Nutritional Diseases of Goats

Enterotoxemia, also called overeating disease, is a feed-associated malady in goats that can be peracute, acute, or chronic. The peracute and acute forms, which most often result in death, are common in young kids. Chronic enterotoxemia is occasionally observed in older goats.

The causative agents of enterotoxemia are exotoxins produced by various types, or strains, of Clostridium perfringens bacteria. Most often, enterotoxemia results from infection with C perfringens type D and sometimes type C; however, type A enterotoxemia has been recognized in goats. (The different types of C perfringens reflect the exotoxins produced.) C perfringens appears to be widespread in nature and is a normal inhabitant of goats' enteric environment. Under conditions of high carbohydrate consumption or high intake of immature succulent forage, the resultant intestinal conditions allow for C perfringens to multiply rapidly and produce toxins that increase intestinal permeability and hemorrhage.

Diarrhea, depression, lack of coordination, digestive upset, coma, and death may occur after excessive carbohydrate feeding in both kids and mature goats due to enterotoxemia. Enterotoxemia may be a secondary disease after a bout of ruminal acidosis.

The best method for preventing enterotoxemia in stable-fed goats is frequent, small-volume feeding of milk, grain, and forage to control the rate of fermentation and alteration of the intestinal environment. Large meals of milk or concentrates fed every 12 or 24 hours should be avoided. In at-risk goat populations, such as growing kids and lactating does that are fed high-concentrate diets, feeding good-quality forages (instead of cereal grains) as an energy or protein supplement helps decrease fermentable carbohydrate intake. If cereal grains are fed, less processing to decrease particle size is appropriate, as goats are good at masticating.

A proper vaccination programs for both dams and kids, using a C perfringens type C and D toxoid, is also valuable in preventing enterotoxemia. For kids to be protected, they must be fed their dam’s colostrum. If the farm's colostrum management program is focused on caprine arthritis and encephalitis control, alternative colostrum sources may be used, and kids must be vaccinated.

Polioencephalomalacia (polio, PEM) is a neurological disease characterized by cortical necrosis of the brain. Clinical signs of PEM in goats 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.

PEM in goats is primarily caused by a deficiency in thiamine (vitamin B₁). PEM also may occur in goats ingesting diets high in sulfur. Diets that produce a low ruminal pH or that are high in grains and low in forages, or that include some contaminants (eg, sulfate or sulfide), may predispose goats to PEM. Such dietary conditions can result in depressed production of thiamine, the production of thiamine antimetabolites, or the production of thiaminases in the rumen.

Differential diagnoses for PEM include lead toxicosis and sulfur toxicosis. Sulfur intoxication occurs when large amounts of sulfates are consumed through feed or water and are then reduced by rumen microbes to sulfides, generating hydrogen sulfide gas.

If the underlying etiology of PEM is thiamine deficiency, affected goats can be treated with thiamine (10 mg/kg, IV bolus, followed by 10 mg/kg, IV, IM, or SC, every 6 hours until resolution of clinical signs). Although response to treatment is dramatic and almost immediate, if substantial brain damage has occurred, goats rarely return to a satisfactory level of production. Prompt treatment of PEM is critical. The diet should be modified to decrease grain and increase forage intake and, when needed, to lower excessive sulfate or sulfide intake. During times of stress, or when predisposing diets are unavoidable, the inclusion of thiamine mononitrate in the diet may aid in prevention. 

Pregnancy toxemia in goats, also called twin kid disease or pregnancy ketosis, is a metabolic disease of late gestation resulting from the doe’s inability to maintain glucose homeostasis. The condition is much more common in does that are carrying multiple fetuses, are excessively thin or fat, live in stressful conditions, and/or have other concurrent diseases.

During late gestation, developing fetuses have high glucose demands. If the doe's glucose intake decreases as a result of environmental or dietary factors, the doe becomes unable to maintain energy balance; this imbalance leads to mobilization of adipose tissue for metabolization into ketone bodies in the liver. Does in heavy body condition may mobilize excessive amounts of fat, overwhelming the liver and leading to secondary hepatic lipidosis (ie, fatty liver disease). Thin does lack body fat reserves but can also experience “starvation” ketosis if they consume poor-quality or inadequate diets to meet their nutritional requirements during pregnancy.

Goats with pregnancy toxemia have abnormally high blood concentrations of ketone bodies and concurrent hypoglycemia. Hypocalcemia is also often associated with pregnancy toxemia, because the doe eats less when experiencing either symptom, leading to negative energy balance. As such, no matter which of these conditions occurs first, the doe is then predisposed to develop the other.

Initial clinical signs of pregnancy toxemia in goats are behavioral in nature. The affected doe may separate from the herd, avoid the feed bunk, and become less active (stage 1). Without intervention, clinical signs progress to include depression, dullness, inappetence, ataxia, and difficulty standing (stage 2). In the final stage of toxemia, clinical signs include recumbency, inability to rise, opisthotonos, and eventually death (stage 3). Fetuses are usually dead in this final stage.  

Intervention for pregnancy toxemia starts with early recognition of behavioral changes. If the condition is recognized in stage 1, the doe can be separated from the herd and fed additional concentrates. Separating the doe also minimizes feeding competition at the bunk.

By stage 2, more aggressive intervention is needed. In addition to dietary alterations, administration of propylene glycol or glycerol (60–90 mL/animal, PO, every 6 hours until resolution of hypoglycemia) can facilitate hepatic glucose production and increase insulin secretion to impede fat mobilization. Dextrose 5% solution is often administered (50–120 mL/animal, IV, as needed to resolve hypoglycemia); however, the response is short-lived. Hypocalcemia can also be addressed by administering calcium borogluconate 23% injection (0.5–1 ml/kg, IV slowly or SC, as needed to resolve hypocalcemia).

Does in stage 3 pregnancy toxemia must be intensively managed. In addition to monitoring glucose status, medical management of acid-base status is required, because goats are prone to ketoacidosis. Fetal removal via surgery or abortifacients should be considered. The prognosis is extremely guarded in stage 3, as most often both doe and fetuses succumb.

Preventive measures include maintaining the doe's proper body condition score, identifying does carrying twins and triplets and feeding them accordingly, lowering the incidence of chronic disease, and not shearing long-fibered does in late gestation. (Shearing can induce a stressor that can precipitate pregnancy toxemia in late gestation.) Forage quality—namely, the plant fiber component (neutral detergent fiber, or NDF)—should be evaluated as a doe's intake capacity decreases. Ensuring sufficient dietary sugar and starch to promote rumen propionate production, without inducing acidosis, is essential. For does in heavy body condition, adding dietary niacin (1 g per day during late gestation) to lower the incidence of ketogenesis is an option. Ensuring adequate winter feedstuffs, while monitoring changes in body condition throughout gestation, helps lower the incidence of pregnancy toxemia.

Hypocalcemia—also called milk fever, gestational hypocalcemia, or parturient paresis—is common in pregnant goats. Clinically affected does present during late gestation. The disruption in calcium homeostasis results from blood calcium loss to fetal bone development and inadequate intake of dietary calcium. High dietary potassium can result in high dietary cation-anion difference, high dietary phosphorus, and low dietary magnesium, all of which have been implicated in hypocalcemia pathogenesis in dairy cows; however, their impact on hypocalcemia in small ruminants is unknown.

Clinical signs of hypocalcemia in goats include depression, decreased appetite, mobility impairment ranging from ataxia to recumbency, and lack of urination or defecation. Pupillary light response is slow to absent, depending on hypocalcemia severity.

Presumptive diagnosis is based on history and physical examination. Diagnosis is confirmed by blood tests indicating low total calcium or ionized calcium concentrations.

Treatment for hypocalcemia is IV administration of 23% calcium borogluconate solution (20 mg Ca/kg) slowly to effect, while listening for cardiac arrhythmias. Additional calcium solution (without dextrose) can be administered subcutaneously for relapses, which are common.

Hypocalcemia is prevented by monitoring calcium content of the late-gestation diet. Dietary calcium should be increased to supply the doe with sufficient calcium. Feeding of legume forage can be useful, as can adding calcium carbonate (limestone) to a concentrate mix. 

Goats can develop ruminal acidosis (grain overload) when they eat large amounts of rapidly fermentable carbohydrates (ie, sugars and starch), resulting in a quick decline in ruminal pH. As ruminal pH drops, the salivary buffering actions and volatile fatty acid absorption capacity become overwhelmed. The bacterium Streptococcus bovis is a primary organism that accounts for lactic acid production under lower ruminal pH conditions. Bacteria that consume lactic acid, a relatively strong volatile fatty acid, are sensitive to low pH conditions and under such conditions are no longer capable of converting lactate to propionate. The ruminal environment continues to spiral down in pH, ultimately allowing Lactobacillus spp to produce d-lactate and L-lactate, further lowering the pH. Depending on the amount of fermentable carbohydrates consumed and the severity of ruminal pH decline, ruminal acidosis can present as a peracute, acute, or subclinical disease process.

In peracute acidosis, ruminal pH declines rapidly to < 4; in acute acidosis, to < 5. Affected goats may be found dead or may be recumbent and possibly bloated, depressed, and dehydrated. The latter is a typical presentation in feedlot kids inappropriately acclimated to a high-concentrate diet. Acute acidosis and a ruminal pH of < 4.8 indicates lactic acidosis, which can lead to secondary complication of enterotoxemia.

Lactating dams are also at risk for ruminal acidosis, because they are fed high-concentrate diets to support milk production. Many lactating dams are fed concentrates only in the milking parlor twice a day and may experience periods of subclinical acidosis or subacute ruminal acidosis, as occurs in dairy cows.

Diagnoses of peracute and acute acidosis are based on history, presentation, and documentation of low ruminal pH. Rumen microbes continue to ferment available carbohydrates, continuing to lower ruminal pH after the animal’s death; therefore, diagnostic ruminal pH testing must be done before death.

Subclinical acidosis is more challenging to diagnose. Affected goats may or may not have diarrhea; however, fecal status may vary within a herd. Sampling rumen fluid via orogastric tube or rumenocentesis can provide some quantitative assessment of pH, within reason. Alterations in milk composition (ie, decreased milk fat production) can also suggest potential subclinical acidosis.

Treatment of acute acidosis is often unsuccessful; therefore, the focus should be on confirming the diagnosis and aggressively treating the rest of the herd. Fluid therapy to address metabolic acidosis and dehydration is necessary. Intervention may not be necessary for subclinical acidosis; however, diet or feeding management should be modified to prevent ongoing bouts.

Preventive dietary modification should assess effective fiber, carbohydrate load and form, and feeding practices. Goats are good at sorting through total mixed diets. Cereal grains should not be highly processed. Wheat intake should be limited, as 90 g/kg will produce lactic acidosis in 12 hours. If possible, concentrate meals should be divided into three meals per day. Substituting fermentable fiber sources, such as beet pulp, wheat middlings, or soybean hulls, for some starch decreases the potential acid load.

Urolithiasis in goats occurs when urinary calculi, or uroliths, form in the urinary bladder and subsequently cause a blockage. Calculi form when minerals crystallize from supersaturated urine in the urinary bladder. (Renal calculi can also develop but are uncommon.) As with urolithiasis in other species, the mineral type is variable, but in goats and other ruminants there is a predisposition for struvite (ammonium-magnesium-phosphate) crystals. Struvite crystals often develop in goats that consume high-concentrate diets and result from excessive phosphorus intake relative to calcium intake. Some breeds seem to have a greater risk for calcium carbonate or calcium oxalate crystal formation. Silicate crystals are also possible and are often associated with consumption of western US forages that are naturally high in silica.

Besides dietary mineral content, other risk factors for urolithiasis include urinary tract infections, low vitamin A status, inadequate water intake, and extremes in urine pH (low or high). Some crystals (eg, struvite) only form in alkaline urine and can be dissolved in acidic urine. Other crystals may form in acidic urine or in either acidic or alkaline urine. Goats excrete an alkaline urine because of the high potassium content of forages.  

Uroliths can form in either males or females; however, urolithiasis is more common in males, because their extended urethras are more prone to blockage. Blockage often occurs in the sigmoid flexure at the glans penis–vermiform appendage junction.

Clinical signs of urolithiasis include difficult and painful urination, as evidenced by straining to urinate, slow urination, stomping of the feet, and kicking at the area of the penis. In some cases, (struvite) crystals may be observed on preputial hairs. Blockage of urine flow can occur in both intact and castrated males. It can cause the urinary bladder to rupture, resulting in a condition known as water belly, and will lead to death.

Struvite urolithiasis is common in animals fed diets high in cereal grains (eg, pet goats). Affected goats excrete alkaline urine with a high phosphorus content. The incidence of urinary struvite calculi can be decreased by lowering phosphorus consumption to minimal levels and maintaining a dietary calcium:phosphorus ratio of > 2:1 (with the phosphorus content being < 0.45% of the diet).

Excessive calcium intake can lead to calcium carbonate stones; however, not all predisposing factors are well defined. Calcium oxalate stones occur when goats are fed diets high in calcium and soluble oxalates, such as diets containing a lot of alfalfa, as some alfalfa varieties can have high oxalate content.

Treatment of urolithiasis is determined by disease severity and duration of blockage. Prolonged blockage results in severe inflammation and swelling of surrounding tissue, making it difficult to pass a catheter to unblock the urethra. Various methods of infusing acidifying agents into the bladder to solubilize struvite or similar acid-sensitive stones have been described. Surgical procedures to redirect and shorten the male urethra have been used.

Urolithiasis prevention is focused on decreasing mineral concentration in urine to prevent supersaturation. Common practices include ensuring adequate dietary vitamin A, increasing salt intake, decreasing dietary mineral sources, minimizing use of pelleted diets, and ensuring free access to fresh, clean, palatable drinking water.

To prevent struvite crystal formation, the dietary cation-anion difference (DCAD) equation can be applied to achieve a desired urine pH. (DCAD equation: (Na + K) – (Cl + 0.6 S); all values on mEq basis.) The most common anionic salt used for this purpose in goats is ammonium chloride; however, this compound is unpalatable, and proper formulation of the rest of the diet relative to DCAD is generally not practiced, so results are often poor. A goal is to obtain a urine pH < 7 to minimize struvite crystal formation. Often, the recommendation for ammonium chloride is 0.5% of complete diet or 1–3% of concentrate; however, this may not be sufficient, depending on cation load in the diet. An alternative recommendation is ammonium chloride, 200–450 mg/kg, PO or in feed, every 24 hours until desired urinary acidification is achieved. Feeding goats more palatable anionic salt products, as is done for dairy cattle, should be considered.

Nutritional myodegeneration, also called white muscle disease or nutritional muscular dystrophy, is a pathological process of Zenker necrosis (Zenker degeneration) affecting skeletal and cardiac muscle. It is due to nutritional deficiencies of selenium and vitamin E. Selenium and vitamin E work in concert as antioxidants to protect cell cytosol and plasma membrane, respectively, from oxidative damage. More commonly, younger animals are affected; however, older animals are occasionally affected.

Clinical signs of nutritional myodegeneration in goats include stiffness (especially in the hindquarters), tucked-up rear flanks, arched backs, pneumonia, and acute death. On necropsy, white striations are found in affected cardiac and skeletal muscles. Skeletal muscles are bilaterally affected. White striations are a result of calcification of muscle necrosis. Antemortem diagnosis can be suggested based on clinical signs, elevated muscle enzyme activities (ie, AST, CK, and LDH), and low selenium and vitamin E concentrations in the blood.

Treatment is generally ineffective, as the fibrous necrosis lesions cannot be reversed.

Prevention efforts are aimed at providing sufficient dietary selenium supplementation.

Goats can experience both copper deficiency and copper toxicosis.

Goats have relatively high copper requirements compared to other species. Moreover, as ruminants, they are susceptible to a variety of mineral interactions in the body that decrease dietary copper bioavailability. For example, sulfates found in drinking water or feed can inhibit copper bioavailability, either alone or in combination with molybdenum as they form various thiomolybdate compounds. In addition, iron from water or diet can decrease intestinal copper uptake.

To ensure adequate copper bioavailability from diet, feeds should be tested for iron, sulfates, and especially molybdenum. A dietary copper:molybdenum ratio in the range of 6:1 to 10:1 is recommended. If dietary molybdenum content is high, additional copper should be added to the diet. Commercial sheep feeds containing sodium molybdate (to help decrease copper bioavailability and minimize copper toxicosis risk in sheep) should not be fed to goats, as these products can lead to copper deficiency in goats.

Copper toxicosis can be an unwanted outcome of treatment for parasites. Internal parasites, especially the abomasal worm Haemonchus contortus, are a major disease concern in goats. H contortus has become resistant to many anthelmintics, requiring alternatives in parasite control programs. This nematode parasite is sensitive to copper ions, and administration of copper oxide wire particle (COWP) boluses can help decrease the H contortus burden in goats. COWP boluses have a 6-month or longer ability to supply copper ions that can be absorbed in the small intestine and contribute to dietary copper. However, repeated bolus administration to control abomasal parasites increases the risk of copper toxicosis. Goats accumulate excess copper in the liver until it reaches a saturation point, at which point copper ions are released, inducing localized cellular necrosis of the liver.

Clinical signs of copper deficiency in goats vary, depending on the biological function of copper being compromised. Microcytic hypochromic anemia occurs when the body is unable to mobilize stored iron for incorporation into developing RBCs, a process normally facilitated by the copper-containing protein ceruloplasmin. Other clinical signs include achromotrichia (bleaching of hair color) and bony or cardiac lesions. Subclinical copper deficiency may present as impaired reproduction, increased perinatal kid losses, and greater disease susceptibility or severity as a result of decreased immune function.

Clinical signs of copper toxicosis are less obvious. Decreased feed intake and depression, as in pregnancy toxemia, are first observed. Serum concentrations of hepatic enzymes may be elevated. Unlike sheep, goats typically do not present with a hemolytic crisis and icterus but may show some signs of hemoglobinuria.

Diagnosis of copper-related disease is best accomplished through postmortem determination of copper concentration in the liver or by antemortem liver biopsy. In the case of copper toxicosis, determination of copper concentration in the kidneys is more diagnostic; concentrations > 10 mcg/g (wet-weight basis) indicate potential toxicosis. Serum copper concentration in an individual goat is not highly diagnostic, unless the concentration is extremely low (< 0.3 mcg/mL) or high (> 2 mcg/mL). If multiple serum samples are taken from a herd (10–12 samples suggested), results can provide some assessment of copper status.

Treatment for copper toxicosis is generally ineffective once clinical signs appear. Once a diagnosis is confirmed in an individual goat, dietary modifications can be made to lower the risk to others in the herd. For goats with confirmed toxicosis, all sources of dietary copper should be decreased to the lowest level possible, and calcium sulfate should be added to the diet to help tie up dietary copper, placing the goat in a state of copper deficiency. It takes a few months to correct the overage of hepatic copper.

Goiter is a pathological enlargement of the paired thyroid glands; both iodine deficiency and iodine toxicosis can cause goiter. Most often in goats, the underlying issue is iodine deficiency, either primary or secondary (ie, induced).

Sodium iodide or potassium iodide are readily leached from mineral mixes used to supplement goat diets when these mixes are exposed to moisture. As a result, goats may receive inadequate iodine. Iodine content of goat forage varies geographically, and forages in the Great Lakes region and northern US are generally low in iodine. Forage iodine content determination is not readily available. Thus, organic iodine is provided in goat diets at 0.5 mg/kg dry matter to meet requirements.

Induced iodine deficiency occurs when dietary goitrogens act to either decrease iodine uptake by the thyroid gland or prevent iodine from being incorporated into thyroid hormones. 

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