Nutritional Effects on
SHEEP HEALTH
by
Helen A. Swartz, Ph.D.
State Sheep, Goat and Small Livestock Specialist
Lincoln University Cooperative Extension
Jefferson City, Missouri
INTRODUCTION
Sheep are hardy, resourceful ruminant animals that live and produce for
several years when adequately fed. Being ruminants, they convert forages,
forbs (weeds) and browse into meat, milk and wool. Either by artificial
or natural selection, certain genotypes produce more effectively in one
environment than in others. The environment of temperature and rainfall
is not provided by man. Management, however, is. Utilizing feedstuffs that
are readily available and providing nutrition for sheep that is the least
costly is how money is made in a sheep operation.
FEED NUTRIENTS
Energy
Nonmilking and some milking sheep can often meet their energy needs
by grazing. Sources of energy are grass, alfalfa, and (starch and cellulose)
grains. Lactating (milking) ewes with the genetic capability for raising
triplets require supplemental nutrients. Inadequate diets of lactating ewes
will lead to weight loss, infertility and reduced production.
Protein
High quality protein feeds such as soybean meal or by-pass protein such
as blood meal and fish meal are needed in the diet of high producing sheep.
High quality legume hay which contains 16 to 20 percent crude protein is
usually sufficient.
Other nutrients required are calcium, phosphorus, magnesium, selenium, and
vitamins A, D and E. In a ruminant animal, the microorganisms synthesize
B and K vitamins.
The nutritional requirements of sheep have been determined for each state
of production. Providing these nutrients on a constant basis allows for
the optimization of the genetic response in breeds and crossbreeds of sheep.
We must keep in mind that in a ruminant, we are feeding the microbes in
the rumen. Also, we need to remember that the newborn lamb functions as
a single stomached animal (like humans and pigs). The rumen is sterile at
birth and gradually as the lamb begins to eat hay, grain or grass, the rumen
expands and becomes functional. The rumen is usually fully functional between
6 and 10 weeks of age (Figure I ).
In the lamb, vitamins B and K must be provided as they begin life with a
nonfunctional rumen.
Fat
A level of 1.5 -2.5 percent fat in a grain mixture is normal.
Feed Additives
Sheep owners should avoid feed additives that make extravagant claims. There
is no research to show that sheep require any miracle feed supplement or
"organic" health feeds. These additives can be expensive and offer
no advantage over other supplements. They often cost so much that the profit
goes out of the enterprise.
Some grain mixtures for growing lambs are shown in Table 1.
Some of the problems that result from insufficient nutrient compositions
of feed or grazing are the following:
Table 1. SAMPLE GRAIN MIXTURES FOR GROWING LAMBS
-------------------------------------------------------
1 2 3 4
----------------------------
Level of Protein in Finished Mix
-----------------------------
Ingredients 14% 16% 18% 20%
---------------------------------------------------------------
Pounds
-------------------------
Rolled Corn 900 800 720 656
Crimped Oats 421 300 240 200
Beet/Citrus Pulp 200 200 200 200
Dried Brewer's Grain --- 150 200 200
40% Protein Supplement 300 --- 516 --
Soybean Meal --- 356 --- 600
Molasses 150 150 100 100
Trace Mineralized Salt 10 20 10 20
Dicalcium Phosphate --- 10 10 20
Monosodium Phosphate 15 10 --- --
Magnesium Oxide 4 4 4 4
---------------------------------------------------------------
Ton 2,000 2,000 2,000 2,000
===============================================================
Table 2. SAMPLE MIXTURES
1. 13.5% of crude protein (to be used with good quality hay).
---------------------------------------------------------------
Crushed oats 75 pounds
Cracked corn 75 pounds
Wheat bran 25 pounds
Soybean oil meal 25 pounds
Salt 2 pounds
---------------------------------------------------------------
2. 16.0% of crude protein (to be used with fair-to-poor hay).
---------------------------------------------------------------
Crushed oats 65 pounds
Cracked corn 65 pounds
Wheat bran 20 pounds
Soybean oil mea 50 pounds
Salt 2 pounds
---------------------------------------------------------------
The second formula is more suitable for high producing lambs and ewes and
instances where only fair quality grass or mixed-legume grass hays are available;
otherwise the first formula is satisfactory and usually less expensive.
ACIDOSIS (grain overload)
Cause
a. Excessive ingestion of grain or moderate amounts by animals not accustomed
to grain or by hungry animals.
b. Grain fermentation results in abnormally high
levels of D-lactic acid and lactate.
c. The rumen pH falls to 4.0 to 4.5
Signs
a. Occur 6-12 hours after grain ingestion
b. Associated with indigestion and dehydration.
c. Off-feed, irritability, dullness.
d. Distended, paralyzed rumen.
e. Profuse diarrhea, dehydration, sunken eyes.
f. Incoordination, collapse, coma, death.
g. Recovered animals often results in founder.
Treatment
a. Empty rumen, either with stomach tube or surgery.
b. Mineral oil and antacids.
c. Electrolytes and buffers to correct dehydration and acidosis.
d. Fluid treatment may need to be supplemented and antibiotics, antihistamines,
steroids, and calcium borogluconate, depending on severity of clinical signs.
Prevention
a. Remove the offending cause: properly managed feedbunks are best prevention.
b. Do not offer free-choice grain to unaccustomed, hungry or starving sheep.
c. Ionophers (e.g.: Bovatec) in concentrate, at recommended level, are useful
BLOAT
Cause
a. Interaction of several factors in rumen:
· reduction of gas elimination
· increased gas production from fermentation
b. Associated with:
· Iush, rapidly growing legumes
· changes in diet composition
c. May follow oral antibacterial treatment. Impaired gas elimination from
solid objects lodged in esophagus or esophageal groove.
Signs
a. Distention of rumen (LEFT side of animal)
b. Often is moderate, with no great consequences.
c. If progressive:
· respiratory distress
· profuse salivation
· bluish mucous membranes
· prostration...death from asphyxiation
Treatment
a. Remove offending cause; usually feed
b. Relieve ruminal pressure: stomach tube
· trocharization of LEFT paralumbar fossa ("last" resort)
· Defoaming agents: vegetable oils are usually as effective as more
expensive commercial preparations
· May use surfactants (e.g.: Poloxalene, Therabloat, etc.)
Prevention
a. Knowledge of circumstances leading to bloat and avoidance of source.
b. Pasture management, especially legume pastures.
c. Poloxalene blocks: relative value, although quite useful when flocks
are first turned into pasture.
d. Bovatec (Lasalocid) in concentrate, at recommended level, is useful.
e. Increase salt intake to increase water consumption.
CALCIUM DEFICIENCY IN PREGNANT EWES
Cause
a. Lack of free access to mineral supplement containing calcium.
b. Winter grazing of forages low in Ca.
· prolonged residue grazing during open winter.
c. Feeding forages low in Ca (straws, corn, silage...)
Signs
a. Affected ewes are lethargic and recumbent with no previous signs of other
illness.
b. Depression, inappetence, muscle tremors and weakness late in gestation.
c. Serum calcium level less than half its normal value.
d. Signs mimic "Pregnancy Disease".
Treatment
a. Results are "dramatic", as in Milk Fever of dairy cows.
b. 200 ml of calcium gluconate, I.V.s, slowly, (results occur in
15-30 min.)
c. Untreated ewes usually die in 12-18 hours.
Prevention
a. Free-choice limestone, mixed with 1/3 salt.
b. Specially needed if feeding forages low in Ca or if ewes are grazing
"residues" during open winters.
GOITER
Cause
a. "Simple" goiter (known also as "colloid" goiter)
of newborn lambs is due to iodine deficiency in the pregnant ewe's diet.
Signs
a. Defined, symmetrical enlargement of the thyroid gland.
b. The thyroid gland is located in the ventral part of the "throat
latch" in the upper part of the trachea (wind-pipe).
c. Affected lambs have a swollen throat, are often born with little or no
wool, act weak and often succumb to starvation.
Treatment
a. Does not improve chances of survival.
Prevention
a. Stabilized iodized salt in diet of gestating ewes.
b. Salt mix should contain at least 0.007% available iodine.
POLIO (Polioencephalomalacia)
Cause
a. Usually a digestive upset which:
· impairs thiamine (vitamin Bl) production, or
· hampers thiamine absorption.
· results in thiamine destruction before its
. absorption
b. Thiamine is indispensable for the vital functioning of the brain...if
thiamine is unavailable or its required level is decreased, the brain
cortex degenerates.
Signs
a. Clinical signs are the result of brain degeneration:
· incoordination
· depression
· prostration
· arrested ruminal movement
· blindness
b. Fever is usually absent.
c. May at times be easily confused with enterotoxemia.
Treatment
a. Thiamine (B1) is the specific treatment.
b. Affected sheep should receive (preferably intravenously) 1 '/: gm to
2 gm thiamine, depending on size and severity of condition. Treatment should
be repeated every 6 hours for at least 24 hours.
d. Thiamine may be provided alone or in a B complex preparation.
e. Recovery is not always complete. Animals severely affected for more than
24 hours cannot be expected to respond adequately to treatment.
f. Do not administer dextrose IV's to affected animals, because their carbohydrate
metabolism is impaired.
Prevention
a. Slowly increase dietary carbohydrates (concentrate) intake, especially
for feedlot lambs.
b. May consider supplemental dietary thiamine: 100200 mg/head/day for 7-10
days, during periods of high risk.
PREGNANCY DISEASE ("Lambing paralysis", Ketosis)
Cause
a. "A disease of men, the symptoms of which are seen in sheep."
b. Inadequate carbohydrate (concentrate, energy) intake during late pregnancy.
c. Common in both older ewes with poor teeth and ewe lambs carrying twins.
d. Overfat ewes carrying twins or triplets appear more susceptible than
ewes in poor condition or those with single lambs.
e. Stress, storms, transport, fasting, excessive heat, etc., aggravate the
adverse effects of poor nutrition.
f. Basically, pregnancy disease results from hypoglycemia leading to ketosis,
liver degeneration and decreased liver glycogen.
Signs
a. Affected ewes exhibit signs of impaired nervous function:
· listlessness
· lack of appetite
· aimless walking
· leaning against objects
· twitching of ears, eyes, tail, etc.
· grinding of teeth
· blindness
progressive loss of reflexes
· paralysis: laying on chest
· coma...death
b. The usual course of the disease lasts from 2 to 5 days.
c. Mortality rate may be as high as 80% regardless of treatment.
Treatment
a. Seldom effective. May try the following:
b. Glucose-producing substances, such as
· glycerol, or
· propylene glycol
· administer orally 7-8 oz. twice daily
c. Intravenous dextrose.
d. Removal of lamb by C-section usually increases survival rates. May need
to abort lambs to save ewe. Should also administer glucocorticoids.
f. Vitamin B12 to increase appetite.
g. Good nursing, such as plenty of water and stomach tube administration
of finely ground quality hay.
h. Insulin is contraindicated. Glucose treatment may be used only
in conjunction with glycerol or propylene glycol.
Prevention
a. Prevention of pregnancy disease can be achieved only through adequate
nutrition of the breeding flock.
b. Prevent obesity in early pregnancy.
c. Adequate energy intake is paramount, especially during the last 6-8 weeks
of gestation.
d. Avoidance of stress is also necessary.
PROLAPSES
Cause
a. Rectal prolapse is seen mainly in creep fed or feedlot lambs. The role
of coughing and heredity cannot be overlooked. Estrogenic substances may
trigger the problem, although cough, parasites and loose stools are usually
complicating factors.
b. Vaginal prolapse is primarily observed among fat pregnant ewes and those
eating large quantities of roughage. Susceptibility is influenced by heredity.
Common among ewe lambs.
c. Docking tails too close contributes to prolapse.
Treatment and Control
a. Treatment of prolapses vary from repositioning to amputation. Suturing
or retainers may be used.
b. For all practical purposes, the prevention of these problems requires:
· adequate management of diet, both quantity and quality.
· consistent culling of individuals affected by either rectal or vaginal
prolapses. The odds are that a young ewe with rectal prolapse will have
a prolapsed vagina come lambing time.
c. Suturing of rectal prolapse is only a temporary solution. Permanent correction
requires amputation (may use "rectal" rings).
RICKETS
Cause
a. A disease of young lambs associated with:
· inadequate calcium or phosphorus, or vitamin D intake
· any disruption of the Ca:P balance
b. Calcium, phosphorus and vitamin D are required for:
· bone formation, and
· bone growth
Signs
a. Lameness associated with enlargement of the ends of fast growing bones.
b. Deformities of long bones which bear the body weight.
c. Weak, demineralized bones which may break easily. Sometimes lambs act
as if paralyzed because of the severe pain associated with fractures. The
head of the femur (by the hip socket) is a common site of fractures, as
well as the ribs.
Treatment
a. Effective treatment requires:
· accurate diagnosis
· careful evaluation of the diet and correction of diet deficiencies
or imbalances. Vitamin D without calcium or phosphorus will make the problem
worse and vice versa.
prevention
a. Adequate nutrition of gestating ewes and lambs.
b. If in doubt, have the ration analyzed, balanced
and properly supplemented with calcium.
c. Sunlight is the cheapest source of vitamin D.
SWEET CLOVER POISONING (Bleeding disease)
Cause
a. Sweet clover contains coumarin, a substance of no consequence
per se.
b. Under the right conditions, such as spoilage, "heating", moldiness,
etc. --the coumarin present in either sweet clover hay or silage is converted
into DICOUMAROL.
c. Dicoumarol is an anticoagulant, no different than D-con or Warfarin.
Dicoumarol disrupts the normal clotting mechanisms of blood in sheep ingesting
contaminated sweet clover forage.
d. Dicoumarol has a "cumulative" effect: the longer sheep ingest
dicoumarol, even very small amounts, the greater the chances for poisoning
to occur.
Signs
a. Some sheep are just found dead, victims of extensive internal hemorrhages.
b. Others may have subcutaneous hematomas (large blood blisters), may bleed
through their noses, be anemic, and eventually die from excessive bleeding.
Many animals will appear stiff and/or lame due to bleeding into the muscles
and joints. Lambs born to ewes consuming toxic sweet clover may be born
weak and will die from hemorrhages.
c. Pregnant ewes may abort.
Treatment
a. It is essential to STOP FEEDING the offending sweet clover forage (hay
or silage).
b. Severe cases respond only to blood transfusions, and/or vitamin K, (vitamin
K3 is of value for treatment). c. Mild to moderate cases may be treated
with vitamin K. Affected animals should be handled with care to avoid further
bruising and hematomas.
d. Affected animals should be handled with care to avoid further bruising
and hematomas.
Prevention
a. The best prevention is not to feed sweet clover hay or silage, although
this is not always economical.
b. If sweet clover hay or silage must be used in a given operation, proper
haying or ensiling practices are essential. The prevention of sweet clover
poisoning starts at harvest time.
c. Plant sweet clover varieties which are low in coumarin.
d. It is a good practice to have sweet clover forage analyzed before offering
to sheep. The Toxicology Section of the Veterinary Science Department can
perform such an analysis. Sweet clover forage should not be fed to pregnant
ewes, especially during the last 8-10 weeks of gestation.
f. If one must feed sweet clover forage which is known to contain
dicoumarol, no guideline is strict enough. At any rate, such sweet clover
should not be fed continuously for over 6 days, and if fed, forage other
than Sweet clover must be fed at least 3 consecutive weeks...(1 week
sweet clover followed by 3 weeks without it).
URINARY CALCULI (Water Belly)
Cause
a. Urinary calculi --primarily a problem of rams and wethers --result from
mineral salts deposited within the urinary organs: kidneys, bladder, ureters,
urethra, around the preputial orifice, etc. Nutritional and seasonal factors
are associated with the incidence of urinary calculi:
· concentrates, high phosphorus
· silicates, present in either grasses or grain
· cold weather which reduces water intake
a. Vary from mild to severe when the urinary passages are obstructed.
b. Arched back, straining, tail twitching.
c. Subcutaneous edema.
d. The distended urinary bladder may eventually rupture and the affected
animal may actually appear improved for several days...UNTIL SIGNS OF UREMIA
DEVELOP. The urethra may also rupture from excessive pressure.
Treatment
a. Treatment requires the reestablishment of ability to urinate.
b. Some mild cases may response to ammonium chloride:
· either in feed: 1/4 oz/head for 7-10 days
· or drench: 3/4-1 fluid oz/head for every other day up to 3 times.
Use 30% NH4CI solution.
c. Severe cases may be saved only through surgical intervention.
d. Smooth muscle relaxants may help.
e. Nutrition, water availability and mineral balance must be adjusted, as
needed.
Prevention
a. Through management practices intended to reduce predisposing factors:
· plenty of water
· supplement ration with feed grade limestone: 20-30 lb/ton of feed
· may add sodium chloride (common salt) to ration: 3-5%
· balanced mineral intake.
· may add ammoniumchloride to ration: 0.5-1% more effective than sodium
cloride
WHITE MUSCLE DISEASE
Cause
a. Not every stiff or weak lamb is affected with WMD...differentiate from
other conditions:
· Vibriosis
· Polyarthritis
· Enterotoxemia
· Rickets
b. Mortality rate is high in lambs born with WMD.
c. The delayed (or acquired type) may be corrected more easily. This type
has nutritional basis
(Selenium-vitamin E deficiency) and is often triggered by vigorous exercise.
Lambs affected by WMD
· move slowly...are in pain
· their backs are arched
· may be down, as paralyzed
· may not nurse and starve out
e. When the heart muscle is severely damaged, death may be sudden.
Treatment
a. Affected lambs should be given injections of sodium selenite -vitamin
E. In aqueous solution such as Bo-Se, dosage: newborn lambs, lcc Bo-Se;
lambs 2 weeks and older, 4cc of Bo-Se. Inject intramuscularly or subcutaneously.
b. Injection should be repeated every 12-14 days, but not to exceed 4 doses.
c. Maternal diet should be reevaluated. Recently cut, "good" hay
(especially legumes) should provide a vitamin E source. If none is available,
use Bo-Se or Mu-Se injections to provide ewes with Selenium and vitamin
E.
d. The maternal ration may be supplemented with sodium selenite not to exceed
0.3 pp or available selenium.
e. Do not overdose with selenium, toxicity may occur.
Prevention
a. Dietary inclusion of recommended NRC levels selenium and vitamin E.
b. Areas or flocks with past experience of WMD may consider injecting pregnant
ewes with selenium-vitamin E preparations at least 4-8 weeks prior to lambing.
Use Bo-Se at the rate of a 1 1/2 cc/100 lb.
c. The incidence of WMD may be reduced by incorporating wheat and linseed
oil meal in rations of pregnant ewes.
d. May feed pellets containing 5 mg selenium and 350 IU vitamin E before
lambing. These pellets are manufactured commercially; follow label instructions.
Some information taken from North Dakota
Extension Guidesheet: "Common Diseases of Sheep"
Author: Helen A. Swartz, Ph.D.
State Sheep, Goat and Small
Livestock Extension Specialist
Publisher: William Helvey, Coordinator
Agricutlural and Extension
Information Center
Editor: Carole E. Johnson, Secretary I
Lincoln University at Jefferson City, University of Missouri
and the U.S. Department of Agriculture cooperating.
Dr. Dyremple Marsh, Interim Director of Cooperative
Extension.
Distributed in furtherance of Food and Agriculture Act, 1977 PL
9S-113 Section 1444 and 1445, as amended by PL 97-98.
December22, 1981
Publications are distributed without regard to race, color,
national origin, sex, age, or religion.