Veterinary College, Bengaluru Monthly e-Bulletin
Newsletter Date : 28 February 2015
Volume No: 4 Issue : 2
Dr. Deepti B. R Assistant professor Dept. of Veterinary Medicine, Hebbal, Bengaluru. ( Deeptidr@gmail.com) Neonatal lamb mortality is one of the major factors in impairment of productivity in sheep-raising enterprises around the world. It is also a welfare concern. Majority of neonatal mortality is due to non-infectious diseases. Three main causes of lamb mortality are: 1. The complex of hypothermia/ exposure/ hypoglycaemia / starvation: This is the most important cause of postnatal disease and mortality. The determinants for the occurrence of this complex are • Birth size of the lamb: determined by the nutrition and genetics of the ewe, and by litter size which is also determined by the parity and genetics of the ewe. A birth weight of less than 2.5-3.0 kg in exotic breeds has increased risk for death. Most Indian breeds have a birth weight of 2-3 kg normally. • The energy reserves of the lamb • Environmental factors like temperature, wetness and wind at birth and during the following 48 hours. The influence of environment varies according to the management system. • Greater mortality in lambs born to maiden ewes is associated with poor mothering and desertion. 2. Stillbirth: Occurs due to placental insufficiency or dystocia. Stillbirth occurs largely as a result of prolonged birth and fetal hypoxemia. Prolonged birth and dystocia is a particular problem in large single lambs. Higher rates of stillbirth can also occur in flocks that are in poor condition. 3. Abortion: Abortion storms in sheep are often accompanied by significant mortality in live born animals. Infections leading to placentitis cause abortion in late pregnancy. Diseases that cause abortion in sheep include toxoplasmosis, E.coli, Camplylobacter, Listeria, Brucella and Chlamydia infections and stress. An abortion rate in excess of two per cent is suggestive of an infectious cause and veterinary investigation is essential. Predation may be an important cause in some parts of the world. Major infectious diseases of lambs that cause mortality are enteritis and pneumonia. These usually occur after 2 days of age. PREVENTION OF LAMB MORTALITY Simple improvements or modifications in the overall management of the flock before, during and after lambing will greatly reduce the number of deaths.
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Volume No : 4 Issue : 02
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Adequate ewe nutrition during the last six weeks of pregnancy, when 75 per cent of foetal growth ocurs, is essential to ensure appropriate lamb birth weight. Sheep should have a body condition score of 2 to 3.5. Ewes with multiple lambs must be fed appropriate levels of high quality roughages and supplementary concentrate feeding to prevent pregnancy toxaemia. Ewes must be vaccinated against the clostridial diseases (Eg: tetanus, enterotoxemia) four weeks before lambing. Improving facilities to avoid overcrowding and accidents and to provide a healthier environment. Navel disinfected with 2% iodine within 15 minutes of birth after clamping and cutting the umbilical cord is important. Ensure 50 ml/ kg intake of colostrum within the first two hours, if not sooner. Assist every lamb with its first meal. This is followed by careful scrutiny of ewes and lambs two or three times a day. Unless lambs receive colostrum within two or three hours of birth, body energy reserves become critically depleted and become prone to hypothermia and hypoglycemia. Interpretation of body temperature: Above 40°C (104 oF): infection likely 39–40°C normal 37–39°C mild hypothermia Below 37°C severe hypothermia (39oC = 102.2oF, 37oC= 98.6oF) Lambs can lose body heat very quickly. Unless they are well fed they can, particularly in cold, wet and windy conditions, become hypothermic. Hypothermic lambs are lethargic, tucked up, tend not to follow the ewe readily and may show signs of distress. Treatment of hypothermia: The lamb should first be vigorously towel-dried and then given colostrum. If it can nurse, encourage it; if not, feed by stomach tube at two hour intervals. The lamb can be warmed with a heat lamp in a draft-free pen. If the lamb is more than 5 hours old, warm (39oC) glucose solution is administered by intraperitoneal injection. The dosage is 10 ml per kg body weight of a 20% glucose solution. Record keeping: It is essential to eliminate problem ewes (Ewes that were poor mothers, had low milk production, had lambing difficulties or created a problem in previous lambings). Use of markers on rams to know when mating has occurred allows shepherds to know when the ewes are due for lambing. Shearing ewes before lambing is a good practice to improve hygiene. Freedom from most infectious causes of abortion is best achieved by maintaining a closed clean flock. Note: Many infectious causes of abortion can also infect humans i.e. zoonotic infection. Increased supervision can allow a reduction in mortality associated with dystocia and the hypothermia/ exposure/ hypoglycemia/ starvation complex.
REARING OF ORPHAN LAMBS Orphans lambs can be reared very successfully on artificial rearing systems. Colostrum can be milked from other ewes or cow colostrum may be used with caution. Orphaned lambs have to be fed 4-5 times a day at the rate of 50ml/kg BW per time.
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Lambs can also be fostered on to other ewes. • Fostering can be done by rubbing an orphan lamb in the foetal fluids of the new born single lamb before introducing to the ewe. • Fostering can also be done by skinning a ewe’s dead lamb and applying this “lamb skin jacket” to the lamb to be fostered. • Triplet lambs can be fostered onto those ewes which have lost a lamb. In addition, lambs are also fostered onto those ewes which produce a single lamb. • From the second week of life, lambs should also have access to palatable and nutritious solid food (which may include grass) and always have access to fresh, clean water. TO SUMMARISE: To increase lamb survival: 1. Have a sound pre‐breeding management program. 2. 3. 4. 5. 6. 7. 8.
Pay close attention to ewe nutritional and health status during late gestation. Keep facilities clean, well ventilated and draft free. Make sure lambs get adequate colostrum intake. Develop a health program for specific flocks. Select sheep that are easy lambing, good mothers, heavy milking, and vigorous at birth. Select against problem sheep. Use crossbreeding when applicable.
Sunilchandra.U., Vijaykumar.M., Vinay.P.Tikare and Ravikumar.C1 Department of Pharmacology and Toxicology, Veterinary College, Bidar. 585401. 1 Veterinary College, Hassan.( Email: sunivet29@rediffmail.com ) An adverse drug reaction (ADR) is any noxious or unintended response to a drug that occurs at appropriate doses used for prophylaxis, diagnosis or therapy. They may vary from minor annoyances to severe life threatening events. Drug toxicity includes all toxicity associated with a drug; including that observed in overdose/ poisoning with drugs. Side effects generally refer to deleterious/non-deleterious effects that may occur during therapy. Common adverse drug reactions of veterinary importance are described briefly. IDIOSYNCRACY : It refers to a genetically determined a unusual abnormal reactivity to a normal/ ordinary dose of a drug , usually observed in smaller percentage of population. The idiosyncratic reactions are difficult to predict and manage. Some of the drugs used in veterinary medicine that have been associated with idiosyncratic reactions in humans are : Penicillins, cephalosporins, erythromycin, sulfonamides, trimethoprim, chloramophenicol, anticonvulsants(phenobarbitol, phenytoin, carbamazepine) , phenyl butazone, dipyrone and phenothiazine derivatives. Some of the examples of idiosyncratic adverse drug reactions noticed in animals are: sulfonamide polyarthritis, hepatotoxicity in dogs, diazepam hepatotoxicity in cats, mebendazole hepatotioxicity in dogs and carprofen hepatitis.
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DRUG ALLERGY/ HYPERSENSITIVITY: Is defined as an immune-mediated response to a drug agent in a sensitized patient. True hypersensitivity adverse drug reactions are great imitators of disease and may present with involvement of any organ system, including systemic reactions such as anaphylaxis. . • Drug reactions commonly manifest with dermatologic symptoms caused by the metabolic and immunologic activity of the skin. Urticaria is typically a manifestation of a truly allergic, Type I reaction. • An anaphylactic reaction or anaphylaxis is an exaggerated immunological response to a substance to which an individual has become sensitised from anaphylaxis, but are mediated by the drug or substance directly, and not by sensitised IgE antibodies. • Any drug can potentially cause an allergic reaction ; but most common drug allergens implicated in producing anaphylactic reactions in domestic animals include Penicillins, cephalosporins, sulfonamides, streptomycin, tranquliisers, vancomycin, vitamins, insulin, tetracyclines, quinolones, salicylates, phenothiazines, chloramhenicol, heparin, lidocaine, erythromycin, angiotensin converting enzyme inhibitors, methyl dopa, vitamin K, iron injections, exogenously administered repeated injections of hormones(LH,hCG,PMSG) thiopentone, suxamethonium, non-depolarising muscle relaxants, ester local anaesthetics and plasma expanders (dextrans, starches and gelatins). • Clinical manifestations are usually minor and consist of urticaria (skin redness and swelling), usually along the line of the vein, flushing and occasionally mild hypotension. • Adrenaline (1:1000 epinephrine) is the most useful drug for treating anaphylaxis as it is effective in bronchospasm and cardiovascular collapse. The dose of 0.01ml/kg.IV or 0.2 – 0.5ml/kg, IM is repeated in 10-15minutes if clinical signs are not resolving. Venous return may be aided by lifting the patient's legs or tilting the patient head down Antihistamine agents: H1 blockers (eg: chlorpheniramine) and corticosteroids are administered for further management. HEPATOTOXICITY: Drug-induced liver damage is one of the most important adverse drug reactions and hepatic injury is the most common reason cited for withdrawal of an approved drug. The risk factors for drug-induced liver injury are age (elderly persons at increased risk of hepatic injury because of decreased clearance), sex(females)and genetic factors. Drug formulation as in case of long-acting drugs, which may cause more liver injury than shorter-acting drugs. The clinically important potential hepatotoxic drugs are Acetaminophen, amoxicillin, amiodarone, Tetracycline, glucocorticoids, phenobarbitone, chlorpromazine, ciprofloxacin, diclofenac, phenytoin, primidone, diazepam (in cats), erythromycin, fluconazole, isoniazid, methyldopa, mebendazole, carprofen, diethylcarbamazine, oxibendazole, sulfonamides, anabolic steroids, oral contraceptives, statins/, rifampin, vincristine etc •
No specific treatment is indicated for drug-induced hepatic disease. Treatment is largely supportive and based on symptoms. The first step is to discontinue the suspected drug. Specific therapy against drug-induced liver injury is limited to the use of N -acetylcysteine in the early phases of acetaminophen toxicity.
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Volume No :4 : 3 Issue : 02 01
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L-carnitine is potentially valuable in cases of valproate toxicity. In general, corticosteroids have no definitive role in treatment.. Cholestyramine may be used for alleviation of pruritus. Ursodeoxycholic acid may be used.
NEPHROTOXICITY: The most common drugs associated with nephrotoxicity are aminoglycosides, NSAIDs, sulfonamides, tetracyclines, amphotericin B, antiviral agents, methotrexate, the older cephalosporins, cimetidine, ciprofloxacin, furosemide, penicillins, phenytoin, rifampin, thiazide diuretics, polymixin etc. • Crystalluria, hematuria and obstruction of renal tubules occurring with sulfonamides are prevented by adequate water intake during the therapy and alkalinisation of the urine with urinary alkaliser (eg: sodium bicarbonate ) supplementation • The prevention or minimizing the drug induced nephrotoxicity is by administering single daily dose; reducing the treatment course as much as possible and avoiding concurrent administration of other nephrotoxic drugs. If at all, needs to be used, the doses of these agents should be reduced in conditions of renal insufficicency/impairment INCOMPATIBILITY: Multiple drug therapy is often used in veterinary practice; occasionally, inappropriate combinations of drugs. Drug incompatibilities are chemical interactions that occur between drugs invitro. Drugs that are incompatible should not be mixed together in a syrienge or infusion bottle. As a general rule, it is always not advisable tio mix drugs unless necessary and then only if we know they are compatible. Such interactions may occur in vitro because of physically or chemically incompatible drugs having been mixed before administration or in vivo. DRUG INTERACTIONS : Drug interactions refer to invivo interaction between drugs, with the possibility that one drug may alter the intensity of pharmacological effects of another drug given simultaneously or in relatively short time. Drug interactions may lead to diminished or an enhanced effect of a drug or may lead to toxicity. 1. Some of the pharmacodynamic drug interactions include : • Glucocorticoids and NSAIDs ( increased gastrointestinal toxicity) • Fuorosemide and ACE inhibitors (increased diuretic effect) • sucralfate and gastric acid secretion inhibitors(decreased efficacy of sucralfate) • NSAIDs and anticoagulants(increased bleeding) • Opioids and general anaesthetics(enhanced respiratory depression by opioids) . 2. Pharmacokinetic drug interactions in dogs that may affect negatively the absorption of the administered former drug include • Fluoroquinolones with cations Na+ and Cl-. Al and Mg, • Orally active penicillins with antacids • Tetracyclines with milk, antacid, laxatives • Digitalis with phenolphthalein (laxative) • Erythromycin with anti-cholinergic drugs • Lincomycin with kaolin 3. Pharmacokinetic drug interactions during the metabolism • Orally administered antibiotics with large dose of atropine.
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Phenobarbital with griseofulvin (decreased efficacy), • Any drug with chloramphenicol (decreased efficacy), •
With primidone/phenytoin, corticosteroids (decreased efficacy);
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Fluoroquinolones with theophylline (theophylline toxicity-CNS stimulation)
TERATOGENICITY: A teratogen is an agent that can disturb the development of the embryo or fetus.by halting the pregnancy (embryotoxicity) or producing a congenital malformation (a birth defect). The major body structures are formed in about the first 12 weeks after conception . Interference in this process causes a teratogenic effect. If a drug is given after this time it will not produce a major anatomical defect, but possibly a functional one. Classes of teratogens include radiation, maternal infections, chemicals, and drugs. The important ones with reference to veterinary field are : all Cytotoxic drugs (Busulphan, Cyclophosphamide, Methotrexate,vincristin etc), Anticoagulants(Warfarin), Vitamin A analogues (Etretinate, Isotretinoin), Anticonvulsants ( Carbamazepine, Phenytoin Sodium valproate), Cardiovascular drugs( Angiotensin-converting enzyme inhibitors, Angiotensin II inhibitors – losartan, spironolactone), Endocrinological drugs (Carbimazole, Propylthiouracil,Chlopropamide,Sulphonylureas), Antifungal drugs (griseofulvin, ketoconazole, Triazoles – Fluconazole, Itraconazole, Terbi afine), Cardiovasculardrugs, Antiinflammatory drugs (NSAIDs;3rdtrimester), antibiotics (tetracycline, ciprofloxacin, chloramphenicol, nitrofurantion, vancomycin, minoglycosides), Endocrinological drugs (Radioactive iodine, sex hormones, octreotide), antihelminthic drugs (mebendazole,albendazole, oxfendazole) and others( Misoprostol, Statins). CNS DISTURBANCES: The common drugs of veterinary importance stimulating CNS are Levamisole, tetramisole, loperamide, tinidazole, metronidazole, quinolones and fluoroquinolones, metoclopramide, promethazine, prochlorperazine, chlorpromazine, methyl xanthines, piperazine, respiratory stimulants (doxapram, nikethamide) and antihistaminics, all of which may result in transcient CNS stimulation under various circumstances depending on the dose and condition PHOTOSENSITIZATION: Photosensitive animals are photophobic Immediately when exposed to sunlight; scratch or rub lightly pigmented, exposed areas of skin (eg, ears, eyelids, muzzle). Bright sunlight on prolonged exposure can induce typical skin lesions,: erythema, edema, serum exudation, scab formation, and skin necrosis . In cattle, exposure of the tongue while licking may result in glossitis, characterized by ulceration and deep necrosis. Animals should be shaded fully or, preferably, housed and allowed to graze only during darkness. Corticosteroids, given parenterally in the early stages, may be helpful. Secondary skin infections and suppurations should be treated with basic wound management techniques, preventing fly strike. Examples : tetracyclines, fluoroquinolones, sulophonamides, antihistaminics, diuretics (thiazides,loop), tricyclic antidepressants, phenothiazines and corticosteroids GASTROINTESTINAL DISTURBANCES: Gastrointestinal disturbances as manifested by nausea, vomition, diarrhoea, abdominal pain are most commonly observed after the oral administration of Macrolides, tetracyclines, piperazine, cephalosporins, oxyclozanide, fluoroquinolones, penicillins, nitrofurans, rafoxanide, NSAIDs, sulphonamides, antineoplastic drugs. Unless severe as in case of antcancerous drugs, most of them are transcient and are self limiting.
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Volume No : 43 Issue : 02 01
LOCAL PAIN, TISSUE INJURY AND IRRITATION:
Both the drug itself and the vehicles may
cause tissue damage. The substances commonly used as drug vehicles such as glycerol formal or propylene glycol caused damage to muscle tissue. •
Bleeding from the injection site and hematoma formation can occur if blood vessels are injured during particularly intramuscular injections. Intravascular injections.. Skin necrosis, neurological damage, and loss of limb can follow.
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Nerve injury is another serious complication of intramuscular(IM) injections. The sciatic nerve is commonly injured by gluteal injections and the radial nerve injury at the shoulder, commonly manifested by paresis, necrosis etc.
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Necrosis of the surrounding tissue following IM installation of a medication may occur after any IM injection. Forceful placement of a volume of fluid into a closed space will cause damage. In other words, the surrounding muscle and tissues in the immediate area of the needle tip are subjected to the pressure of the mass of fluid that has been instilled into the area, which causes pressure necrosis. The toxicity of the medication, the volume injected, and even the speed at which the injection is given also will influence the size of the necrotic lesion.
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Numerous drugs like cephalosporins, tetracyclines, NSAIDS, oil based injectables, the long-acting injectable medications
may result in
complications at IM injection sites.
The extravasation of
anticancerous drugs outside the vein may result in thrombophlebitiis and tissue necrosis AVOIDING INJECTION SITE COMPLICATIONS •
Avoidance of infection at the injection site can be minimized by cleansing and drying the skin thoroughly prior to the injection.
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The use of disposable needles and syringes reduces the chance of inadequate sterilization of the equipment.
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Using single-dose medication vials will help to prevent contamination of the medication.
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Needle of appropriate size and length be used to avoid injecting the medication into the subcutaneous tissues.
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Repeated injections into the same site is to be avoided and alternating the injection site can prevent complications from tissue necrosis.
Pashubandha 2015 2014
Volume No : 43 Issue : 02 01
Sudha G Assistant Professor Veterinary College , Bangalore ( dineshtumkur@gmail.com) Deficiencies of most nutrients have been associated with reproductive failure in the cow yet many of these associations have not been proven. Even research-proven interactions may be difficult to prove in commercial herds. This diagnosis of nutrient-sensitive infertility is similar to other diagnoses through the 1. Recognition of infertility through history and evaluation of the cows / records 2. Determination of inadequate or excessive nutrient intake with supportive testing of the 3. animals or feed 4. Confirmation of the diagnosis after intervention Challenges in detection of nutrient-sensitive infertility 1. Nutrition is continuous (15-20%) whereas pregnancy is absolute 2. Hard to define an average pregnancy 3. Statistics: It takes 1500 cows to detect the difference between 50 and 55% pregnancy rate at p < 0.05 Production and Fertility Should we accept the premise that high producing cows are less fertile? As milk production of dairy cows increases over time, cow fertility appears to be declining. Presently, first service conception rate decreases as milk production increases Conversely, days open and days to first service decreased as milk production increased in the same herds. Thus we see mixed trends in milk production and reproduction and management must certainly be considered. Fertility for virgin heifers, appears to remain the same, or may be improving, as age of first calving has tended to decrease. Does a ration designed for maximum milk production also optimize fertility or does the cow put a higher priority on production than reproduction? Malnutrition vs. metabolic disease vs. nutrient-sensitive infertility Gross malnutrition is easily diagnosed with its associated reproductive failure. Infertility caused by malnutrition is usually associated with adverse environmental and/or climatic conditions. Reproduction fails at a point prior to the expression of loss of condition, emaciation, and death. Nutritional infertility would most commonly be observed in beef cattle and dairy replacement heifers on poor pastures. One could suggest that a dairy cow that is 60 days fresh, milking 50 lbs, and lost 2 body condition scores since calving is exhibiting malnutrition. In addition, metabolic diseases have a negative impact on subsequent reproduction. Displaced abomasums, retained placentas, or mastitis after AI decrease the odds of pregnancy at first service by more than 50% in dairy cows. Feeding programs designed to minimize metabolic disease should indirectly enhance reproduction.
Pashubandha 2015 2014
Volume No : 43 Issue : 02 01
The dynamic ovary The ovary should be considered a dynamic tissue that has tremendous production capability and the production changes rapidly over a 21-day cycle. For example, plasma concentration of progesterone in a cow is similar to testosterone concentration in a bull. However, progesterone is produced by one corpus luteum about 3/4” in diameter as compared to 2 testicles in a bull. Other issues with high metabolic rates and cell turnover like intestinal mucosa or bone marrow are considered very sensitive to nutrient intake. In addition, the ovum and embryo use glucose as their primary energy source and have limited to no ability to use fatty acids as an energy source. The periparturient cow relies on fat mobilization in late gestation and early lactation to support energy requirements. Thus subtle changes in glucose could have a more profound effect on the ovary and reproduction than milk production. Consider that the postpartum cow has to decide if pregnancy, while lactating, is in her bestinterests. If the last calving went poorly or body condition is lost after calving, the cow would have protective mechanisms to not get pregnant again. Energy balance In the post-partum cow, return to cycling is associated with energy balance. If the cow consumes less energy than she needs for maintenance and milk production, she is considered in negative energy balance. Most cows are in a negative energy balance for the first 2-3 months of lactation, however the lowest energy balance or “nadir” of energy balance appears to be associated with return to cycling. DeVries and Veerkamp (2000) estimated that each decrease of 2.3 Mcals in energy balance nadir resulted in about a 1.5-day increase in time to resume luteal activity after calving. 75% of the variation inenergy balance in early lactation Holsteins was associated with intake, while 25% was associated with milk yield. The transition program from the dry period and the early lactation ration should be considered when minimizing the negative reproductive effects of negative energy balance. Protein and reproduction Excessive protein, especially soluble or degradable protein, has been suggested to decrease fertility of cows, possibly though early embryonic death. Cows make use of non-protein nitrogen in the rumen to make microbial protein, which is very high quality. The rumen microbes combine non-protein nitrogen with carbohydrate skeletons, such as volatile fatty acids, to make protein. If we feed protein in excess of the rumen’s ability to make protein, the urea concentrations in blood, milk and urine will increase. One suggestion was that excess urea was broken down to ammonia in the reproductive tract and that ammonia was toxic to embryos. Regardless, excess protein costs money and adds to environmental pollution. So if you avoid excess protein to save money and protect the environment, reproduction should not be altered. Feed storage and delivery The feed may be harvested at a desired nutrient content but can lose nutrients with improper storage or feeding methods. Heat and improper moisture can destroy nutrients or alter essential nutrients. Fat soluble vitamins are susceptible to temperatures associated with hot summer days and thus stored feed can lose vitamin content over weeks to months. Fermented feeds are also prone to losses. Silages and haylages that are too wet may lose water-soluble nutrients in the run-off below the silo.
Pashubandha 2015 2014
Volume No : 43 Issue : 02 01
qÁ: J£ï.©.²æÃzsÀgÀ ¸ÀºÀ ¥ÁæzsÁå¥ÀPÀgÀÄ, ¥À±ÀĪÉÊzÀåQÃAiÀÄ OµÀzsÀ±Á¸ÀÛç ªÀÄvÀÄÛ «µÀ±Á¸ÀÛç «¨sÁUÀ ¥À±ÀĪÉÊzÀåQÃAiÀÄ ªÀĺÁ«zÁå®AiÀÄ, ºÉ¨Áâ¼À, ¨ÉAUÀ¼ÀÆgÀÄ-24, (E ªÉÄʯï: sridhar_vet@rediffmail.com) ºÀ°èAiÀÄÄ CºÁgÀzÀ°è ©zÀÝgÉ «µÀ JA§ÄzÀÄ MAzÀÄ ¥ÀæwÃw. ªÉÄðAzÀ ªÉÄÃ¯É F PÀÄjvÀÄ ¥ÀwæPÉUÀ¼À°è ªÀgÀ¢UÀ¼ÀÄ §gÀÄvÀ¯Éà EgÀÄvÀÛªÉ. EzÀgÀ°è ºÀ®ªÀÅ ¸ÀvÀå ªÀÄvÀÄÛ «ÄxÀåUÀ½ªÉ. ¸ÀvÀåUÀ½VAvÀ®Æ «ÄxÀåUÀ¼Éà eÁ¹Û JAzÀgÀÆ vÀ¦à®è. GzÁºÀgÀuÉUÉ PÉÃAzÀæ ªÀÄvÀÄÛ gÁdå ¸ÀPÁðgÀUÀ¼À ¸ÀºÀ AiÉÆÃUÀUÀ¼À°è ¥ÁæxÀ«ÄPÀ ±Á¯ÉUÀ¼À°è ªÀÄzÁåºÀßzÀ ©¹AiÀÄÆl AiÉÆÃd£É PÉ®ªÀÅ ªÀµÀðUÀ½AzÀ eÁjAiÀÄ°èzÉ. AiÀiÁªÀÅzÉà ªÀÄPÀ̼ÀÄ Hl ªÀiÁr C¸Àé¸ÀÜ UÉÆAqÀgÀÆ ¸ÀºÀ ªÉÆzÀ® C¥ÁzÀ£É §gÀĪÀÅzÀÄ ºÀ°èUÀ¼À ªÉÄïÉ. ºÁVzÀÝgÉ F ºÀ°èUÀ¼À §UÉÎ ªÉÆzÀ®Ä ¸Àé®à w½zÀÄPÉƼÉÆîÃt. £ÁqÀ ºÀ°èAiÀÄ£ÀÄß DAUÀè ¨sÁµÉAiÀÄ°è Gecko gecko JAzÀÄ PÀgÉAiÀÄÄvÁÛgÉ. EzÀÄ UÉÆÃqÉUÀ¼À ªÉÄÃ¯É ºÀjzÁqÀÄvÁÛ ºÀļÀ ºÀÄ¥ÀàmÉUÀ¼À£ÀÄß wAzÀÄPÉÆAqÀÄ §zÀÄPÀĪÀ MAzÀÄ ²ÃvÀ gÀPÀÛzÀ ¥ÁætÂ. EzÀgÀ°è AiÀiÁªÀÅzÉà «µÀ ªÀ¸ÀÄÛªÀÅ EgÀĪÀÅ¢¯®. ªÀÄvÀÄÛ EzÀÄ ªÀÄ£ÀĵÀå£À£ÁßUÀ°Ã CxÀªÁ ¥ÁætÂUÀ¼À£ÁßUÀ°Ã PÀrAiÀÄĪÀ C¨sÁå¸ÀªÀ£ÀÄß ºÉÆA¢®è. PÉêÀ® PÉ®ªÀÅ ºÀ°èUÀ¼ÀÄ ªÀiÁvÀæ ºÀjvÀªÁzÀ ºÀ®è£ÀÄß ºÉÆA¢zÀÄÝ EªÀÅ ªÀÄ£ÀĵÀå£À£ÀÄß CxÀªÁ ¥ÁætÂUÀ¼À£ÀÄß PÀrAiÀħ®èªÀÅ. EªÀÅUÀ¼À ºÀ®ÄèUÀ¼À ¸ÀAzÀÄUÀ½AzÀ M¸ÀgÀĪÀ «µÀ ªÀÄ£ÀĵÀå£À ±ÀjÃgÀªÀ£ÀÄß ¸ÉÃj C®fð CxÀªÁ GjAiÀÄÆvÀªÀ£ÀÄßAlÄ ªÀiÁqÀ§®ÄèzÀÄ. DzÀgÉ ºÀ°è CºÁgÀzÀ°è ©zÀÝgÉ «µÀªÁUÀ§®è z ÉÃ? CxÀªÁ ºÀ°è AiÀ ÄÄ CµÉÆÖ A zÀÄ «µÀPÁjAiÉ ÄÃ? EzÀPÉÌ ªÉéöÊeÁÕ¤PÀªÁV GvÀÛgÀ«zÉ. £ÁqÀ ºÀ°è RArvÁ «µÀPÁjAiÀÄ®è. EzÀÄ PÀrAiÀÄĪÀÅ¢®è. EzÀÄ ¨ÉPÀÄÌUÀ¼À ¸Áé¨sÁ«PÀªÁzÀ MAzÀÄ CºÁgÀ ªÀÄvÀÄÛ £Á¬ÄUÀ¼ÀÆ ¸ÀºÀ PÉ®ªÀÅ ¸À® EªÀÅUÀ¼À£ÀÄß ¨ÉÃmÉAiÀiÁr w£ÀÄßvÀÛªÉ. DzÀgÉ EzÀjAzÀ MAzÀÆ ¨ÉPÀÄÌ CxÀªÁ £Á¬ÄUÀ¼ÀÄ ¸ÀvÀÛ §UÉÎ ªÀgÀ¢UÀ½®è. aãÁ ªÀÄwÛvÀgÀ zÉñÀUÀ¼À°è “ºÀ°èUÀ¼À ¸À¯Áqï” ªÀiÁr w£ÀÄßvÁÛgÉ JAzÀgÉ ªÉÄÊ dÄA J£ÀÄßvÀÛzÉ. MAzÀÄ ªÉÃ¼É ºÀ°èUÀ¼À°è «µÀ«zÉ JAzÀÄ PÉÆAqÀgÀÆ ¸ÀºÀ CzÀÄ CºÁgÀzÀ°è AiÀiÁªÁUÀ ©¢ÝzÉ J£ÀÄߪÀÅzÀÄ §ºÀ¼À ªÀÄÄRå. AiÀiÁªÀÅzÉà «µÀªÀÅ ¥ÉÇænãï CA±ÀªÀ£ÀÄß ºÉÆA¢gÀĪÀÅzÀjAzÀ CzÀgÀ°è «µÀ«zÉ CAzÀÄPÉÆAqÀgÀÆ ¸ÀºÀ ¨ÉìĸÀĪÀ ªÉÆzÀ¯Éà CºÁgÀzÀ°è ©zÀÝgÉ CzÀgÀ°ègÀĪÀ «µÀzÀ CA±ÀªÀÅ ¸ÀA¥ÀÇtðªÁV ¤¶ÌçAiÉÄUÉƼÀÄîvÀÛzÉ. PÁgÀt ºÀ°è CºÁgÀªÀ£ÀÄß ¨ÉìĸÀĪÀ ªÉÆzÀ®Ä CzÀgÀ°è ©zÀÝgÉ D CºÁgÀªÀ£ÀÄß wAzÀgÉ AiÀiÁªÀÅzÉà «µÀPÁjà ¥ÀjuÁªÀÄ GAmÁUÀĪÀÅ¢®è. §ºÀ¼ÀµÀÄÖ ¥ÀæPÀgÀtUÀ¼À°è CºÁgÀzÀ°è ºÀ°èAiÀÄ£ÀÄß £ÉÆÃrzÀgÉà ªÁAw ªÀÄvÀÄÛ ¨Éâü ¥ÁægÀA¨sÀªÁUÀÄvÀÛzÉ. EzÉÆAzÀÄ ¸ÀªÀÄƺÀ ¸À¤ßAiÀiÁV ¥Àjt«Ĺ J®ègÀÆ ªÁAw ¥ÁægÀA©ü¸ÀĪÀ ¸ÁzsÀåvÉAiÀÄ£ÀÄß vÀ½î ºÀ°è ºÁPÀĪÀAw®è. DzÀgÉ PÉ®ªÀÅ ªÉÊeÁÕ¤PÀ ¯ÉÃR£ÀUÀ¼À£ÀÄß N¢zÁUÀ PÉ®ªÀÅ ¸ÀvÀåUÀ¼ÀÆ EgÀ§ºÀÄzÀÄ C£ÀÄߪÀ C©ü¥ÁæAiÀÄ §gÀÄvÀÛzÉ. ºÀ°èAiÀÄAvÀ ¸ÀjøÀæ¥ÀUÀ¼À fÃuÁðAUÀ ªÀÇåºÀzÀ°è ¥sóÀÅqï ¥ÉÇAiÀÄì¤AUï GAlÄ ªÀiÁqÀ§®è ¸Á¯ÉÆä£É¯Áè, ¸ÀÖ¥sÉʯÉÆÃPÉÆÃPÀ¸ï ªÀÄvÀÄÛ E.PÉƯÉÊ EvÁå¢ ¨ÁåQÖjAiÀiÁUÀ¼ÀÄ EgÀÄvÀÛªÉ JA§ §UÉÎ ªÀgÀ¢UÀ½ªÉ. PÁgÀt CºÁgÀªÀ£ÀÄß ¨ÉìĹ EmÖ £ÀAvÀgÀ CzÀgÀ°è ºÀ°è CxÀªÁ CzÀgÀ EPÉÌ CºÁgÀzÀ°è ©zÀÝ°è F ¸ÀÆPÁë÷ätÄUÀ¼ÀÄ PÉ®ªÉà ¤«ÄµÀUÀ¼À°è PÉÆÃmÁå£ÀÄ ºÀ°èAiÀÄ «µÀ¨ÁzsÉ MAzÀÄ ¸ÀªÀÄƺÀ ¸À¤ßAiÉÄÃ? PÉÆÃn ¸ÀASÉåAiÀÄ° C©üªÀÈ¢ÞUÉÆAqÀÄ CºÁgÀzÀ°è «µÀªÀ£ÀÄß ¸À櫸ÀĪÀÅzÀjAzÀ CºÁgÀ «µÀªÁUÀĪÀ ¸ÁzsÀåvÉAiÀÄ£ÀÄß
Pashubandha 2015 2014
Volume No : 43 Issue : 02 01
C®èUÀ¼ÉAiÀÄÄAw®è. F CºÁgÀªÀ£ÀÄß wAzÀ°è ªÀÄPÀ̼ÀÄ C¸Àé¸ÀÜUÉƼÀÀÄzÀÄ. DzÀgÉ E°è UÀªÀĤ¸À¨ÉÃPÁzÀ CA±ÀªÉAzÀgÉ ¹zÀÝUÉƼ¹zÀ CºÁgÀzÀ°è ºÀ°è ©zÀÝ £ÀAvÀgÀ CzÀÄ ¸ÀvÀÄÛ CxÀªÁ CzÀgÀ PÀgÀĽ£À°è£À ¨ÁåQÖjAiÀiÁUÀ¼ÀÄ CºÁgÀªÀ£ÀÄß ¸ÉÃj C°è ªÀÈ¢ÞUÉÆAqÀÄ «µÀ ¸ÀÈ«¸À®Ä ¸ÀĪÀiÁgÀÄ 4-5 vÁ¸ÀÄ ¨ÉÃPÀÄ. C®èzÉà J¯Áè ºÀ°èUÀ¼À PÀgÀĽ£À°è F QÃmÁtÄUÀ¼ÀÄ EgÀĪÀÅ¢®è. CzÀÄzÀjAzÀ ¹zÀÝUÉÆAqÀ CºÁgÀzÀ°è ºÀ°è ©zÀÝ ªÀiÁvÀæPÉÌ CzÀÄ CºÁgÀ C¸Àé¸ÀÜvÉAiÀÄ£ÀÄßAlÄ ªÀiÁqÀ§®èzÀÄ J£À߯ÁUÀzÀÄ. MnÖ£À°è F ºÀ°è ©zÀÝ CºÁgÀªÀ£ÀÄß d£À ¸Éë¹zÁUÀ DUÀĪÀ “¸ÀªÀÄƺÀ ¸À¤ß” ªÁAw ¨Éâ¬ÄAzÀ d£ÀgÀÄ §¼À®ÄªÀ §UÉÎ CjªÀÅ ªÀÄÆr¸ÀĪÀÅzÀÄ ¸ÀzÀåzÀ CUÀvÀå.
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§rzÉ©â¹vÀÄ. UÀÄ©â Hj£À ºÀwÛgÀzÀ £À£Àß ¸ÉßûvÀgÁzÀ £ÀAeÉÃUËqÀjAzÀ vÀPÀët CªÀgÀ PÉÆý ¥sÁgÀAUÉ ¨sÉÃnPÉÆqÀ®Ä PÀgÉ. £ÀAeÉÃUËqÀgÀÄ §ºÀıÀ: C¼ÀÄvÀÛ¯Éà ºÉýzÀgÀÄ “ qÁPÀÖgï ¸ÁºÉçgÉà vÀPÀët ¥sÁgÀAUÉ §¤ß PÉÆý ªÀÄjUÀ¼ÀÄ vÀÄA¨Á ¸Á0iÀÄÄvÁÛ EªÉ, OµÀzsÉÆ¥ÀZÁgÀ ªÀiÁrzÀgÀÆ ¸Á«£À ¸ÀASÉå vÀUÀÄÎwÛ®è, FUÀ ¤ÃªÉ ¢PÀÄÌ”. ¨sÁ£ÀĪÁgÀzÀ ªÀÄdPÉÌ gÀeÉPÉÆlÄÖ UÀÄ©âPÀqÉUÉ £À£Àß PÁgÀ£ÀÄß Nr¹zÉ. zÁj0iÀÄÄzÀÝPÀÆÌ PÉÆýªÀÄjUÀ¼À ¸Á«UÉ J£ÀÄ PÁgÀt«§ºÀÄzÀÄ JA§ÄzÀ£ÀÄß 0iÉÆÃa¸ÀÄvÁÛ UÀÄ©â0iÀÄ£ÀÄß vÀ®Ä¦zÁUÀ £ÀAeÉÃUËqÀgÀÄ HgÀ ¨ÁV°£À°è0iÉÄà PÁ0iÀÄÄvÁÛ ¤AwzÀÝgÀÄ. CªÀgÀ ªÀÄÄRzÀ°è DvÀAPÀ JzÀÄÝ PÁtÄwÛvÀÄÛ. ¸Àj £ÀAeÉÃUËqÀjUÉ PÉýzÉ “K£ÀÄ vÉÆAzÀgÉ PÉÆýUÀ½UÉ K£ÁVzÉ?” £ÀAeÉÃUËqÀgÀÄ ºÉýzÀgÀÄ “ 10 ¢£ÀUÀ½AzÀ PÉÆýUÀ¼ÀÄ ¸Á0iÀÄÄvÀÛ°ªÉ ¸ÀܽÃ0iÀÄ ¥À±ÀĪÉÊzÀågÀÄ ¸ÀvÀÛ ªÀÄjUÀ¼À ªÀÄgÀuÉÆÃvÀÛgÀ ¥ÀjÃPÉë £Àqɹ PÉÆýUÀ½UÉ coccidiosis PÁ¬Ä¯É §A¢zÉ CAvÀ OµÀ¢ü §gÉzÀÄPÉÆlÖgÀÄ. CzÉà jÃw OµÀ¢ü vÀAzÀÄ qÁPÀÖgï ºÉýzÀ jÃw0iÀÄ°è0iÉÄà PÉÆýUÀ½UÉ OµÀ¢ü ¤Ãj£À°èü PÉÆmÉÖ MAzÀÄ ¢£ÀzÀ ªÀÄnÖUÉ PÉÆýUÀ¼ÀÄ ¸Á0iÀÄĪÀÅzÀÄ vÀVÎvÀÄ. DzÀgÉ FUÀ ªÀÄvÉÛ PÉÆýUÀ¼ÀÄ ¸Á0iÀÄĪÀÅzÀÄ ºÉZÁÑV FUÀ zÉÆqÀØ vÉÆAzÀgÉ0iÀiÁVzÉ. §ºÀıÀ: F ¨ÁåZï £À£Àß PÉÊUɺÀvÉÆÛîè C¤¸ÀÄwÛzÉ.” EµÀÖgÀ°è £ÁªÀÅ £ÀAeÉÃUËqÀgÀ PÉÆý ¥sÁgÀA vÀ®Ä¦0iÀiÁVvÀÄÛ. zÉÆqÀØ PÉÆý ¥sÁgÀA, CzÉà jÃw PÉÆýUÀ¼À ¸ÀASÉå0iÀÄÆ ºÉZÀÄÑ. ««zsÀ ªÀ0iÀĹì£À PÉÆýUÀ¼ÀÄ ¨ÉÃgÉ ¨ÉÃgÉ ªÀÄ£É0iÀÄ°è ¨É¼É0iÀÄÄvÉÛzÀݪÀÅ. ¸Àj £ÀAeÉÃUËqÀgÀÄ £À£ÀߣÀÄß MAzÀÄ PÉÆýªÀģɺÀwÛgÀ PÀgÉzÉÆ0iÀÄÄÝ ºÉýzÀgÀÄ “ qÁPÀÖgï, £ÉÆÃr EzÉà ¨ÁåZï£À PÉÆýUÀ½UÉ coccidiosis
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Pashubandha 2015 2014
Volume No : 43 Issue : 02 01
JAzÀÄ UÉÆvÁÛ U À°®è . ¸Àj PÉÆýªÀÄ£É M¼ÀUÉ ºÉÆÃV PÉÆýUÀ¼À£ÀÄß £ÉÆÃrzÉ. PÉÆýUÀ¼ÀÄ ¸ÀĸÁÛ V PÀĽwzÀݪÀÅ £ÉÆÃqÀ£ÉÆÃqÀÄwÛzÀÝAvÉ ªÀÄvÀÛµÀÄÖ PÉÆýUÀ¼ÀÄ ¸ÀvÀÛªÀÅ coccidiosis gÉÆÃUÀ®PÀëtªÁzÀ gÀPÀÛ¨sÉâ J®Æè PÀAqÀħgÀ°®è. §ºÀıÀ: coccidiosis PÁ¬Ä¯É C®è CAvÀ ªÀÄ£À¸ÀÄì ºÉývÀÄ. Coccidiosis PÁ¬Ä¯É C®è¢zÀÝgÉ ªÀÄvÉÛãÀÄ? JA§ ¥Àæ±Éß ¥Àæ±Éß0iÀiÁUÉà G½¬ÄvÀÄ. ¸ÀvÀÛ PÉÆýUÀ¼À ¥ÀjÃPÉë C¯Éèà MAzÀÄ ªÀÄgÀzÀ PɼÀUÉ ¥ÁægÀA©ü¹zÉ. Coccidiosis gÉÆÃUÀ ®PÀëtzÀ 0iÀiÁªÀ PÀÄgÀĺÀÆ PÁt°®è DzÀgÉ PÀgÀĽ£À vÀÄA¨Á ¤ÃgÀÄ vÀÄA©zÀAvÉ PÁtÄwÛvÀÄÛ. PÀgÀĽ£À°è vÉÆAzÀgÉ EzÉ, DzÀgÉ EzÀPÉÌ PÁgÀt K£ÀÄ? JA§ ¥Àæ±ÉßUÉ GvÀÛgÀ ¹UÀ°®è. £À£Àß ¥À±ÀĪÉÊzÀåQÃAiÀÄ ªÀÈwÛAiÀÄ C£ÀĨsÀªÀPÉÌ EzÀÄ ¸ÀªÀ¯ÁV ¤AwvÀÄ. ªÀÄvÉÛ ªÀÄÆVUÉ CzÉà WÁlÄ ªÁ¸À£É. £ÀAeÉÃUËqÀgÀ£ÀÄß PÉýzÉ,”K£ÀÄ OµÀ¢ü ºÁQ¢ÝÃj?, JµÀÄÖ OµÀ¢ü ªÀÄvÀÄÛ ºÉÃUÉ OµÀ¢AiÀÄ£ÀÄß PÉÆnÖ¢ÝÃj?” £ÀAeÉÃUËqÀgÀÄ OµÀ¢ü aÃn £ÉÆÃqÀÄvÁÛ, amprollium
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Pashubandha 2015 2014
Volume No : 43 Issue : 02 01
Dr A. S. Patil, Dr Ramesh Rathod, Dr B. N. Nagaraj and Dr L. Ranganath Veterinary Hospital, University of Agricultural Sciences Dharwad-580 005 (Email: patilas@uasd.in; anilpatiluasd@yahoo.co.in ) The omasum is the 3rd compartment of the bovine stomach, located toward the right of the median plane and opposing the 7th to 11th ribs (Fig. 1). Omasal leaves provide a large surface area for the absorption of volatile fatty acids, electrolytes, and water. The omasum also acts to reduce the size of feed particles. In tropical countries omasal impaction is prevalent in cows and buffaloes. The omasum is secondarily involved in forestomach disorders after primary involvement of other compartments of the forestomach. The clinical differentiation of omasal impaction from other gastrointestinal problems is difficult and often exploratory rumenotomy is required for confirmation of the diagnosis. Because of its position under the costal part of the abdominal wall, the omasum is not easily accessible for clinical examination by palpation, percussion and auscultation, and it cannot be palpated through the rectum. So an insight into the condition is presented here. Causes: Feeding of rough fibrous feed during fodder scarcity periods, Alfaalfa stalks and feeding of machine harvested wheat straw have been reported as the causes of omasal impaction. Most of animals are presented during the months of fodder scarcity (usually Mayâ&#x20AC;&#x201C;June and sometimes in winter also). This machine-made straw is low in both digestible proteins and energy, may contribute to the cause and is also very fine as compared to manually harvested straw and contained soil particles because of the low height of machine blades from the ground, which introduce dust / sand into feed. It seems that this fine straw and soil became entrapped between the omasal leaves, leading to omasal impaction. Clinical signs: Omasal impaction as a clinical entity is difficult to define and is usually diagnosed at necropsy where the omasum is grossly distended and excessively hard with dry coarse particles (Fig 2 a and b) and patches of necrosis were present on the omasal leaves. The most common initial owner complaints (decreased or absent fecal output, anorexia, reduced milk yield and pain) and clinical signs will be consistent with abdominal disease. Clinical examination usually reveal a significant increase in pulse rate, normal body temperature and reduced ruminal movement with weakness in the ruminal contractility. The clinical signs of omasal impaction observed include anorexia, moderate to severe dehydration, dullness, abdominal distention, mild colicy signs, ruminal hypomotility or atony, no palpable abnormalities of intestine, and an empty rectum with cessation of defecation. There may be a history of mild to moderate pain observed for the first 1â&#x20AC;&#x201C;2 days at the right abdominal wall (7thâ&#x20AC;&#x201C;9th intercostal space). Complete loss of defecation and pain on palpation of the omasal area could be a diagnostic feature for omasal impaction.
Pashubandha 2015 2014
Fig. 1: Topography of the omasum depicting the dorso-ventral and craniocaudal extents over the right side.
Volume No : 43 Issue : 02 01
Transrectal abdominal palpation is a valuable diagnostic procedure in examination of bovine abdominal diseases. Only mucous or mucous with a few pellets of feces in the rectum along with slippery or sticky rectal mucosa, unappreciable intestines, and a doughy normal-sized rumen will be consistent findings on rectal examination (Table 1). Table 1. Rectal exploration findings may vary in animals with primary omasal impaction. Rumen consistency
Doughy
Rumen size
Normal to Moderately distended or Severely distended
Intestines
Normal to Mild distension
Rectal mucosa
Normal to, Sticky
Fecal quantity in rectum
Scanty to Negligible or Absent
Feces
Absent / Pelleted / Hard / Pasty
Presence of mucus
Mucus only to, Mucus and feces or Absent
Haematological examination demonstrates in the majority of animals, a neutrophillic leukocytosis and lymphocytopenia. Primary omasal impaction appears to elicit an inflammatory reaction even in the absence of other complications (e.g., peritonitis). attributable to inflammatory complications of impacted feed material. Neutrophilia might have resulted from chronic irritation of the forestomach wall by impacted feed materials, leaving the wall exposed to secondary infection, which resulted in inflammation. Decreased lymphocytes could be due to release of corticosteroids as a result of stress. Serum biochemical analysis shows significantly reduced glucose and albumin levels which may be ascribed to chronic starvation or failure of the liver to synthesize adequate amounts of protein. There is increased AST, ALT, BUN, Creatinine, Lactate dehydngenase (LD) and Creatinine phosphokinase (CPK) levels. Absorption of toxic products from the rumen or alimentary tracts, starvation and constipation leading to cellular disturbances of liver parenchyma could result in increased levels of plasma AST and ALT. The increased BUN and creatinine levels could be attributed to decrease in renal blood flow as a part of compensatory mechanisms to maintain circulation in hypovolemia associated with dehydration, leading to azotemia. Lactate dehydngenase (LD) and creatinine phosphokinase (CPK) increase might be attributed to affection of liver, heart and skeletal muscles. The main function of the omasum is to absorb water and electrolytes; failure to do so leads to dehydration. Serum electrolytes analysis shows that calcium, potassium, sodium and chloride will be significantly decreased in cases of omasal impaction. The hypokalaemia observed in the diseased cows could be attributed to fasting and adaptive response to continued hypoadrenocortical activity. An intracellular shift of potassium might have occurred subsequent to generation of metabolic alkalosis. The hypochloraemia might be due to the long-standing anorectic status of the animals and also be attributed to chloride retention in rumen contents, which was evident by increased rumen chloride concentration (>30 mEq/L). Hypocalcemia, hypokalemia, and hypophosphatemia may be due to less assimilation of feed materials.
Pashubandha 2015 2014
Volume No : 43 Issue : 02 01
Radiographic and ultrasographic examinations reveal the contour of the omasum and provide a definitive diagnosis on dilation and motility. Treatment: The objective of treatment should be to relieve the impaction. Moreover, electrolyte imbalance must be assessed to avoid complications associated with hypokalemia, hypochloremia, and hypocalcemia. •
Medical Treatment: omasal impaction can be treated medically by repeated dosing with mineral oil and laxatives. The animals may be given purgatives. They may also be administered with Mifex 500 ml, DNS 2 lts, and RL 2 lts given as intravenous injection along with Cremaffin liquid 200 ml orally. The animals may be made to walk briskly for 1-2 kms.
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Surgical treatment: Through rumenotomy site, a soft flexible rubber pipe may be introduced through the reticulo- omasal orifice and irrigate with water and also evacuate the omasal contents into the rumen using fingers. 500 ml of glycerine / mineral oil may also be pushed though orifice and kneading of omasum may be attempted. 30 liters of water along with 500gms jagary, 100gms salt, 100 gms baking soda may also be introduced through the pipe.
Fig. 2 (a and b): Impacted food particles in omasum.
Dr. Naveen Kumar G.S., Dr. Basavaraj Inamdar & Dr. Shrikant Dodamani Assistant Professors, Department of AGB, Veterinary College Hassan-573201 ( Email: shri537@gmail.com ) Synonyms: Kavalu Dana, Mysore Dana, Kadu Dana, Number Dana & Poornaiana Dana •
It is known for power & endurance, Mysore rulers developed this breed from Hallikar, Hagalvadi and Chitaldoorga.
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White to Black or Grey in color
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Muzzle, Face and Tail switch are usually black, cows are white and bulls are darker in color
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Head is long and tapering towards muzzle
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Forehead is narrow and furrowed in middle
Pashubandha 2015 2014
Volume No : 43 Issue : 02 01
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Horns are long and emerge from top of the poll
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Eyes are bright and look bloodshot
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Ears are small, horizontal and taper to a point
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Hump is well developed
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Dewlap is fine and naval flap is small and close to the body
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Hooves are hard and close together Traits
Male
Adult male weight
500 kg
Adult female weight
318 kg
Daily Milk yield
0.5-4 kg
Average Lactation Milk yield
572±24 kg
Lactation Length
299±10 days
Age at First calving
1337.6±115.52 days
Calving Interval
577.6±24.32 days Female
Breeding Farms: CBF Ajjampur, Com-posite Livestock farm Hesarghatta Accession no: INDIA CATTLE 0800 AMRITMAHAL_03001
monthly e-Bulletin Published and circulated by Veterinary College, Hebbal, Bengaluru. Editor: Dean, Veterinary College, Hebbal, Bengaluru Dr. S. Yathiraj (Ex-Officio)
Associate Editior: Head, Dept. of Vety.& Animal Husbandry Extension Education Dr. K. Satyanarayan (Ex-Officio)
Contact : Dept of Veterinary and Animal Husbandry Extension Education Veterinary College, Hebbal Bangalore email: pashubandhavch@gmail.com Blog: pashubandhavch.blogspot.in
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Pashubandha 2015 2014
PELVIC
Volume No : 43 Issue : 02 01