Line of Treatment of common Metabolic diseases in Bovines(Cattle & Buffalo)-A Brief discussion
Harshit Saxena
Uttar Pradesh Pandit Deen Dayal Upadhyaya Pashu Chikitsa Vigyan Vishwavidyalaya Evam Go Anusandhan Sansthan, DUVASU, Mathura srhiharshit@gmail.com
The Pandora box of resources in Indian subcontinent holds what not!!! In context to livestock resources,India is Paramount in the milk production. Apodictically when it comes to milk it is mainly Cattle and Buffalo without which the story of triumph of Dairy Industry can’t be completed. India with about 125.85 million milch cattle and buffalo (both dry and lactating) is hub of Dairying. Producing not only quantity but quality milk from indigenous varieties. But despite of such a high number of Milch Animals and Total milk production the per capita milk production is quiet low and the rationale lies behind this is Extensive Dairy management, Lack of education in farmers and prevalence of diseases in herds. When comes to diseases they can be classified on the basis of different etiologies like bacterial,viral, fungal, parasitic and metabolic. All other diseases except metabolic are mainly attributed to the entry of exogenous agent/pathogen in the the body of the animal .However, when it comes to metabolic diseases it is attributed to the failure of homeostatic and homeorrhetic mechanism of the animals. Leading to deficit of nutrients store of the animal assimilating factors like variation in metabolic needs during pregnancy and lactation, age-related decline in body homeostasis both in young and old animals and lastly mis-managed diet of the animals are keyplayers of pathogenesis. Though diseases can be prevented by taking appropriate prophylactic measures but when it comes to metabolic diseases the prophylaxis become more tricky and sometimes with all efforts the change of metabolic needs of animal cannot be concurrent with our management & this Metabolic depreciation leads to direct fall in production of the animal and hence devising a proper line treatment is of utmost importance for Veterinary professionals so that farmers and corporates can prolong their business with livestock to positive side. And also healthy and Happy animals produce healthy food!!! Thus, this article describes in brief the line of treatment of common metabolic diseases in Cattle and Buffalo.
Milk fever:
Animals with high milk yield, geriatric animals and those with mismanaged diet both pre and post partum are susceptible to milk fever. Administration of Calcium is the main line of treatment which is prescribed both orally and through parenteral route. Parenteral treatment of stage 2 and stage 3 of milk fever is done by administration of commercially available Calcium borogluconate and Calcium gluconate former preferred being more soluble. As a thumb rule 2g Ca/100 body weight IV @ 1g Ca/mint is injected. Calcium borogluconate preparation commercially available as 500ml ; 23% solution having 19.78 mg Ca/ml supplies 8.5g to 11.5g Ca/500 ml of preparation. As Ca through intravenous route elevate serum level of Ca only for approx 4 hrs. Thus dose must be divided equally between Intravenous and Subcutaneous route of administration with 50-75 ml of preparation/site that is 1-1.5 g Ca /site. Oral administration of calcium is generally not preferred in clinical cases but as prophylactic measure and in stage 1 of milk fever. The aim of PO Ca administration is to increase intestinal ionised Ca to a level so that passive absorption of large amount of Calcium can occur independent of Vitamin D. Oral preparations include concentrated solutions and gels of Calcium chloride and Calcium propionate former being irritant is less preferred but contains high proportion of Calcium as compared to Calcium propionate thus requiring lesser dose. Next approach is by modifying Dietary cation anion difference (DCAD) inducing moderate metabolic acidosis. Strong cations such as CaCl2 ,CaSO4, MgCl2, MgSO4 and NH4Cl or acids of anions such as HCL or H2SO4 is used for this. Ammonium chloride is one the best acidifier prescribed at the rate of 62-100/g/day/ cow for 14 to 21 days before parturition & at least five days after postpartum. Sometimes PO dose of 20 million Vitamin D2 for 5 days before parturition is also prescribed or IM dose of 1 million IU/45 kg of body weight before 2-8 days of Calving is suggested. Lastly hypomagnesemia if present must be resolved because such animals are very highly susceptible to milk fever. The golden rule of reducing dietary calcium concentration in closeup dairy animals in order to prevent quiescence of homeostatic calcium mechanism must also be kept in mind.
Ketosis:
Transition from non-lactational to lactational phase is regulated through many homeorhetic changes. Energy metabolism generally fails during this transition due to several factors like reduced voluntary DM intake (type1), increase demand of energy for milk and over conditioned/fatty (type2) cows leading to a state of negative energy balance and accumulation of ketone bodies.
Ultimate aim of therapy is to increase the glucose level in the blood, reduce ketogenesis , lipolytic activity and thrust liver to undergo gluconeogenesis. Replacement therapy include in fusion of 500 ml 50% solution of glucose or glucogenic precursors such as propylene glycol, glycerol and propionate. Propylene glycol 225g BID followed by 110g each for 2-2 days each prescribed with care because overdosing of it may lead to CNS depression. The glucogenic precursors resolve the condition by converting into propionate which act as strong stimuli for insulin synthesis and also convert into glucose via gluconeogenesis. Hormonal therapy aims at administration of glucocorticoids like Dexamethasone 21-isonicotinate @10mg for 4-6 days, Dexamethasone sodium phosphate @40 mg, Flumetasone @5 mg. Isoflupredone acetate@ 5- 20mg IM is also recommended but it can produce profound hyperkalemia which can exaggerate the condition. In type 2 ketosis that occur 1-2 week after calving long acting insulin like protamine zinc insulin is given subcut@ 200 to 300 IU/day in combination with glucose (to prevent hypoglycemia) here insulin actually suppresses mobilization of fat from adipose tissue and also ketogenesis and facilitates glucose cellular uptake and hepatic gluconeogenesis. Anabolic steroids such as Trenbolone acetate can also be prescribed in overfat and stressed animals. Miscellaneous treatment involves biological precursor of coenzyme A -Cysteamine @750 mg IV repeated 3 times at interval of 2-3days, Methyl donors choline and methionine to increase FFA oxidation efficiency of of hepatocytes. Electron transporters of NADP like Niacin reduced phosphorylation of HSL and has antilipolytic effect. Monensin which indirectly inhibit adipose lipolysis inhibiting growth of Gram positive bacteria and increasing propionic acid production is also given. Trivalent chromium given to potentiate effect of insulin.
Acute Hypokalemia:
Treatment aspect of acute hyperkalemia is convexed to the lactating dairy animal which are at high risk of the condition due to excretion of potassium during glycogen catabolism. Anorexia of 24 to 48 hours plays a pivotal role in developing hypokalemia. Administration of corticosteroids particularly Isoflupredone acetate and also sometimes Dexamethasone develops hypokalemia. Other conditions like metabolic alkalosis, hyperglycemia and hyperinsulinemia , dehydration also associated with the above condition thus the first attempt to prevent hyperkalemia is to minimize use of of above mentioned corticosteroids and keep an eye over potassium levels via clinical signs during administration of dextrose & insulin. Anorexia in case of hyperkalemia is virtual means animal is inappetant due to inability to reach the feed due to to neck that doesn’t supports weight with typical S shaped posture thus animal must be kept in close vicinity of feed and water so that the two can remain accessible to animal. The treatment is is based on supplementing the deficit of potassium exogenously, preventing alkalemia dehydration and surgical correction of Abomasal displacement. Recommended dose of Potassium chloride is 240250g/cow/day. Orogastric intubation & administration of 120 gram KCL should be done twice in 24 hours. Dose can be standardized as 4g/kg body weight. IV administration of KCl can be dangerous and thus must be done with utmost care. It is advised to use isotonic solution of potassium chloride 1.15% @ 3.5 ml/kg/hr at maximum delivery speed of 0.5 Meq of Pottasium /Kg/hour.
Hypomagnesaemic Tetany/ Grass Tetany/ Grass Staggers/ Winter Tetany:
Maintenance of normal magnesium level in bovine blood is not controlled by feedback regulatory mechanism but depends only upon dietary magnesium absorption through Mg2+ ion channel and Mg2+/2Cl- cotransporter. Clinical signs of hypomagnesemic tetany is manifested when serum level of Mg falls down below 1.8mg/dl in high yielding lactating animals due to secretion of 120 to 150 mg of Mg/kg of milk. Feeding of fast growing grasses with high potassium and low sodium content can a precipitate the condition called grass tetany while feeding of cereal forages like wheat, barley, and rye can cause the condition winter tetany. Hypomagnesemia is also observed in calves of 2-4months (when concentration of Mg < 0.8mg/do) which are solely dependent on whole milk and rapidly growing with incorporation of Mg in the soft tissues. Line of treatment aims supplementation of magnesium exogenously. IV infusion of 200-300 ml of 20% MgSO4 Subcut. administration of 200 ml 50% solution of Magnesium lactate or MgSO4 is done by keeping a close monitoring of respiratory and heart rhythms and must be administered slowly to prevent cardiac arrest. PO administration of 30g MgSO4/day and Rectal infusion of 30g of Magnesium Chloride in 100ml solution is also prescribed. It is advised to administer Chloral hydrate or tranquilizers in order to calm animal and avoid respiratory paralysis during treatment. Animals must be provided with mineral mixture blocks and forages must be given only after the reach the stage of maturity > 6 inches length. Fertilizers like of N and K must not be used in the pastoral land.
Postparturient Haemoglobinuria(PPH):
Hypophosphatemia is attributed as the main cause of PPH but deficiency of Cu and Se, feeding of Brassica specie, sugar beets, cruciferous plants with haemolytic toxins like saponins also cause the disease even ingestion of cold water in extreme cold weather can also precipitate the condition. Intravascular hemolysis of RBC due to increased osmotic fragility is due to decrease in ATP and Creatine phosphate, impaired cell membrane stability, decrease glycolysis and glycogenolysis in RBC due to lack of Pi for phosphorylation, and shift of oxygen hemoglobin dissociation curve leading to hypoxia may occur in hypophosphatemia. Line of treatment involves administration of Inorganic phosphate(Pi) over organic phosphate like Butafosfan & Toldimfos. Sodium acid phosphate is used as 60g in 300 ml of distilled water IV and Subcut. injection at every 12hrs , 3 times. During IV administration of phosphorus it should not accompany cations like Ca, K, Mg because they may precipitate Pi. Generally iron preparation should be restricted to prevent deposition of iron in organs like liver and oral hematinics are advised. Inclusion of bone meal 120g twice daily can also be suggested for 5 days. Transfusion of whole blood 5l/450 kg animal or crystalloid fluid administration is also recommended to prevent haemoglobinuric nephrosis. Fluid containing dextrose and alkalinizing property must not be used.
The syndrome counts for clinical science which are mainly due to four reasons that is muscoskeleton injuries, nerve paralysis, systemic inflammatory illness and imbalance of electrolytes. The diverse plethora of etiologies may be associated with downer cow syndrome. However despite of all primary causes it is the prolonged recumbency whitch exaggerates the the case. Anti inflammatory therapy in order to alleviate pain and also to prevent neuropathy and myopathy is prescribed. Dexamethasone 0.20.3mg/kg IV is recommended in early recumbency. Also IM injection of Dexamethasone 0.05mg/ kg/day & Flunixin meglumine 1mg/kg every 12 hour can also be given. Precautions must be taken in pregnant animal before anti-inflammatory therapy. Regular monitoring of faeces for presence of melena should be done because anti-inflammatory therapy can induce gastric ulcers. Fluid and electrolyte therapy must be prescribed in animals with inadequate water and feed intake in non alert downers cows. Treatment must not exceed 40 litre fluid per animal to prevent risk of reflux due to increase of intraruminal pressure. Comfortable bedding should be provided for the animal and it should be moved from side to side daily to prevent stomach damage due to prolonged recumbency. In absence of complete bedding animals resist standing and worsen condition. Assisted lifting must be opted by using hip lifters for 20-30 min. Recent Aqua Cow Rise System gives impressive result.
Hypovitaminosis and Hypervitaminosis:
Hypovitaminosis A in calves is manifested typically as a nervous form and is identified by typical tonic clonic convulsion, syncope and also sometimes even death. However in adult animal there is xeroophthalmia, seborrheiic dermatitis, placental retention, fall in fertility of both males and female Cattle is observed. Treatment is to supplement 10-20 times administration of daily maintenance requirement- 440IU/kg BW parenteral injection (aqueous).Supportive treatment is administration of anticonvulsant drugs, neurotonics.
Hypervitaminosis A symptoms that dominate include pseudotumor cerebri, rough and dry skin, bone pain and anorexia, ataxia and exostosis of third phalanx at its plantar aspect. Therapeutic effect of vitamin E and 2-hydroxypropyl-ß- cyclodextrin has been observed.
Thiamine deficiency in bovines is manifested as sudden onset of blindness muscle tremors, abnormal gait, frothy salivation, head pressing & tetany. Young animals being more susceptible and can die within 24 to 48 hours. IV or IM administration of 10mg/kg BW Thamine hydrochloride, 5X, every 3hour. General treatment of cerebral edema by administration of Mannitol, NS and parenteral dexamethasone is also indicated.
Hypovitaminosis H(Biotin)- the main lesion is is disruption of the integrity of keratinized tissue such as horn and hoof. And becomes one of the major reason of lameness in cattle. Supplementation of 40 mg biotin per day for 50 days is being recommended to correct horn deformity and supplementation of 20mg/day Biotin for 4 to 6 months interval can reduce lameness and foot lesions.
Mineral Deficiencies:
Cu deficiency- deficiency of copper occur in animals feeding on forages that grow on the soil lacking copper,during pregnancy & Calves with 2-3 months of age are more susceptible due to lesser reserves of Cu in milk fed to them. Typical deficiency include leucoderma or hypomelanosis in Buffalo loss of hair around eye called as spectacled eye and depressed immunity and also anaemia. Treatment indicated is oral dosing of 4g Cu to calves & 8-10g to buffaloes/day for 3-5wks. Cu glycinate @ 400mg to mature cattle & 100-200mg to calves is prescribed. Buffaloes show impressive results for leucoderma when treated with Cu glycinate with ZnO.
Iodine deficiency- resorption of foetus in the uterus, stillbirths, fall in fertility, deficient metabolism & psychomotor disturbances are some of the signs of iodine deficiency in humans. Painting flank skin with 5% tincture iodine in lactating dairy cattle is used.
Concludingly, by following a proper line of treatment for metabolic diseases at proper time and phase of animal’s life really a revolutionary change can be made in dairy industry . This could necessarily prolong the production phase of the animal and give better returns to the dairy owners. As most of the treatment protocols give not only immediate but sure results thus by acquaintance of knowledge on treatment aspect of metabolic diseases Veterinary Professionals can do good to animals, farmers, corporates and to themselves.
Harshit Saxena BVSc & AH- 4th Proffessional (Student)
CoVsc & AH, DUVASU, Mathura srhiharshit@gmail.com
