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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.

Pashubandha 2015 Volume No : 4 Issue : 02


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 40C (104 oF): infection likely
3940C normal
3739C mild hypothermia
Below 37C 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 ewes 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 prebreeding management program.
2. Pay close attention to ewe nutritional and health status during late gestation.
3. Keep facilities clean, well ventilated and draft free.
4. Make sure lambs get adequate colostrum intake.
5. Develop a health program for specific flocks.
6. Select sheep that are easy lambing, good mothers, heavy milking, and vigorous at birth.
7. Select against problem sheep.
8. 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, sux-
amethonium, 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,
oral contraceptives, statins/, rifampin, oxibendazole, sulfonamides, anabolic steroids,
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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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);
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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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.
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.
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.
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.
The use of disposable needles and syringes reduces the chance of inadequate sterilization of the
equipment.
Using single-dose medication vials will help to prevent contamination of the medication.
Needle of appropriate size and length be used to avoid injecting the medication into the subcutaneous
tissues.
Repeated injections into the same site is to be avoided and alternating the injection site can prevent
complications from tissue necrosis.

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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.

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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 rumens 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.

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2014 Volume No : 43 Issue : 02
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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 MayJune 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 12 days at the right abdominal wall (7th9th
intercostal space). Complete loss of defecation and pain on palpation of Fig. 1: Topography of the
omasum depicting the
the omasal area could be a diagnostic feature for omasal impaction. dorso-ventral and craniocaudal
extents over the right side.

Pashubandha 2015
2014 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.
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.
White to Black or Grey in color
Muzzle, Face and Tail switch are usually black, cows are white and bulls are darker in color
Head is long and tapering towards muzzle
Forehead is narrow and furrowed in middle

Pashubandha 2015
2014 Volume No : 43 Issue : 02
01
Horns are long and emerge from top of the poll
Eyes are bright and look bloodshot
Ears are small, horizontal and taper to a point
Hump is well developed
Dewlap is fine and naval flap is small and close to the body
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 57224 kg
Lactation Length 29910 days
Age at First calving 1337.6115.52 days

Calving Interval 577.624.32 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: Associate Editior:


Dean, Veterinary College, Hebbal, Bengaluru Head, Dept. of Vety.& Animal Husbandry Extension Education
Dr. S. Yathiraj (Ex-Officio) 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

PELVIC

Pashubandha 2015
2014 Volume No : 43 Issue : 02
01