ewes is highly fatal and may occur as an outbreak

• Ketosis in cows is mostly sporadic

• Regardless of specific etiology bovine ketosis is

• Most common during 1st month of lactation
• Less common during 2nd month of lactation
• Occasionally during late pregnancy
• Higher frequency in 20 – 30 days of calving
• Low prevalence at 1st calving
• Peak prevalence at 4th calving

Clinical findings

Bovine ketosis

Wasting form

1. Gradual but moderate decrease in appetite and decreased milk yield over 2-4 days
2. First refuse grains, ensilage but continue to eat hay.
3. Loss of body weight is rapid due to off-feed
4. Woody appearance (due to loss of cutaneous elasticity and s/c fat)
5. Feces firm and dry
6. Cow moderately depressed
7. Disinclined to move
8. Normal temperature, pulse, and respiratory rates.
9. The rate and amplitude of ruminal movements are normal and may be decreased in prolonged cases
10. Ketone odor from mouth and milk
11. Staggering and partial blindness may occur transiently.
12. Severely affected animals die.
13. Spontaneous recovery in about a month, but milk yield never returns to normal level; a sharp drop in SNF content of milk in wasting form.

Nervous form

1. Suddenly appear Bizarre, delirium, walking in circles, straddling or crossing of legs, head pushing or leaning onto stanchion, apparent blindness, aimless movements, wandering, vigorous licking of the skin, and inanimate objects
2. Depraved appetite
3. Chewing movements with salivation
4. Hyperaesthetic- bellowing on pinching or stroking
5. Moderate tremor and tetany
6. Gait is usually staggering.
7. Nervous signs usually occur in short episodes which last for 1 or 2 hrs and may recur at intervals of about 8 to 12 hrs
8. Affected cows may injure themselves during the nervous episodes

source: krishijagran.com

Ovine and Caprine ketosis

1. Similar to the nervous form of ketosis in cows
2. Separate from the flock and apparent blindness (alert but disinclined to move).
3. Stand still when approached by man or dog and no attempt to escape, head pressed against the obstacle, stand in water through all day and lap the water.
4. Feces – constipation, dry and scanty
5. Grinding of teeth
6. Later stages – more severe nervous signs, tremors of muscles of the head, twitching of lips, champing of jaws, and salivation
7. Clonic contraction of cervical muscles, dorsal flexion or lateral deviation of head, circling, convulsions spread to the whole body.
8. Recurrent attack and drowsiness between convulsions
9. Stargazing, incoordination, falling when attempting to walk
10. The smell of ketone in the breath.
11. Course: become recumbent in 3-4 days and then coma for 3-4 days

Source: University of Florida

Clinical pathology of ketosis

Metabolite	Level when diseased	Normal
Primary hypoglycemia	20-40mg/dl	50mg/dl
Secondary hypoglycemia	>40 mg or above normal
Ketones – Primary	10-100mg/dl	Up to 10 mg / dl
Ketones – Secondary	< 50 mg /dl
Urinary ketones (primary/secondary)	80-130 mg/dl	10-70 mg/dl
Milk ketones	Average 40mg/dl	3 mg/dl
Liver glycogen	Low
Glucose curve	Normal
VFA in blood and rumen	Increased

• Field test (Rothera’s reaction): Milk and urine can be tested. It measures only Aceto acetic acid.

• β hydroxybutyric acid – no reaction
• Acetone – very little reaction
• Primary ketosis – strong color
• Secondary ketosis – moderate reaction

Diagnosis

• History regarding the time of calving, duration of pregnancy in ewes, feeding program
• Biochemical examination reveals hypoglycemia, ketonemia, and ketonuria
• In cases of subclinical ketosis: Ketonemia with the absence of clinical signs
• Ovine ketosis: die within 6-7 days

Differential Diagnosis

• TRP,
• Bovine pyelonephritis,
• Indigestion,
• Abomasal displacement,
• Metritis and
• Mastitis.
• The nervous form of ketosis should be differentiated from Listeriosis and Rabies.

Treatment

• Response is less satisfactory. It depends on the severity of the cases and the duration of the disease.

Neither replacement therapy nor hormonal therapy has any effect.

• Oral- glucose 45 g, NaCl 8.5 g, glycine 6.17 g, and electrolytes in 160 ml every 4-8 hrs.

• The flock should be examined for any evidence of ketosis and to be treated with propylene glycol or glycerol.

• Increased carbohydrate intake in the flock.

• In clinical cases – caesarian section, glucocorticoids parentally, glucose or glycerol.

Replacement therapy

1. 50 % glucose 500ml I/V, 20 % glucose I/P,
2. Propylene glycol or glycerine @ 225 mg / day for 2 days then 110 mg / day for 2 days.
3. In sheep, a common complication is acidosis. So sodium bicarbonate is to be given along with replacement therapy.
4. Sodium propionate is 110 -225 mg/ day but shows a very slow response.
5. Lactates: Ca or sodium lactate 1 kg initially, later. kg/day for 7 days or
6. Sodium acetate 110-500 g/day.
7. Ammonium lactate 200g/day for 5 days.
8. Ewes: Sodium ethyl oxaloacetate I/V (costly).
9. Anabolic steroids: Effective treatment for pregnancy toxemia of cows. Trenbolone acetate @
10. 60mg to 100 mg as a single injection.
11. Insulin with glucose or glucocorticoids 200 – 300 I.U. Repeat every 24 – 48 hrs. There is no marked therapeutic advantage.

Miscellaneous treatment

1. Chloral hydrate- Initially, 30 g orally as a capsule, later 7 g bid for several days as a drench in molasses or water. It breaks the starch in the rumen and stimulates the production and absorption of glucose. Also, selectively influence rumen fermentation to produce more sodium propionate.
2. Potassium chlorate can also be given but in some cases, it causes severe diarrhea.
3. Vitamin B12 and cobalt – for the activation of coenzyme A.
4. Cysteamine (precursor of co-enzyme A)- 750 mg i/v
5. Sodium fumarate (precursor of co-enzyme A) 3 doses at 1-3 days interval.
6. Provide adequate food and water.
7. Sheep at pasture is to be driven to shade to avoid heatstroke.
8. Caesarian or corticosteroid to induce parturition.
9. Monensin sodium enhances propionate production in the rumen. Dose 25mg/day in a grain feed mix.

Control measures

Cattle

1. Should not be starved or over fat at calving.
2. Adequate calorie intake at early lactation.
3. Feeding in preparation for the next lactation should not begin until about 4 weeks to calving.
4. 4 weeks before calving: silage or hay or pasture maintenance + 1 Kg concentrate/ day; gradually increase to 5 kg concentrate/day at calving.
5. After calving, increase concentrate as production increases i.e. 3 kg hay/ 100 kg b.wt. or 9 kg ensilage/ 100kg b.wt. as maintenance + 1 kg concentrate /3 kg milk produced.
6. Protein should not exceed 16-18 %.
7. Exercise is a must in intensive rearing.
8. The ration should contain Co, P, and I2.
9. Avoid wet ensilage or moldy hay or dusty hay (as they have increased levels of butyrate).
10. Prophylactic feeding of sodium propionate @ 110g daily for 6 weeks.
11. Sodium propionate 110 g/ day for 6 weeks
12. Propylene glycol @ 350 ml / day for 10 days after serving or 6% of concentrate ration for 2 months.
13. Blood glucose and milk ketone estimation during the 6th week of lactation.

Sheep

1. Same as in cows. Monensin sodium @ 25 mg/day as feed mix.
2. Ensure that the plane of nutrition is raising in 2nd half of pregnancy.
3. During last 2 months: concentrates containing 10% protein @ 0.25 kg/ day, increasing to 1 kg/ day during last 2 weeks.
4. Avoid sudden change in feed.
5. Ensure extra food during bad weather.
6. The shelter should be available in the pasture.
7. Ewes should be driven out for 1/2 hour twice daily in well-fed flocks.
8. If pasture is available, only concentrate should be fed.

General

Manipulation of ration to produce more propionate in the rumen (ration of finely ground roughage, cooked grain, cod liver oil with certain unsaturated fatty acid are anti ketogenic and produces less milk fat thereby reducing energy loss).

1. Blood glucose estimation at 2-6 weeks of lactation (< 35 mg % needs attention). Regular tests for ketone in urine are to be done from the 2nd week.
2. Estimation of β hydroxy-butyrate levels in early lactation.
3. Palatable feeds and frequent feeding.
4. 1/3rd of total D.M consumption through good quality roughage helps to maintain appetite.