Metabolic & Nutritional
Diseases of Goats
Table of Contents
- Pregnancy Toxaemia / Ketosis
- Periparturient Hypocalcaemia (Milk Fever)
- Lactic Acidosis (Grain Overload)
- Urolithiasis (Urinary Stones)
- Posthitis (Pizzle Rot)
- White Muscle Disease
- Iodine Deficiency Abortion
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.
Pregnancy Toxaemia / Ketosis
- Predisposing Factors
- Inadequate Nutrition
- Factors Affecting Intake
- Clinical Picture
- Clinical Pathology
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
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.
Factors Affecting Intake
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
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.
Table 1. Interpretation of serum ß-hydroxybutyrate
levels in the evaluation of late gestation ewe nutritional status
|| Serum ß-hydroxybutyrate (mmol/L)
|| < 0.70
| Moderate under feeding
|| 0.80 - 1.6
| Severe under feeding
(subclinical pregnancy toxaemia)
| 1.6 - 3.0
| Pregnancy toxaemia
|| > 3.0
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
- 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
- Correction of ketoacidosis using bicarbonate or bicarbonate
- Since hypocalcaemia is often a secondary disease associated
with pregnancy toxaemia, clinical signs of hypocalcaemia should
- 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
- Systemic antibiotics.
- Nursing care. Does need to be encouraged to eat and will need
- 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
Periparturient Hypocalcaemia (Milk Fever)
- Clinical Picture
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
Lactic Acidosis (Grain Overload)
- Clinical Picture
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.
Urolithiasis (Urinary Stones)
- Clinical Signs
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 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.
Posthitis (Pizzle Rot)
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.
White Muscle Disease
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
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.
Iodine Deficiency Abortion
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.