COPPER DEFICIENCY IN A HERD OF ANGORA GOATS
A 3-month old female Angora goat kid was admitted to PurdueUniversity
Large Animal
Hospital because
she was unable to stand on her rear legs. This kid came
from a farm of approximately 25 does and two other kids
at the farm were showing similar clinical signs. Upon presentation,
the kid was bright and alert but emaciated and infested
with lice. Feces were matted to the fleece on her rear
legs but diarrhea was not clinically evident. The kid made
several unsuccessful attempts to stand. She did not appear
to be in pain and held herself in sternalrecumbency with
her rear legs on either side of her body rather than with
both legs folded to one side. Questioning of the owners
revealed that there had been no additions to the herd, no
goats showed any signs of swollen joints or arthritis and
that there had been four kids born weak or dead, an unusually
high number of perinatal deaths for that herd. The does
had access to pasture and were fed a grain/protein supplement
mix and trace mineral salt formulated for sheep. Despite
the lack of clinical signs of Caprine Arthritis-Encephalitis,
or CAE, this was the primary differential diagnosis. Other
differentials were spinal abscesses, trauma and copper
deficiency.
Blood samples were taken for serology for CAE and blood
copper levels. By the third day in the clinic, after
consuming high quality hay and a commercial goat ration
(containing copper sulfate), the kid was able to stand
without assistance and remain standing when downward pressure
was applied to her hindquarters. Serology for CAE was
negative. Blood copper levels were 0.20 ppm. (Deficient
is 0.04-0.40 ppm.) The cause of ataxia in this particular
kid was presumed to be copper deficiency because of deficient
blood copper levels and rapid response to adequate copper
in the diet. To hasten her recovery, we decided to supplement
the copper already in the diet. No approved source of
copper could be obtained from the pharmacy, so the goat
was treated orally with copper sulfate crystals dissolved
in water at a dose of 80 mg. copper per day for 7 days.
By the end of the treatment period, the kid's blood copper
level was 1.06 ppm. (Normal
is>0.80 ppm.) The kid was also treated with VI-Sorbin(R)
for a mild anemia and procaine penicillin for pneumonia,
most likely due to her debilitated condition. The kid
improved steadily throughout her hospital stay.
Copper deficiency in this kid was thought to be a herd
problem because of two similarly affected kids at the
farm. Blood samples were taken from the two affected
kids and a representative sample of unaffected kids and
does. Of the ten animals tested, one doe had blood copper
levels in the low marginal range (0.40-0.80ppm.) while
the remaining nine animals were in the deficient range.
The water was analyzed and no sulfates were found. Both
the grass and grain samples had copper:molybdenum rations
in the copper deficiency-causing, or toxic range, thus
making this a case of secondary copper deficiency.
The two affected kids were treated with copper sulfate
solution orally, 80 mg. copper per day for 7 days. We
also recommended that the rest of the herd be supplemented
with copper by feeding a calf protein supplement for
6 weeks and that they use a free choice salt mix containing
0.2-0.25% copper sulfate. Other methods of supplementing
copper in the diet are: Fertilize pasture with copper
sulfate (only works in acidic soils) or giving a parenteral
injection of copper glycinate or copper EDTA.
We visited the herd about three months later to check
the progress of the kids. No weakness or ataxia could
be detected in any of the kids, even when they were driven
around the pasture. The horns of the kids, which had
previously been flattened, dry and flaky, showed a more
normal appearance with the new growth. Since the goats
were white, no pigmentation changes were seen, nor were
any hair changes.
REFERENCES AVAILABLE UPON REQUEST
Darcy dark-Class of 1994 Edited by W.G.VanAlstine