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Pregnancy toxaemia and

ketosis in goats


The diseases pregnancy toxaemia and ketosis can cause severe problems in goats. While the diseases are clinically different and occur during different stages of pregnancy and lactation, the basis of the disorder is essentially the same: a decrease in blood sugar levels and an increase in ketones.

In ruminants, glucose is synthesised mainly from propionic acid (a volatile fatty acid produced in the rumen) and from amino acids. The amount of glucose that is absorbed directly depends on how much dietary carbohydrate escapes rumen fermentation and is digested in the small intestine. This form of glucose uptake varies with different feeds as well as their treatment.

Ruminants can use products from rumen fermentation, such as volatile fatty acids, for most of their energy requirements. However, the nervous system, kidneys, mammary gland and foetus have a direct requirement for glucose. During periods of peak glucose requirement (late pregnancy and early lactation) problems may arise due to a glucose deficiency.

The incidence of pregnancy toxaemia and ketosis varies with the two main types of goats. In dairy goats with a genetic potential for high milk production, ketosis may be a potential problem; in non-milch goats (Angora, Cashmere and meat) pregnancy toxaemia is more common.

PREGNANCY TOXAEMIA

Main causes

The most important cause of pregnancy toxaemia is a decline in the plane of nutrition during the last six to eight weeks of pregnancy. This places the pregnant female in a difficult situation because the developing foetus imposes an unremitting drain on available maternal nutrients.

Pregnancy toxaemia can arise from starvation and an over-fat condition.

Starvation - The natural tendency for goats in an autumn breeding cycle, with most Angora flocks having a late winter or spring kidding. If the last third of pregnancy coincides with the spring flush of pasture growth, pregnancy toxaemia should not be a problem under extensive grazing. However, in the South-West of Western Australia a late break in the season followed by cold weather usually results in little pasture growth, and animals are frequently in poor condition during late pregnancy.

Some feral goats and the lower grades of Angora crosses may have an extended breeding cycle, with some breeding twice a year. With these goats there may be periods where late pregnancy coincides with poor feed, especially during autumn.

Over-fat - Over-fat does are usually found in a small enclosure and get very little exercise. Their appetite may be reduced, they become lazy and excessive fat breakdown begins in an attempt to maintain blood glucose levels. This can result in abnormally high levels of ketones. Another problem is fatty degeneration of the liver.



A healthy doe and kid. Early diagnosis can

prevent pregnancy toxaemia and ketosis.

Other causes

Psychological considerations - Goats tend to form small family groups. When an animal is removed from its group it can fret and refuse to eat. Fretting is more common with one or two house goats. Bonding may also include humans; the goat may refuse to eat when its human friend is away. These periods of voluntary starvation may be critical in late pregnancy, triggering off excessive fat breakdown leading to pregnancy toxaemia.

Appetite-depressing factors - Gastro-intestinal worms are known to depress voluntary feed intake, as well as causing an increased leakage of protein into the animal's small intestine. A deficiency of vitamin B12 (due to a cobalt deficiency) will also result in a drastic reduction in voluntary feed intake.

Stress - Various forms of stress, such as transportation, prolonged yarding and shearing, may decrease energy intake and increase energy expenditure.

Disease - Other diseases, such as the causes of lameness and bad teeth, may impede the animal's ability to forage.

Clinicial findings

Clinical findings will vary depending on whether the animal is run in a backyard or in a flock.

The over-fat and/or backyard doe - About four weeks before kidding the doe becomes lazy, spends much time lying down and typically defaecates while recumbent. Her appetite may become capricious. Eight to ten days later, the feet and lower parts of the legs may swell and the doe is reluctant to walk. This period of reduced exercise is accompanied by a decrease in feed intake, until about one week before kidding the doe stops eating and will not stand unless assisted.

In the terminal phase the doe will moan and have laboured respiration and sunken eyes, indicating a rapid loss of condition. She usually dies two to three days before she is due to kid.

Starvation — In the paddock or flock situation, affected animals are often not noticed until they have reached a terminal stage. The affected doe is usually found on her own near some shelter. Respiration is laboured and often through the mouth. Her "camp" is surrounded by small, flinty, mucous-covered droppings, indicating she has not eaten for a few days. She may attempt to kid on the day she dies.

Diagnosis

Pregnancy toxaemia is usually suspected when heavily pregnant does have a history similar to that outlined previously. The characteristic signs at autopsy are:

  • The liver is swollen, friable and greasy.

  • The fat in the abdominal cavity has whitish flakes of necrosis throughout.

  • Well developed kid or kids in the uterus.

Treatment

Treatment is seldom successful unless the condition is diagnosed early. It is aimed at correcting the doe's energy imbalance by a direct energy supplement with a twice-daily drench of 120 to 180ml of glycerine or propylen glycol mixed with an equal volume of water. Or, an intravenous injection of 100 to 200ml of a 50 per cent dextrose or glucose solution will give a rapid initial effect.

Other supportive measures include forcing the overfat doe to exercise, premature induction of kidding or caesarian, and stimulating the doe's appetite by using selected shrubs and vitamins, if needed.

Prevention

Avoid an over-fat condition during early pregnancy. In the last two months, gradually increase the plane of nutrition. If this is not possible on existing paddock feed, either supplement the feed or select a different kidding time. Avoid periods of sudden stress during the last two months of pregnancy.

KETOSIS (Acetonaemia)

Cause

All high-yielding dairy animals in early lactation may experience a net loss of energy and may be in a state of sub-clinical ketosis. About four to six weeks after kidding, hormonal stimuli for lactation may overcome the effects of inadequate food intake. However, it takes only a small nutritional inadequacy of metabolic imbalance for does to develop clinical ketosis.

Predisposing factors

In the last four weeks of pregnancy, rumen activity is restricted, resulting in a depressed food intake. This may continue into the first few weeks of lactation.

Over-fatness during late pregnancy may reduce appetite further and predispose the goat to a subsequent rapid fat breakdown.

Other factors may include faulty ration formulation and feeding regime.

Ruminal digestion will be upset if a big quantity of concentrated feed is eaten over a short period. In the extreme form this results in a complete lack of ruminal motility and acidosis. Sudden changes in types of feed may result in indigestion or periods of low volunatry feed intake. Short periods of starvation, either voluntary (pregnancy toxaemia) or imposed (yarding, transport) may cause problems.

Stress may have a direct effect on feed intake as well as having a hormonal effect on the metabolic process.

Clinical findings

The clinical evidence of ketosis usually appears during the period leading up to peak lactation (six to eight weeks after kidding).

Sub-clinical form — Many high producing dairy animals are on the borderline for ketosis. Intermittent periods of indigestion may take place with excessive amounts of highly digestible food, which may result in high levels of volatile fatty acids. Excessive acidity is liable to cause a stand-still of rumen activity and a chain of metabolic events resulting in excessive fat breakdown and ketosis. In this mild form, does will have irregular milk production and days of inactivity.

Clinical form — In the more severe form, the clinical findings include:

  • A decrease in appetite and milk production.

  • A rapid loss in condition.

  • Hard droppings which tend to have pointed ends.

  • The doe is moderately depressed and frequently exhibits signs suggestive of milk abdominal pain.

  • A "sweet corn" (acetone) smell may be detected on the doe's breath or in the milk.

Diagnosis

Diagnosis is generally based on the doe's history (time of kidding) and the clinical findings. However, the clinical signs can be confused with hypocalcaemia (milk fever), enterotoxaemia (pulpy kidney), bloat, impaction, reticulitis and nephritis.

The presence of ketones can be established by using acetest tablets in a urine sample.

Treatment

The general principle of direct energy supplementation is the same as outline for pregnancy toxaemia.

With non-pregnant animals, the second option is hormone therapy (cortisone) which affects the activity of certain key enzymes, thereby increasing the blood glucose supply.

In cases where problems with grain digestion are suspected, acidosis may be reduced by dosing the doe with sodium bicarbonate (500ml of a 5 per cent solution). A small dose of sodium bicarbonate (100 to 150ml) will stimulate the oesophageal groove to close, ensuring fluid flows directly to the fourth stomach. It is useful as a preliminary drench to be followed by the other forms of oral drenching outlined previously.

Prevention

The main preventative measures are:

  • The doe must not be excessively fat at the beginning of the dry period.

  • The production ration should be introduced about one month before kidding to allow the rumen micro-organisms to adapt.

  • After kidding, feed the doe as much as she will eat of a good quality roughage diet up to peak lactation yield.

© 2000 W.A. Dept. Ag.