Metabolic & Nutritional Diseases of Goats
Table of Contents
This talk discusses some of the more common disorders seen in goats due to nutritional error. The discussion is to help identify potential problems goat producers may encounter. It is important to work with your veterinarian and nutritionist to best diagnose and solve nutritional diseases.
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.
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.
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.
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.
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.
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.
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.
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:
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.
Hypocalcaemia is usually seen in high producing dairy goats one to three weeks post-kidding and is much rarer than pregnancy toxaemia. Initially the doe is ataxic, nervous and hyperactive but quickly becomes sternally recumbent. The doe stops eating and the ears are cold. The pupils are dilated and respond very slowly or not at all to a flashlight being shone directly at them. The head may be turned back to the flank. Sometimes the hind legs are splayed out behind the doe. The heart is very hard to hear or feel) and beats quickly and weakly. Death follows bloat, regurgitation of rumen contents and aspiration.
The course of disease can be as little as a few hours and occasionally may occur as "sudden death", i.e. the doe is found dead in the morning. Serum calcium levels are decreased, usually less than 1.7 mmol/L (normal 2.1 - 2.8 mmol/L). To help in diagnosing hypocalcaemia at a postmortem examination, serosanguinous blood obtained from heart clots can be centrifuged and the serum analysed for Ca++ levels. The values obtained will accurately reflect pre-mortem values as long as haemolysis and putrefaction have not yet occurred.
Again, this disease may look like other diseases and the doe must be examined by a veterinarian in order to differentiate from polioencephalomalacia, advanced grain overload, toxic mastitis, lead poisoning, listeriosis, etc.
Clinical cases of hypocalcaemia are usually treated with calcium borogluconate solution (20 mg Ca++/ml) iv and sc. Response should be dramatic. The doe usually starts to shiver and brightens up by the time treatment is finished. If she does not, it may be that the diagnosis is incorrect or is complicated by another disease. It is important that iv treatment only be given in the face of strong clinical evidence of disease. Calcium can easily cause death if given i.v. to an animal with normal calcium levels.
Long term under nutrition is required for primary hypocalcaemia to develop. Goats require calcium rich diets after kidding. Alfalfa hay can provide this. Cereal crop forages such as wheat or oat hay are very low in calcium (0.15% and 0.24% dry matter (DM) basis respectively) as opposed to alfalfa hay (1.4% DM) and should be avoided unless the ration is balanced with other calcium sources. Over-feeding of calcium in late gestation by feeding alfalfa without balancing with anionic salts has been associated with hypocalcaemia in cattle. Feeding an anionic ration in late gestation will also improve calcium absorption from the gut and from the bones. The ration in late gestation and early lactation should also have a calcium:phosphorus ratio of greater than 1.5 to 1. Prevention of pregnancy toxaemia will also help to prevent hypocalcaemia as well.
The rumen microflora can only handle gradual changes in forage:grain ratio. If the proportion, absolute amount or type of grain changes too quickly, then lactic acidosis will develop. Feeding order (i.e. grain before forage) also can cause lactic acidosis. The type of rumen bacteria change to gram positive from gram negative and lactic acid is produced. This lowers the pH of the rumen. Once below 5.5, protozoa and bacteria start to die. The acid gets absorbed into the body creating general acidosis. If the pH is low enough, the rumen gets "burned" and, if the goat survives, it often gets secondary rumen and liver infections from bacteria or fungi. Fibre (e.g. hay or silage) is important in the diet as well as it stimulates the goat to chew, thus producing alkaline saliva which serves to buffer the rumen. Diets with little fibre or chopped too finely are more at risk of lactic acidosis.
Simple indigestion may be the first indication of a feeding problem. The goat backs off her feed, usually only for one feeding. If longer than 24 hrs then something else is wrong. Chronic feeding problems will manifest as variable appetite, depressed milk fat and chronic laminitis. Acute laminitis shows up as painful feet. What is more common is the chronic form in which the toes grow abnormally fast with "rings". The quality of the horn is poor and flaky. Goats may be lame and prone to foot abscesses. Milk fat is depressed because fibre is necessary for the rumen flora to produce the correct volatile fatty acid to make milk fat (acetate). With more severe lactic acidosis, the protozoa die, the rumen becomes static and the goat becomes depressed and dehydrated. The rumen is fluid filled and "sloshy". Diarrhea smells acidic and is yellow in colour. In very severe cases, there is no diarrhea because of total gut stasis. The goat may appear "drunk" and ataxic. She will go down and will look very similar to milk fever, i.e. cold with dilated pupils. Rumen examination (pH and examination of flora) need to be done to confirm a diagnosis.
In severe cases, treatment is heroic and may involve a rumenotomy in which the rumen is surgically emptied out. Supportive therapy includes iv fluids, rumen transfaunation (rumen juice from a healthy animal), alkalinizing solutions for the rumen (only done with caution), antibiotics and nursing care.
Rations should be formulated and balanced correctly for the correct production group. Forage should be fed before grain and the daily amount divided into at least 3 separate feedings. A total mixed ration (TMR) helps keep the rumen flora happy by not overwhelming them with carbohydrate at any one time. Feed changes all need to be made gradually over several days so the flora have time to adapt. For small holders with a few goats, grain security is an important issue.
Bucks and wethers are prone to urinary tract blockage due to urinary calculi (stones). The most common type in Ontario are calcium phosphate and struvite (magnesium phosphate) from high grain diets rich in phosphorus but deficient in calcium. The calculi often have the appearance of sand. The male urethra is narrow and long. At the end of the penis is the urethra process (vermiform appendage). Sand may become blocked anywhere but most frequently is at the urethral process, sigmoid flexure (about the level of the testicles) and ischial arch as the urethra travels out of the pelvis.
The blocked goat will be uncomfortable and will strain and act depressed. Often the presenting complaint is constipation. If observed carefully, the producer may notice frequent dribbling of small amounts of urine which may be blood tinged. If not sure if the goat is urinating, place in an unbedded, cement pen by himself for several hours. Prepucial hairs may have dried crystals on the end. If not noticed and blockage is total, the bladder ruptures in 24 to 36 hrs. After rupture, the abdomen swells with urine and the goat appears more depressed. He may live another few days before succumbing to the toxins in his system. Occasionally the urethra ruptures and the urine pools under the skin. This condition is called "water belly".
In bucks, the penis can be exposed and the urethral process examined. Sand or stones, discolouration and swelling may be evident. A normal appearing process may mean the blockage is higher. In wethers, often the prepuce is adherent to the penis and it is difficult to expose the end. Veterinarians may "tap" the abdomen to detect urine in cases of suspected bladder rupture. Catheterization of the urethra is difficult and should only be attempted by a vet. It isn't possible to catheterize into the bladder as there is a diverticulum at the pelvis that the catheter cannot get past.
If the blockage is at the urethral process, then it can be snipped off. If urine is voided after this "surgery" then the prognosis, while not good, has some hope. Oral therapy with ammonium chloride which dissolves the remaining stones is highly recommended. If the blockage is higher, then there are two options, both with major problems. A perineal urethrostomy, in which the penis is exposed and cut in its location below the rectum and the urethra exposed, often results in failure if the blockage is higher. In addition, even if immediately successful, it is a salvage procedure as the hole heals up in a few weeks and the goat re-blocks. Therefore it is not a suitable option for breeding bucks or pets. The second option is very expensive and few practitioners will undertake the surgery. The abdomen is opened and the bladder opened. A catheter is introduced from the bladder into the urethra and the stones flushed down the penis. If successful, all stones are removed and the buck is still capable of breeding. Often the stones are firmly lodged, there is tissue damage from the stones and recovery is very prolonged. Only valuable bucks or valued pets are recommended for this option.
As usual, this is a condition better prevented than treated. The diet should have a calcium:phosphorus ratio of 1.5 to 2:1. Salt should be included at 1% of total dry matter intake. Plenty of fresh, palatable water should always be available. Diets high in potassium should be avoided. Vitamin A requirements should be met (good quality green hay and pasture will do this). For herds with previous problems, it is sometimes recommended to include ammonium chloride in the ration at ½ % of dry matter intake. This is particularly true with kids on creep grain. Other diseases such as coccidiosis, pneumonia, etc. which might cause decreased water consumption or increased needs may spark an "outbreak" of urolithiasis so these diseases should be managed as well.
This is a nutritional disease of bucks and wethers that are on high protein diets, often with high inclusion rates of alfalfa hay. The urine is high in urea and, therefore, very alkaline. The urine scalds the prepuce and allow specific bacteria (Corynebacterium renale group) to grow. The prepuce becomes ulcerated, swollen and very painful. The condition is worse in wethers that don't extend their penis to urinate. Affected breeding bucks are often reluctant to extend their penis and may not breed does because of it. Occasionally the condition is so severe that scarring of the prepucial opening mechanically prevents extension of the penis, rendering the buck infertile. Treatment consists of diet change to lower protein rations (e.g. 12 to 14%), clipping the prepucial hairs, cleaning the area and local antibiotics. Pets or valuable breeding bucks may require surgery if scarring is severe.
Southern Ontario soil is very deficient in selenium. Feeds often have less than 0.1 mg Se/kg. dry matter. Vitamin E may also be deficient in the ration but is usually not assayed for on feed analyses. Selenium and vitamin E are anti-oxidants. Deficiency causes acute muscle necrosis known as white muscle disease. Usually young fast growing kids are affected anywhere from birth to full grown. Kids are acutely painful, reluctant to move but may still eat. Sometimes it manifests itself as sudden death as the heart muscle is affected. Selenium deficiency has also been identified as a cause of illthrift in growing lambs. Cattle supplemented with selenium (when deficient) have fewer problems with toxic mastitis and retained placentas. It has also been shown that selenium supplementation helps with cell mediated immunity. Oxidized milk (cardboard off-flavour) has been associated with Vitamin E deficiency in cattle.
Injection of kids at birth with 1/4 cc of a commercial Vitamin E Selenium preparation is common practise [read the label to confirm dosage as there are different formulations out there!]. It is advisable to inject with a sterile 22 g (blue) needle under the skin (instead of into the muscle). Does can be injected two to four weeks prior to kidding as well. Kids should be re-injected at one month of age if no feed supplementation.
Feed supplementation should be done with caution. Selenium can be added to feed supplements and premixes to a maximum of 0.3 ppm. Read the feed label to discover what is in the premix currently. Veterinarians can script in higher levels but this should be done after forages and grains have been analyzed. Too high levels can result in death.
The Great Lakes basin is deficient in iodine. If goats are not supplemented with iodized salt, iodine deficiency will result. Because the needs of pregnant does are highest (0.8 ppm DM of feed), the most common manifestation of iodine deficiency is abortion or birth of stillborn, and weak kids with enlarged, goitered thyroid glands. The kids may have a reduced hair coat but the most obvious sign are the large bilateral swellings on the neck. The thyroid gland may be several times normal size. Fetuses should be sent to the Animal Health Lab for diagnosis and immediate supplementation of the pregnant does should be done. If iodized salt is already fed, the needs may have increased if the does are grazed on brassica plants (turnips, cabbage, forage rape) while pregnant.
This is a neurological disease caused by real or relative thiamine deficiency. Thiamine (vitamin B1) is made by the normal bacteria in the rumen. Kids or does on high carbohydrate diets may have an upset in normal rumen flora. A change in bacterial types may cause either a deficiency of thiamine or production of an enzyme which inhibits thiamine activity. The end result is the disease polioencephalomalacia (softening and necrosis of the grey matter of the brain). Overdosing with amprolium (in the treatment of coccidosis), exposure to high levels of sulphur in the diet, or grazing on mare's tail (equisetum) can also result in "polio" but are unusual in comparison to high CHO diets.
Early on in the course of the disease, the goat may show a stiff legged gait. The head may be held high and the animal is anxious. As the disease progresses (often within 6 hours), the goat is blind and the head may be pulled straight back towards its shoulders. The front legs are stiff and the animal may fall down. Once down the abnormal head and neck stance is more evident (opisthotonus). The pupils will constrict to light but the goat will not react to a hand menace. Other rule outs are tetanus (the animal is not blind), pulpy kidney, lead poisoning, listerosis, and other toxins e.g. organophosphates and organochlorines.
Sometimes the only way to make a diagnosis is through a response to treatment. Early polio cases often respond, at least partially if not completely to thiamine administration (by a veterinarian). Often some response occurs within a few hours of initial treatment. Most other neurological diseases respond slowly or not at all to indicated treatments (unless specific poisonings). Because thiamine deficiency does cause brain necrosis however, time is important. The longer treatment is delayed, the more likely irreversible brain damage may occur. One case may not necessarily mean a herd problem but the feeding management should be reviewed. Some problem herds do require routine thiamine supplementation but first feeding management should be investigated.
There are many more nutritional diseases e.g. copper deficiency/toxicity, zinc deficiency etc. but the previously reviewed diseases are the most likely ones for Ontario goat producers to encounter.
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