VETERINARY NUTRIENT

NUTRITION is the science of dealing with the utilization of food by the body processes which
transforms food into body tissues and energy.
To obtain and utilize surplus or unusable feed stuffs and convert them to desirable products such
as meat, milk, eggs, fiber and work.
NUTRIENT is a single class of food or group of like foods that aids in the support of life and
makes it possible for animals to grow or provide energy for physiological processes.

INTRODUCTION TO ANIMAL NUTRITION

There are six major classes of nutrients, carbohydrates, fats, minerals, protein, vitamin, and
water. The main components of food are water and dry matter. The dry matter consists of organic
material and inorganic material.
WATER is essential in the transport of metabolic products and wastes throughout the body and
for most chemical reactions in the body. The amount of water required varies with the amount of
feed consumed, body size, species and the surrounding temperature. However, if water intake
declines, feed intake usually declines.
Animals require ENERGY for maintenance, growth, work and for the production of milk and
wool. Feeds are evaluated in terms of the amount of energy an animal can obtain from them. The
digestible energy (DE) is the gross (total) amount of energy in the hay and grain fed an animal
less the amount lost in the feces. Energy is usually reported in megacalories (Mcal) per kilogram.
(One kilocalorie is equal to 1,000 calories. One megacalorie is equal to 1,000,000 calories).
Amount of DE needed by an animal per day varies according to body size, weight gain, milk
production and work. The amount of energy required to maintain an animal for one day without
loss of body weight is called the energy required for maintenance. Most symptoms of slight
energy deficiency are not very noticeable: slightly reduced gains, less than maximum milk
production and small increases in calving interval. The more severe the energy deficiency, the
more noticeable are the symptoms described. Excess energy is stored as fat.
The most common energy source is from the CARBOHYDRATES contained in feeds. These
are the sugars, starches, cellulose and hemicellulose which have been stored in plant tissues.
Chemical reactions which take place in the animal release the energy in the feed (originally
trapped from the sun by the plant) and convert it to other forms of energy which the animal can
use.
LIPIDS are another energy source found in plants. They are fats and compounds closely related
to them. They contain about two and a half times as much energy as carbohydrates.
PROTEINS are composed of amino acids, which contain carbohydrates, nitrogen and
sometimes sulphur. Ten amino acids are essential to monogastrics, whereas ruminants only need
a source of nitrogen, or a poor quality protein, from which the microbes in the rumen can then
construct the essential amino acids. Protein is absolutely essential for growth, reproduction and
maintenance in monogastrics and ruminants. Mature animals require less protein on the basis of
percentage of the feed offered than young ones. Excess protein is utilized as an energy source.
 Measures of Energy and Energy Utilization
The major MINERALS in cattle nutrition are calcium, phosphorus, sodium, chlorine,
magnesium and potassium. An essential mineral performs specific functions in the body and
must be supplied in the diet, but too much of any may be harmful or even dangerous.
Calcium (Ca) and Phosphorus (P) are the most abundant minerals present in the animal. Both
are found in the teeth and bones, but calcium is also found in milk and eggs. In addition, Ca is
necessary for the clotting of blood, the contraction of muscles, and the functioning of numerous
biochemical reactions in the body. All biochemical reactions which allow the energy in food to
be utilized by animals require phosphorus.
Diets high in legume hay usually require supplemental P only, while diets high in grain often
require supplemental Ca. Young animals, including humans, that do not receive adequate
amounts of Ca or P may develop rickets, which in cattle show up as arched backs. A deficiency
of vitamin D may also contribute to the problem. Older animals fed inadequate amounts of
vitamin D develop osteomalacia, the symptoms of which are weak and easily fractured bones.
Animals having diets low in Ca and P will show a drop in milk production. A low level of P in
the diet may also cause poor reproductive performance in females and lower the availability of
vitamin A.
Sodium (Na) and Chlorine (Cl) are found together as sodium chloride (NaCl or common salt)
and serve to maintain proper acidity levels in body fluid and pressure in body cells. The
hydrochloric acid found in the stomach contains chlorine.
Even though many feeds contain enough sodium and chlorine to meet the requirements of cattle,
supplemental cobalt iodized (blue) salt or trace mineral salt should be available at all times.
Potassium (K), like sodium, serves to maintain proper acidity levels in body fluids and pressure
in body cells. It is also required in a number of enzyme reactions in carbohydrate metabolism
and protein synthesis. Forages normally contain more than adequate amounts of potassium.
Supplemental potassium may be necessary for high-grain feedlot diets.
Magnesium (Mg) is necessary for the utilization of energy in the body and for bone growth.
Cattle fed on lush, immature pasture may have a low level of Mg in the blood, which can result
in grass tetany, a disease characterized by convulsions, twitching of muscles, staggering gait
and falling.
Sulphur (S) is a component of body protein, some vitamins, and several hormones. It is involved
in protein, fat and carbohydrate metabolism as well as blood clotting and the maintenance of
proper body fluid acidity. Most feeds contain adequate amounts of S for cattle. Supplemental S
may be necessary when non-protein nitrogen sources are being utilised in high grain feedlot
diets.
Feeding TRACE MINERALS is not a simple matter. They are required only in very small
amounts. Some minerals fed in excess amounts may cause a deficiency in others; a slight
deficiency or excess may cause a decrease in performance that is hard to pinpoint. Even though
the level in the diet appears adequate, an animal may occasionally respond to an increased supply
of a particular mineral because other dietary factors may have decreased its availability.
Iron (Fe) is an essential part of hemoglobin, a compound that carries oxygen in the blood. A
deficiency of Fe may cause anemia and reduce growth. Generally there is no need to supply extra
iron.
Zinc (Zn) affects growth rate, skin conditions, reproduction, skeletal development and the
utilization of protein, carbohydrates and fats in the body. While Zn deficiency is not common in
ruminants, it can cause a mange-like skin condition called paraketerosis.
Copper (Cu) deficiency can result in anemia, depigmentation in hair, infertility, scouring, and
cardiac failure. Feed testing laboratories find that many samples contain less than the estimated
RDA of 10 ppm. Although the symptoms of copper deficiency are rarely evident, improved
growth and performance is often seen after Cu supplementation.
Manganese (Mn) is essential for the utilization of carbohydrates. Symptoms include retarded
bone growth and reproductive failure. The RDA for Mn is 50 ppm.
Cobalt (Co) is necessary for the microorganisms in the rumen to synthesize vitamin B12.
Iodine (I) is needed in trace amounts by the thyroid gland, which influences the rate of
metabolism in the body. A deficiency causes goitre.
Molybdenum (Mo) forms an essential part of some enzymes. It may also have a stimulating
effect on fibre-digesting microorganisms in the rumen. Excessive quantities of Mo interfere with
the utilization of Cu and may cause a Cu deficiency, symptoms of which include severe scours
and loss of body weight. If the diet is high in sulphur, the problem is more severe.
Selenium (Se) deficiency may result in "white muscle disease" in calves, lambs and foals. A
vitamin E deficiency increases the amount of selenium required to prevent this form of
nutritional muscular dystrophy. Cows on Se deficient diets may have lower fertility and an
increased incidence of retained placentas. The RDA for Se is 200 parts per billion.
Chromium (Cr), tin (Sn) and nickel (NI) appear to be present in sufficient quantities to meet
the requirements of most farm animals.
Fluorine (FI) is essential for proper bone development but will cause toxicity if fed at too high a
rate. It is used on domestic water supplies to reduce the incidence of tooth decay. Too much FI
causes abnormal bone growth, mottling and degeneration of teeth, and delayed growth and
reproduction. To avoid excessive consumption of FI, be sure any rock phosphate fed is
defluorinated.
VITAMINS are the organic compounds, required in minute amounts by the body. They are
essential to metabolism, and some must be supplied in the feed of ruminants.
Vitamin A is the most important vitamin in cattle nutrition. It is the only one that normally must
be added to cattle diets. It is necessary for bone development, sight, and maintenance of healthy
epithelial tissues (i.e. lining of digestive and reproductive tracts). A deficiency can cause an
increased susceptibility to disease, night blindness and reproductive failure.
Vitamin A may be supplied by green forages that contain carotenoids. Carotenoids are broken
down in the body to vitamin A.
Cattle can convert 1 mg of carotene to 400 international units (IU) of vitamin A, while chickens
can convert 1 mg to 1667 IU of vitamin A. Animals on green grass can store vitamin A in the
liver and draw on it for 2-3 months. Vitamin A is inexpensive. The dry granular product is the
most economical source. Animals may also be injected with a 2-3 month supply. It should be
injected twice during the winter.
Water-soluble vitamin A is sometimes added to the water; however, it is difficult to tell whether
the animal is getting its daily or monthly quota this way. Mineral supplements should not be
relied upon to supply vitamin A as they only contain very small amounts.
Vitamin D is called the sunshine vitamin because ultraviolet light acting on a compound on
animal skin changes that compound into vitamin D. Vitamin D is found in sun-cured forages.
Animals kept outdoors or fed sun-cured hay do not usually suffer a deficiency, whereas animals
kept indoors and fed silage may do so.
Vitamin D is involved in the uptake to Ca and P, so that a vitamin D deficiency resembles a Ca
and P deficiency: rickets in the young animals, weak bones in older animals, and a decreased
growth rate.
Vitamin E and selenium have similar and interrelated functions in the body. Use supplements
containing vitamins D and E in addition to vitamin A. They may not always be necessary but
cost little to add.
ACETONAEMIA (KETOSIS)
Cause
Ketosis is a metabolic disorder that occurs in cattle when energy demands (e.g. high milk
production) exceed energy intake and result in a negative energy balance. Ketotic cows often
have low blood glucose (blood sugar) concentrations.
When large amounts of body fat are utilised as an energy source to support production, fat is
sometimes mobilised faster than the liver can properly metabolise it. If this situation occurs,
ketone production exceeds ketone utilisation by the cow, and ketosis results.
In the beef cow, this is most likely to occur in late pregnancy when the cow's appetite is at its
lowest and the energy requirement of the growing calf near its peak.
In the dairy cow, the mismatch between input and output usually occurs in the first few weeks of
lactation, because the cow is not able to eat enough to match the energy lost in the milk.
Symptoms
 Reduced milk yield
 Weight loss
 Reduced appetite
 Dull coat
 Acetone (pear drop) smell of breath/ or milk
 Fever
 Some develop nervous signs including excess salivation, licking, agression etc.
For every cow with clinical signs there are probably a number of others with sub-clinical signs.
Treatment
The initial aim of treatment is to restore the lack of glucose in the body.
A quick-acting glucose supplement is required immediately. Follow-up treatment is aimed at
providing a long term supply of glucose.
Glucose replacement
Intravenous administration of a dextrose solution by a veterinarian is effective in the short term,
but follow-up treatment is essential if relapses are to be avoided.
Drenching with propylene glycol or glycerine has longer term effects. It also has the benefit of
ease of administration. Treatment should be continued for two to four days. Several commercial
compounds contain propylene glycol and glycerine.
Hormonal therapy
Many of the long-acting corticosteroids have beneficial effects in ketosis. They are administered
by the veterinarian as a single injection.
Corticosteroids have the ability to break down protein in muscles to produce glucose, which
immediately replenishes the depressed blood glucose levels.
When using corticosteroids, it is important to supply an adequate amount of glucose either as a
high carbohydrate diet and/or propylene glycol drenches to prevent excessive breakdown of
muscle protein.
Prevention
It is important to prevent ketosis from occurring, rather than treating cases as they appear.
Prevention depends on adequate feeding and management practices.
In times of feed deficiency because of drought or other reasons, the provision of supplementary
feed with adequate amounts of carbohydrate is essential. The best feeds tend to be good quality
hay, silage, or cereal grain.
The body condition of the dairy cow is important at calving. Cows should be on a rising plane of
nutrition up to calving with the aim to calve in good condition.
After calving, the cow has the potential to reach maximum efficiency in milk production, but
feed requirements for high production are often greater than the voluntary intake of pasture can
provide.
Therefore an energy supplement is required and there is evidence that this will improve
production and reproductive performance, and decrease the risk of ketosis. The best supplements
are good quality hay, silage, or cereal grains. Supplements should be fed at least until the peak of
lactation is reached or longer depending on the quality and quantity of available pasture.
Occasionally, very high-producing cows will be susceptible to ketosis every year. In these cases
a preventive drenching program of propylene glycol immediately after calving may avert ketosis
in individual problem cows.

TWIN LAMB DISEASE

Twin Lamb Disease or Pregnancy Toxaemia is a metabolic disorder where the body’s energy
requirements are not being met, resulting from a significant decline in the level of nutrition. In
the final two months of a ewe’s pregnancy, 70% of the lamb’s growth is taking place. It is
therefore particularly important at this time to make sure the ewe has enough good feed to keep
her and her lamb going. Ewes carrying twins are more often affected, but ewes carrying single
lambs can also get the disease.
Stressful events like worms, feet problems, mouth problems, yarding and transport can bring on
Pregnancy Toxaemia. Late pregnant ewes should not be without feed for longer than 4 hours.
Signs:
 Don’t run away when approached.
 Appear blind.
 ‘Star gazing’ – stands looking into the sky.
Treatment
For any treatment to be successful it must be given early. For treatment to be effective the ewe
should be able to chew and respond to food in her mouth, if not it is unlikely that she will
respond to treatment.
We have had the best treatment results with Botonic Energy oral paste – this is available from
the surgery.
Other treatments are:
 Glycerol (Glycerine) given orally 100ml twice daily
 Glucose, 100ml of sterile 6% solution given under the skin daily
 Glucose Solution, 100 – 200ml given orally twice a day,
Continue treating the ewe until she recovers, if she doesn’t respond to treatment, she must be
humanely destroyed.
For valuable ewes or goats, caesarean section may be considered; this immediately removes the
demand for glucose and alleviates the cause of the disease.
MILK FEVER
Milk fever, postparturient hypocalcemia, or parturient paresis is a disease, primarily in dairy
cattle, but also seen in beef cattle, characterized by reduced blood calcium levels (see:
Hypocalcemia). It occurs following parturition, at onset of lactation, when demand for calcium
for colostrum production exceeds the body’s ability to mobilize calcium. “Fever” is a misnomer,
as body temperature during the disease is generally not elevated. Milk fever is more commonly
seen in older animals.
Cause
During the dry period (late gestation, non-lactating), dairy cattle have relatively low calcium
requirements, with a need to replace approximately 30 g of calcium per day due to utilization for
fetal growth and fecal and urinary losses. At parturition, the requirement for calcium is greatly
increased due to initiation of lactation, when mammary drainage of calcium may exceed 50g per
day. Due to this large increase in demand for calcium, most cows will experience some degree of
hypocalcemia for a short period following parturition as the metabolism adjusts to the increased
demand. When the mammary drain of plasma calcium causes hypocalcemia severe enough to
compromise neuromuscular function, the cow is considered to have clinical milk fever.
Clinical signs
The clinical signs of milk fever can be divided into three distinct stages:
Stage 1: Cows are mobile but show signs of hypersensitivity and excitability such as restlessness,
tremors, ear twitching, head bobbing and mild ataxia. If not treated, symptoms usually progress
to stage 2.
Stage 2: Cows can no longer stand and present in sternal recumbency. Tachycardia, weakened
heart contraction and peripheral pulses. Cows appear dull, have dry muzzles, cold extremities
and a lower than normal body temperature. Smooth muscle paralysis can cause bloat, and the
inability to urinate or defecate. Cows often tuck their heads into their flanks.
Stage 3: Lateral recumbency, muscle flaccidity, unresponsiveness to stimuli, and loss of
consciousness progressing to coma. Heart rate can approach 120 bpm, with peripheral pulses
becoming undetectable. If untreated, progression will continue to death.
Treatment
Treatment generally involves calcium injection by intravenous, intramuscular or subcutaneous
routes. Before calcium injection was employed, treatment comprised inflation of the udder using
a pneumatic pump. Inflation of the udder worked because the increased pressure created in the
udder pushed the calcium in the udder back into the bloodstream of the cow.
Prevention
Proper dietary management will prevent most cases of milk fever. This generally involves close
attention to mineral and fiber levels in the diet prior to calving, as well as improving cow
comfort to eliminate other problems that may interfere with appetite and so trigger
hypocalcemia. Oral administration of a dose of a calcium salt in a gel has been advised by some
veterinarians.
GRASS TETANY
Grass tetany or hypomagnesemic tetany, also known as grass staggers and winter tetany, is a
metabolic disease involving magnesium deficiency, which can occur in such ruminant livestock
as beef cattle, dairy cattle and sheep, usually after grazing on pastures of rapidly growing grass,
especially in early spring.
Cow grazing on rapidly grown pasture with tetany of the neck suggesting Grass Tetany
Symptoms and Etiology
Progressive symptoms may include grazing away from the herd, irritability, muscle twitching,
staring, incoordination, staggering, collapse, thrashing, head thrown back, and coma, followed by
death. However, clinical signs are not always evident before the animal is found dead.
The condition results from hypomagnesemia (low magnesium concentration in blood) which
may reflect low magnesium intake, low magnesium absorption, unusually low retention of
magnesium, or a combination of these. Commonly, apparent symptoms develop only when
hypomagnesemia is accompanied by hypocalcemia (blood Ca below 8 mg/dL).
Low magnesium intake by grazing ruminants may occur especially with some grass species early
in the growing season, due to seasonally low magnesium concentrations in forage dry matter.
Some conserved forages are also low in magnesium and may be conducive to hypomagnesemia.
High potassium intake relative to calcium and magnesium intake may induce hypomagnesemia.
A K/(Ca+Mg) charge ratio exceeding 2.2 in forages has been commonly considered a risk factor
for grass tetany. Potassium fertilizer application to increase forage production may contribute to
an increased K/(Ca+Mg) ratio in forage plants, not only by adding potassium to soil, but also by
displacing soil-adsorbed calcium and magnesium by ion exchange, contributing to increased
susceptibility of calcium and magnesium to leaching loss from the root zone during rainy
seasons. In ruminants, high potassium intake results in decreased absorption of magnesium from
the digestive tract.
Trans-aconitate, which accumulates in some grasses, can be a risk factor for hypomagnesemia in
grazing ruminants. (Tetany has been induced in cattle by administration of trans-aconitate and
KCl, where the amount of KCl used was, by itself, insufficient to induce tetany.) Relatively high
levels of trans-aconitate have been found in several forage species on rangeland sites conducive
to hypomagnesemia. Although at least one rumen organism converts trans-aconitate to acetate,
other rumen organisms convert trans-aconitate to tricarballylate, which complexes with
magnesium. Using rats as an animal model, oral administration of tricarballylate has been shown
to reduce an animal's magnesium retention. Potassium fertilizer application results in increased
concentration of aconitic acid in some grass species.
Epidemiology
In Northern Europe, the disease occurs after winter housing. But in Australia and New Zealand,
where the cows are not housed, the disease occurs in similar conditions, when the animal enters
lush, grass-dominant pastures. In North America, grass tetany occurs most commonly when
range stock are moved onto lush early pasture or when housed stock are turned out onto such
pasture in the spring. A second high-risk period may occur in the fall. Although cereal grasses
(e.g. winter wheat) and crested wheatgrass may be especially conducive to grass tetany, the
problem can also occur with several other grass species. "Winter tetany" may occur with some
silages,[3] low-magnesium grass hays, or corn stover.
Treatment
The affected animal should be left in the pasture, and not forced to come back to stall because
excitation can darken the prognosis, even after adequate treatment.
Intravenous mixed calcium and magnesium injection are used. Subcutaneous injection of
magnesium sulfate (200 ml of 50% solution) is also recommended.
Prevention
Magnesium supplements are used to prevent the disease when ruminants, for obvious economic
reasons, must have access to dangerous pastures.
NUTRITIONAL MUSCULAR DYSTROPHY
Nutritional muscular dystrophy (also called nutritional myopathy or white muscle disease)
is a muscle disease of lambs, calves, and foals and adult horses due to deficiency in selenium
and/or vitamin E.
The condition is observed in all breeds and sexes of lambs, from birth to three month of age. Its
frequency increases with upgrading of sheep breed for increased muscling, especially in areas
with selenium deficiency in soils.
In dairy breeds, it occurs in calves from some days after birth until four months of age. But, in
rustic breeds or beef cattle, heifers and young steers up to 12 months can also be affected.
Clinical symptoms
The most usual form involves skeletal muscles, especially in the back. The animal is weak when
it stands up, and has an awkward gait. Animals tend not stay up for more than a few minutes.
When in recumbency, the animals are normal, and have a good appetite.
Treatment
Affected lambs and calves generally recover after injection of veterinary preparations of
selenium and vitamin E.
In horses
In equids, nutritional muscular dystrophy is most commonly seen in growing foals from birth up
to 1 year of age. It is more common in neonatal foals born to dams that are selenium-deficient.
Two forms exist: a peracute form, and a subacute form. The peracute form is characterized by
recumbency, tachypnea, dyspnea, myalgia, cardiac arrhythmias, and rapid death. The subacute
form produces weakness, fasciculations, cramping, and stiffness of muscles which can lead to
recumbency, as well as a stilted gait, dysphagia, ptyalism, and a weak suckle. It may be treated
with selenium supplementation, but still has a 30–45% mortality rate. Other sequela commonly
seen include aspiration pneumonia, failure of passive transfer, and stunting of growth.
Clinical laboratory changes include evidence of rhabdomyolysis (elevated CK and AST,
myoglobinuria) and low blood selenium levels. On necropsy, muscles are pale with areas of
necrosis and edema evidenced as white streaks.