The metabolic related diseases mostly occur during certain stages of pregnancy or with lactation, which help to differentiate them from other nutritional deficiencies.
It is important to
follow preventive management practices to minimize losses from potentially
costly diseases.
Sheep and goats are exposed to diseases, but fewer would die
if farmers recognized the problem, made the correct diagnosis, and treated them
in the most effective manner.
To make the correct diagnosis is very difficult as it
requires experience. Consulting with a veterinarian can be most helpful. The
following comments are intended to help diagnose, treat, and prevent some of
the more prevalent nutritional health problems in sheep.
Pregnancy Disease
Pregnancy disease is an upset or interference in the
carbohydrate metabolism cycle and is not related in any way to the amount of
exercise the ewe gets. In converting fatty acids and particularly body fat to
glucose, ketones accumulate in the bloodstream and blood glucose levels decline.
The ketones are very toxic to the ewe, resulting in death within two to five
days.
Pregnancy disease occurs only among ewes carrying multiple fetuses
and usually only during the last four to five weeks of gestation. The ewe stops
eating, which reduces her source of carbohydrate. She separates from the flock,
often wanders around aimlessly, and may press her head against the barn or feed
bunk.
Unless a ewe is treated very soon after the first signs are
noticed, little can be done. Separate her from the flock, drench her with 300
ml propylene glycol twice a day until she eats, and offer her grain and hay. Drenching
with glucose, honey, or molasses or injecting 40-50 cc of 5-10 percent glucose
under the skin can also be used with reasonable success. If the ewe is not
treated on the first day, however, the prognosis is poor.
To prevent pregnancy disease, keep ewes gaining weight
during the last four weeks of gestation. (Photo right)
Enterotoxemia (Overeating Disease)
Enterotoxemia can kill sheep and goats of all ages but
usually kills only those that consume high levels of carbohydrates. Feedlot
mortality for vaccinated lambs is 0.5 %; for unvaccinated lambs it is 5 to 10%.
Vaccination is the cornerstone to prevention of the disease.
Clostridium
perfringens type
D, one type of bacteria that causes Enterotoxemia, is most prevalent in feedlot
or in creep-fed lambs. Symptoms are sudden death, occasional pushing, and
staggering, and apparent blindness. For an outbreak, vaccinate with type D
toxoid on day 1 and again 12 to 14 days later, deworm, and reduce grain until
the vaccine takes effect.
C. perfringens type C causes a type of Enterotoxemia
that usually is accompanied by bloody scours. Mortality may be high. It usually
occurs among fast gaining lambs during the first three weeks. Ewes vaccinated
three to four weeks before lambing, provide antibody protection in their milk. Normally,
vaccine won’t “take” on young (3 to 10 days) lambs that are nursing.
Prevention of Enterotoxemia is far more likely to be successful
than trying to treat the disease. Most commonly , the change in diet that
triggers the diseases an increase in the amount of grain! Protein supplement
and/or grass that the sheep or goat is ingesting.
Always make feed
changes slowly.
Acidosis
Overfeeding of highly fermentable carbohydrate diets may
cause acidosis. The high grain intake lowers the rumen pH from about 6.5 + to
below 5.5, at which point lactic acid production increases and causes acidosis.
Ewes fattening on grain, lambs on protein-supplemented carbohydrates, rams
being fed for show or any feedlot animals on a high starch diet are at risk. Affected
animals discontinue eating and showing signs of severe stomach pain. Affected animals
sometimes are very lame and prefer to lie down or walk on their carpi.
This is because, especially the front feet are hot and
painful in the acute stage of acidosis. These symptoms are named laminitis and
may lead to permanent hoof deformities. Affected animals are staggery initially
and have bloated, distended rumens. Some may have acute, watery diarrhoea. Later
they may become recumbent, cold and comatose with sunken eyes indicative of
dehydration.
Animals experiencing acute acidosis should be treated
immediately. Purging with mineral oil or a bicarbonate drench is effective. If
an animal has symptoms of brain disorder an injection of thiamine (Vit. B1)
should be administered. To prevent acidosis the following management tips
should be followed:
grain and hay separately, if possible.
·
Minimise
sorting of diet ingredients by the use
of the same particle size for all
feedstuffs.
·
Feed
slowly fermenting grains (maize;
grain sorghum) with rapidly fermented
grains
(barley; wheat; steam-flaked maize).
Limit wheat to a maximum of 20 % of the
diet
if not accustomed to feeding wheat.
·
Gradually
adapt animals to high-grain
finishing diets in 21 to 28 days using three or
four step-up diets. Suggested step-up diets may contain 45, 35, 25 and 15 %
roughage.
·
Feed
at least 15 to 20 % roughage (90% dry). Roughage
is similar to insurance. The more
roughage fed, the less likely acidosis will be a problem. When acidosis is not a problem, feed
efficiency and cost per gain increase as roughage level increases.
·
Make
sure feed intake is consistent (not increasing or decreasing) before switching
animals to the next diet.
·
Feed
bunks should contain always a sprinkle of feed.
Never allow the animals to be without feed for more than 30 minutes.
·
Feed
animals, as close as possible, at the same time each day.
·
Feed
two or more times a day if possible.
·
Use
an ionophore to increase feed efficiency and reduce variation in feed
consumption. (Ionophores are feed
additives used in sheep and cattle diets
to increase feed efficiency and body weight gain).
·
Balance
feedlot diets for 0.5 to 0.7 % calcium.
·
Keep
daily records of dry matter feed intake.
·
Keep
all water containers clean and fresh
·
Prevent
urinary calculi in feedlot lambs by feeding ammonium chloride and/or ammonium
sulphate at 1.0 % in the complete diet.
Feedlot Rectal Prolapse
Feedlot rectal prolapse occurs in 0 to 10 % of sheep. This condition is caused by high grain diets,
high feed intake, overweight, coughing, or a short dock. There is no particularly effective cure. Procedures usually include suturing the
rectum partially shut or inserting a plastic tube or short piece of hose and
clamping off the protruding position of the rectum with an elastrator ring.
Urinary Calculi
Urinary calculi occur in feedlot wether lambs and rams on
high grain diets and in creep-fed wether
lambs.
Mortality is 80-90 % of those affected.
The usual cause is an improper calcium: phosphorus ratio. High grain diets result in a Ca:P ratio of
1:2 or 1:3. The ratio of Ca:P should be
1.5:1 or 2:1 thus, you must add limestone not dicalcium phosphate to fattening
lamb diets. Another effective preventive measure is the addition of 0.75 to 1 %
ammonium chloride to the grain diets.Lamb Starvation
Lamb starvation, the number one killer of lambs, often
associated with lack of shepherding.
Contributing causes are:
·
The
lamb doesn’t get started (gets no colostrum). Seventy-five percent of lambs that don’t get colostrum die for one
reason or another.
·
The
ewe won’t claim the lamb.
·
Mastitis.
·
The
teat is too big or is too near the ground and the lamb doesn’t find it.
·
Sore
mouth.
·
The
ewe can’t feed two lambs (mastitis, too little feed, etc.).
·
Joint
injury or illness.
·
Pneumonia,
which often is associated with lambs that received no colostrum and thereby
lack immune bodies.
·
Difficult
parturition.
·
A
“genetic will to die”. Actually, the
majority of lambs die for no apparent reason.
A genetically caused lack of vitality may well be the cause.
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