Agriculture Reference
In-Depth Information
anthelmintic for combating nematode infestation of small
ruminants in humid and warm environments (see Chapter
11 for more details). This topic deserves further research
attention.
conditions, hypocalcemia triggers parathyroid hormone
(PTH) release reducing urinary calcium loss, stimulating
calcium resorption, and promoting synthesis of 1,25-dihy-
droxyvitamin D to enhance intestinal transport of calcium.
The lack of a timely response of any of these three mecha-
nisms provokes milk fever. An acid-base imbalance of the
body at parturition is a predisposing factor. Metabolic
alkalosis impairs the ability of PTH to function normally.
Injected calcium gluconate can keep the animal alive until
calcium homeostasis is restored. Preventive measures
include feeding an acidic (low calcium) diet during late
pregnancy to provoke PTH release and prepare the meta-
bolic system to mobilize bone reserves and increase the
effi ciency of urinary and intestinal calcium transport.
Preventive practices include feeding less salt and potas-
sium and improving phosphorous and magnesium intake;
adding anions such as ammonium, calcium chloride, and
magnesium chloride and sulfate to induce mild metabolic
acidosis; and feeding low calcium diets to stimulate PHT
release prior to parturition. Oral calcium drenching and
vitamin D supplementation at kidding also can help.
METABOLIC DISORDERS
Most prominent disorders are caused by improper feeding
management and nutrient imbalances in the feeds offered
to goats. Animals selected for rapid growth or high rates
of milk production may have a genetic predisposition to
these disorders.
Grass Tetany or Hypomagnesemia
Grass tetany is a metabolic disorder associated with hypo-
magnesemia (low magnesium concentrations of blood).
This condition is most prevalent when animals are milking
heavily and have a higher requirement for magnesium or
early in spring when animals are grazing rapidly growing
pastures that are heavily fertilized. Grass tetany occurs
when pastures are low in magnesium but rich in nitrogen
and potassium that result in a low magnesium : potassium
ratio. In addition, plants involved may have high concen-
trations of tricarbalyllic acid (propane - 1,2,3 - tricarboxylic
acid) that binds magnesium. Clinical signs depend on the
severity of the magnesium defi ciency and whether animals
also are hypocalcemic (low blood calcium concentrations).
Affected animals have low feed intake and low milk pro-
duction. The condition may be chronic and if undetected
will predispose an animal to milk fever. Feeding magne-
sium supplements as magnesium oxide is advised.
Magnesium can be mixed with grain for feeding to preg-
nant and lactating does. Feeding ionophores like monensin
to growing animals may increase activity of the sodium-
linked magnesium transport system in the rumen and
increase effi ciency of magnesium absorption.
Ketosis or Pregnancy Toxemia
Ketosis is a metabolic disorder caused by a negative
glucose balance that, combined with an energy drain, pro-
vokes fat mobilization. Ketosis usually occurs during late
gestation (pregnancy toxemia) or 2-4 weeks after parturi-
tion. It commonly is associated with accumulation of tri-
glycerides in the liver combined with depressed glycogen
levels. A high amount of glucose is required either for
development of multiple fetuses at late gestation or for
milk production; this is responsible for the hypoglycemic
condition of the animal. As a result of the energy drain,
body fat is mobilized leading to an increase in nonesteri-
fi ed fatty acid (NEFA) concentrations in blood that fl ood
the liver with lipid. Esterifi ed fatty acids normally would
be exported from the liver or stored. But the mechanism
to export triglycerides in ruminants is slow, leading to fat
accumulation in the liver. With incomplete oxidation of
fat, NEFA are converted to ketone bodies, primarily ace-
toacetate and β-hydroxybutyrate that are released into
blood. Ketone bodies often increase in blood when the
amount of energy needed for milk production exceeds
energy intake. Feeding management that reduces the sever-
ity and length of the negative energy balance can help
prevent ketosis. Extra supplemental concentrate fed 1
week before and after kidding reduces the incidence of
fatty liver and ketosis. Preventive measures include
increasing the feed supply the 2 weeks around kidding;
avoiding overconditioning animals during pregnancy;
Milk Fever
Milk fever is a metabolic disorder apparent as hypocalce-
mia (low blood calcium concentration) of milking does
that occurs just after kidding. This disorder usually is
related closely to hypophosphatemia (low blood phospho-
rus concentration) and hypomagnesemia (low blood mag-
nesium concentration). During milk fever, the calcium
homeostatic mechanism of goats fails to maintain blood
calcium at a normal level. Because calcium is essential for
muscle contractions and nerve function, hypocalcemic
animals cannot rise or eat. At parturition with the onset of
milk production, the drain on blood calcium for milk must
be replenished either by additional absorption of dietary
calcium or mobilization from bone reserves. Under normal
