Nutritional Diseases of Goats

Enterotoxemia, a feed-related malady, causes almost sudden death due to a toxin produced by Clostridium perfringens type D and sometimes type C. The organism appears to be widespread in nature. Under conditions of high carbohydrate consumption or high intake of immature succulent forage, the causative bacteria multiply rapidly and produce an sigma toxin that increases intestinal permeability. ( See also page Enterotoxemias in Animals.) Some cases of enterotoxemia are seen in goats, usually those fed diets with high concentrations of carbohydrates. Diarrhea, depression, lack of coordination, digestive upsets, coma, and death may be seen after excessive carbohydrate feeding of both baby kids and mature goats.

The best method to prevent enterotoxemia in stable-fed goats is frequent, small-volume feeding of milk, grain, and forage. Large meals fed once a day should be avoided. In 'at risk' populations of goat, feeding good quality forages as an energy/protein supplement instead of cereal grains will help reduce fermentable carbohydrate intake. Acute indigestion and a rumen pH of < 4.8 indicates lactic acidosis, which can lead to the secondary complication of enterotoxemia. Proper vaccination programs for both the dam and kid will also be of value in prevention.

Clinical signs of polioencephalomalacia include disorientation, dullness, aimless wandering, loss of appetite, circling, progressive cortical blindness, extensor spasms, and occasionally head pressing. Some animals become recumbent and may eventually die without treatment. Diets that produce a low rumen pH or that are high in grain and low in forages, or with some contaminants (eg, sulfate/sulfide), may predispose ruminants to polioencephalomalacia. Such dietary conditions can result in depressed production of thiamine, the production of thiamine antimetabolites, or the production of thiaminases in the rumen.

Affected animals can usually be treated successfully with thiamine (200–500 mg, IV, IM, or SC). Although response is dramatic and almost immediate, if significant brain damage has occurred, animals rarely return to a satisfactory level of production. Prompt treatment is critical. The diet should be modified to reduce grain and increase forage intake and, when needed, to reduce excessive sulfate/sulfide intake. During times of stress, or when predisposing diets are unavoidable, the inclusion of thiamine mononitrate in the diet may aid in prevention. ( See also page Polioencephalomalacia.)

Seen usually in late pregnancy, pregnancy toxemia is much more common in dams carrying multiple fetuses and that are excessively thin, live in stressful conditions, and/or have other, concurrent diseases. Clinical features include abnormally increased blood levels of ketone bodies with concurrent hypoglycemia. Affected animals exhibit many of the signs described for enterotoxemia. During late gestation, the developing fetuses have high demands for glucose; in an attempt to meet the glucose needs, the dam begins to metabolize adipose tissue (fat). The ability of the liver to metabolize this extra fat load is compromised, with a subsequent increase in the release of ketone bodies into the bloodstream. Signs include depression, dullness, opisthotonos, and eventually death.

In early stages of the disease, when signs first appear, a drench of 200–300 mL of propylene glycol or glycerol can be used as an energy source for the dam to prevent so much body fat from being metabolized. However, the administration of glucose (5% dextrose or 50–120 mL of 23% calcium borogluconate solution into a liter of 5% dextrose IV) is the treatment of choice.

Prevention should be aimed at maintaining a proper body condition score, identifying females with twins and triplets and feeding accordingly, reducing the incidence of chronic disease, shearing long-fibered does in late gestation, and possibly including niacin (1 g/day in the diet during late gestation) in the diet. Ensuring adequate winter feedstuffs while monitoring body condition changes throughout gestation will help reduce the incidence of this condition. ( See also page Pregnancy Toxemia in Sheep and Goats.)

Calculi result from mineral deposits in the urinary tract. Difficult and painful urination is evidenced by straining, slow urination, stomping of the feet, and kicking at the area of the penis. Blockage of the flow of urine generally is seen most commonly in intact or castrated males. The blockage may rupture the urinary bladder, resulting in a condition known as waterbelly, and lead to death. It is common when diets with high concentrations of cereal grains are fed (feedlot lambs, pet goats, etc). Affected animals excrete an alkaline urine that has a high phosphorus content.

The incidence of urinary struvite calculi can be reduced by lowering phosphorus consumption to minimal levels and maintaining a calcium:phosphorus ratio >2:1 (with the phosphorus content < 0.45% of the diet). The use of anionic salts such as ammonium chloride (0.5% of the complete diet), dietary tetracycline, adequate vitamin A (or beta-carotene) intake, increased dietary intake of NaCl, reducing grain intake, minimizing use of pelleted cereal grains, and ensuring an adequate source of fresh, clean, palatable water free choice have proved beneficial. Affected animals drenched with ammonium chloride (7–14 g/day for 3–5 days) may show a good response. In range sheep and goats, the disease is associated with consumption of forages having a high silica content. ( See also page Noninfectious Diseases of the Urinary System in Large Animals.)

White muscle disease is caused by low levels of selenium and possibly vitamin E. It seems to develop less frequently in goats than in sheep. Signs include stiffness (especially in the hindquarters), tucked-up rear flanks, arched backs, pneumonia, and acute death. On necropsy, white striations are found in cardiac, diaphragmatic, and skeletal muscles. Levels of AST and lactic dehydrogenase are increased, indicating muscle damage. Blood levels of the selenium-containing glutathione peroxidase are reduced. ( See also page Nutritional Myodegeneration.)