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Common metabolic diseases of cattle
1. Common Metabolic Diseases Of
Cattle In Nepal
Presenter:
Ganesh Adhikari
B.V.Sc & A.H (TU)
9th Semester
1
Clinical Conference-I
2. COMMON METABOLIC DISEASES OF CATTLE IN NEPAL
Ganesh Adhikari
B.V.Sc. & A.H. 8th Semester
Class Roll No. 15
Institute Of Agriculture and Animal Science (IAAS)
Tribhuvan University
ABSTRACT
Livestock sector in Nepal is not well-developed in terms of nutrition, feeding and
management causing alteration in metabolism of animals which leads to health
disorders. Nutritional imbalances, deficiencies, improper management of feeding
programs for dairy cattle can create large number and various types of health
problems generally categorized as metabolic diseases. High producing dairy cows
are most susceptible to metabolic diseases during the peri-parturient period. In
Nepalese context, common metabolic diseases which cause acute, temporary or
fatal disorders in cattle are Milk Fever/hypocalcaemia, Ketosis, Hypomagnesaemia,
Fat cow syndrome, Hypoglycaemia, Grass Tetany, Acute Hypokalaemia and Post
Parturient Hemoglobinuria (PPH). An important aspect of dealing with production-
induced metabolic diseases is accurate and rapid diagnosis. Most of these
metabolic diseases can generally be treated with systemic administration of
deficient nutrient or metabolite along with supportive therapy.
Key Words: Hypocalcaemia, Hypoglycaemia, metabolic disease, PPH
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3. Introduction:
Nutritional imbalances, deficiencies, or erratic
management of feeding programs for dairy cows can
create large numbers and various types of health
problems generally categorized as metabolic diseases.
High producing dairy cows are most susceptible to
metabolic diseases during the peri-parturient period.
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6. Milk Fever/Hypocalcaemia
It is a metabolic disease caused by a low blood calcium
level.
About 80% of cases occur within one day of calving
because milk and colostrum production drain calcium
(and other substances) from the blood
High producers like jersey are more susceptible than
local nepalese breeds.
Increase in susceptibility with the age.
Estimated to occur at 5-7% nationwide. (Gaire et al.,
2000)
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7. Etio-pathogenesis
Excessive loss of Calcium in the colstrum
Deficiency of Vit. D
It is converted to 1-25dihydroxycholecalciferol
Which is activated form of Vit. D3 which helps in Ca++
absorption in the intestine
Excessive calcitonin level and PTH insufficiency
Causes failure to mobilize calcium
These causes low blood calcium level, hyperexcitability of the
nervous system and weakened muscle contractions.
Paresis and Tetany
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10. Treatment
Supportive Therapy: Treatment generally involves calcium injection by
intravenous, intramuscular or subcutaneous routes.
I/V injection of Calcium Borogluconate 25%
Eg: Thiacal 450ml
Supplementation Therapy: 1 ounce of Sodium acid phosphate + 4
ounces of glucose I/V helps in absorption of Ca++
Corrective Therapy: Inj. Avil 10-15 ml I/M
Immediate response to treatment
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11. Ketosis/ Acetonemia
Ketosis or acetonemia, is an increase of "ketone bodies"
(acetone, acetoacetate, and 3-hydroxybutyrate,
subsequently referred to as ketones) in blood until they
eventually begin to spill over into urine and (or) milk.
In dairy cows, ketosis is a metabolic disorder usually
associated with intense milk production and negative
energy balance.
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12. Etio-pathogenesis
Low in nutrition + Formation of lactose and milk fat
Decrease glusose level in blood
Lack of CHO in hepatic cells
Leading to β-oxidation of fats and Mobilization of Non-esterified
fatty acid(NEFA) from fatty tissues
Production of Ketone bodies
(Acetoacetic acid, β-Hydroxy butyric acid)
Ketosis
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13. ClinicalsignsOccursintwoforms:
Digestive or Wasting form of Ketosis:
• Decrease in apetite
• Milk production falls
• Dull depressed and declined condition
• Vulvar discharge
• Odour of ketone bodies in breath and milk
• Temperature, pulse and respiratory rates are within normal range
Nervous form of ketosis:
• Circling movements
• Blindness and unusual wandering
• Hyperaesthesia
• Profuse salivation
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14. ClinicalPathology
Blood Glucose Level: Reduced to below 30mg/dl
(Normal 40-55 mg/dl)
Ketone bodies in milk: 40 mg/dl (Normally ketone
bodies are not excreted in milk)
Ketone bodies in Urine: 500-1000 mg/dl (Normally very
little or no excretion of ketone bodies in urine)
Serum Magnesium level also slightly reduced to less
than 2.5mg/dl
Diagnosis
History,ClinicalpictureandBiochemicalpropertiesare
valuableaidfordiagnosisofthedisease.
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15. Treatment:
Replacement Therapy:
Glucose or Dextrose 500-800 ml of 40-50% solution I/V
Glycerol @ 100mg twice daily for 3 days. Glycerol helps in
glucogenesis
Sodium Propionate 100-200 gm once daily for 3 days
Hormonal Therapy:
Betamethasone or Dexamethasone 30 mg I/M
Prednisolone 10 ml injection I/M
(Reduce ketone body formation)
Insulin Therapy:
200 I.U. (facilitate glucose transport)
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17. Etio-Pathogenesis
Low phosphorus containing plants
Phospholipid layer of wall of R.B.C
reduced
Increased Fragility of cell wall
Haemolysis
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Toxins like saponin, sulphoxides
Causes irreversible oxidative
changes in haemoglobin
Formation of heinze bodies
R.B.C are erythrophagocytised
in spleen
18. ClinicalSigns
Anorexia, dull, depressed and weakness
Severe depression of milk yeild
Haemoglobinuria- light brown to deep red coffee
coloured urine
Haemolytic jaundice
Dehydration
Cesation of rumination
Heart rate and breathing are rapid
Death due to anaemic anoxia
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19. ClinicalPathologyAndDiagnosis
Phosphorus Level down to 0.5-2.5 mg/dl (Normal 4-7
mg/dl)
Erythrocytic and hemoglobin counts are reduced.
Heinze bodies may be present in erythrocytes
Blood urea Nitrogen level increased
Light brown to coffee coloured urine
Diagnosis is made on the basis of the History, clinical signs
and clinical examination of blood and urine.
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20. Treatment
Immediate Correction of Anaemia
Transfusion of upto 5 litres of whole blood is recommended.
Supportive therapy:
• Fluid therapy to minimize danger of haemoglobinuric nephrosis
• Haemanitic drugs preparation of Cupper, cobalt and iron is
effective
• Livertonic like Vetliv, Livogen 20-30 ml orally.
Specific Therapy:
• Phosphorus supplement in the form of Na-acid phosphate 80 g
dissolved in 400 ml of distilled water given I/V slowly
• Oral dosing with bone meal (120 gm twice daily)
• Tonophasphan Injection can be administered to correct
hypophosphatemia
• Ascorbic acid 5gm per cow I/V
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21. Hypomagnesemic Tetany
It is a metabolic disease characterized by hyperaesthesia,
incoordination, tetany and convulsion as a result of
disturbed magnesium homeostasis.
This disease may occur as a complex accompanied with
varying degrees of hypocalcaemia, ketosis and
hypophosphatemia.
Classified as:
Lactation tetany
Grass tetany
Milk tetany
Transit tetany
21Source: mydairyvet.net
22. Etio-pathogenesis
Following excessive feeding of lush green pastures + High
milking
Low Magnesium level in blood (hypomagnesemia)
Decrease in Mg:Ca ratio
Calcium stimulates secretion of Acetylcholine esterase
(Ach) which is responsible for tetanic signs
Tetany, Convulsion, Hyperaesthesia
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23. Clinicalsigns
Sudden caesation to graze
Twitching of muscles and ears
Hyperaesthesia
Staggering gait
Clamping of jaws and vigorous limb movements
Frequent urination and defaecation
Violent convulsion
Increase in temperature and heart rate
Lead to death by paresis and circulatory collapse
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24. ClinicalpathologyandDiagnosis
Serum Mg level: reduced to less than 0.5 mg/dl (Normal 2-
3 mg/dl)
Serum Calcium level reduced
Urine Mg level: Less than 1 mg/dl (reduced)
Diagnosis: Done on the basis of History, Hyperaesthesia ,
tetany and the clinical pathology of blood and urine
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25. Treatment
Administer Solution Coantaining Calcium and Magnesium Salts.
Mifex @ 1 bottle. Half i/v followed by s/c
Magnesium sulphate can be administered as enema. 60 gm dissolved
in 200ml
Oral preparation of 100gm magnesium oxide, 50 gm Calcium
carbonate and 50 gm of Sodium chloride can be given.
Prevention measures
Preventing cow from feeding to excessive green pastures
Feeding of Magnesium supplement on feed or drinking water on daily
basis
Hay treatment with Magnesium oxide. 25