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Ketosis |
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Ketosis |
Introduction
This is a condition of late pregnancy and early lactation most commonly occurring in the last six weeks
of gestation in does with multiple fetuses and in the first 4 weeks in heavily lactating does. Pregnancy
toxaemia is a more common condition than ketosis in goats. Through recognition of early signs and
symptoms and avoidance of the predisposing factors, it can be reduced to a sporadic condition.
Predisposing Factors:
Factors that predispose does to develop pregnancy toxaemia can be divided into two types: inadequate
nutrition (they are not offered the correct quantity or quality of the required ration) and adequate nutritional
offerings but external or animal factors (e.g. disease) affecting intake.
Inadequate nutrition:
Does carrying multiple fetuses require a much higher level of energy than does carrying singles. These
increased needs are compounded by a decreased capacity to consume. When offered ad lib balanced
feeds, does in late pregnancy will voluntarily increase energy consumption but expanded uterine contents
limit dry matter intake, putting fecund does at even greater risk of developing pregnancy toxaemia. To
counteract this, the producer must offer a ration that is more energy and protein dense, e.g. 35% grain to
65% forage. Prolific does on pasture may have difficulty meeting their energy needs through grazing.
Factors affecting intake:
External factors:
Healthy, well fed goats may tolerate many external factors but does chronically underfed are not able to
compensate. Inclement weather (e.g. rain or snow storms or extreme heat) may interrupt intakes. Feeder
space may have been calculated for non-gravid does and may be inadequate for heavily pregnant does.
When hand feeding, the producer should be warned to watch for excessive competition. Restricted water
intake or poor quality water will reduce dry matter intakes. Rapid feed changes, transport may all
temporarily reduce intakes. Poor quality forage that is too woody may also reduce dry matter intake.
Preventive treatments such as vaccinating, etc. performed in late gestation may reduce intakes,
particularly if they are held off feed for the procedure. Exercise has been shown to increase voluntary
intake.
Animal factors :
Factors that will reduce intakes include dental disease, old age, smaller body size than group (see feeder
space), and other concomitant disease such as hypocalcaemia, lameness (e.g. CAE arthritis),
gastrointestinal parasitism, Johne's disease, etc. The body condition score of the doe entering into late
gestation is important. Does that are very thin (< 2.5) have little fat or muscle reserves to draw upon and
are then at increased risk despite a good ration. Very fat does (> 4.0) will readily use body fat reserves in
late gestation but also experience decreased voluntary intakes, thus predisposing them to formation of
ketone bodies that further suppress appetite.
Clinical Picture:
The course of the disease varies but generally develops over three to ten days. A more sudden onset is
usually associated with a sudden stress or poor producer observation. Does will start to decrease grain
intake, followed by silage and then forage. They separate from the herd, lag behind, and become
depressed and gaunt. Other signs of predisposing disease may also be present. Producers that are
vigilant when hand feeding does will easily recognize these animals. If missed, the doe may go on to
exhibit neurological signs which include an abnormal gait and stance, apparent blindness, stargazing and
severe depression followed by recumbency and coma. Some of these signs are attributable to ischemic
necrosis of the brain cortex secondary to prolonged hypoglycaemia (low blood sugar).
Polioencephalomalacia, hypocalcaemia, toxic mastitis (if near or after kidding), grain overload, listeriosis
and lead poisoning are important differential diagnoses. Some producers can smell acetone on the goat's
breath (not everybody has this capability). This is the ketone bodies being produced because of the
disease.
Clinical Pathology:
Most changes are attributable to primary hypoglycaemia resulting from the failure of nutrient intake to
meet the combined needs of the doe and fetuses or of the doe's milk production. Circulating glucose
demands in late gestation and early lactation are extremely high. The doe must either manufacture this
from the production of propionic acid precursor in the rumen or from gluconeogenesis of amino acids
derived from the diet or body muscle reserves. This prolonged hypoglycaemia results in suppressed
insulin production, which in turn increases fat mobilization. This is limited by the availability of the
glucose precursor oxaloacetate for the tricarboxylic acid cycle. This results in a build-up of acetyl-CoA
which is broken down in the liver to the ketone bodies acetoacetate and ß-hydroxybuterate.
Low blood glucose is a consistent finding in clinical and subclinical pregnancy toxaemia (often much less
than 2.0 mmol/L) but may disappear in cases of severe disease, probably due to the death of the fetuses.
Ketonaemia (blood ketones) and ketonuria (urine ketones) are also consistent findings. The serum level
of ß-hydroxybuterate (ß-HB) is inversely correlated with serum glucose. Serum ß-HB levels may be used
to provide a screening test for flock nutritional status in late gestation. Interpretation of values are
presented in table 1 (sheep values). ß-OH levels have been reported at pregnancy toxaemia levels up to
10 days before the ewe develops clinical signs.
Treatment
It is important that the producer recognizes the predisposing factors to pregnancy toxaemia and takes
action to prevent the disease. Does with reduced appetite and mild depression with no neurological
signs, may respond to the following conservative treatment regime: supplementation with propylene
glycol (600 mg/ml) at a rate of 60 ml/ BID per OS for a minimum of 3 days; improved nutrition and feeding
management; and treatment of any predisposing condition. More severely affected does require
aggressive therapy which includes:
A single injection of glucose iv (more frequent injections have been associated with insulin
suppression and rebound hypoglycaemia
Oral propylene glycol at the above dosage regime if not comatose
Oral and/or intravenous fluid therapy using balanced electrolyte solutions
Correction of ketoacidosis using bicarbonate or bicarbonate precursors.
Since hypocalcaemia is often a secondary disease associated with pregnancy toxaemia, clinical
signs of hypocalcaemia should be evaluated.
Corticosteroid therapy using a single dose of dexamethasone.
Removal of the fetuses. Abortion is the preferred method as it is more affordable and less stressful
to the doe. If the kids are more than 2 to 3 days premature, they will be unlikely to survive but are
already at great risk of death in a severely ill doe. Consult your vet about this procedure. Before a
caesarian section is performed, the doe should be stabilized using appropriate fluid therapy.
Systemic antibiotics.
Nursing care. Does need to be encouraged to eat and will need extra attention.
Correction of other diseases (e.g. if CAE arthritis, a non-steroidal anti-inflammatory could be
considered so the doe is willing to get up to eat)
This is a disease that needs to be prevented rather than treated. It is generally a management disease
and should be initially investigated as a herd level problem rather than an individual sick goat. If one doe
is clinically ill, many more in the herd are likely at risk.
Dr. Paula I. Menzies, Ruminant Health Management Group
Ontario Veterinary College, University of Guelph