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This addresses "dry" gangrene, gangrene resulting from
bacterial infection in the udder, not to be confused with
gas ("wet") gangrene, that can result from wound contamination
with soil containing spores (alpha toxin) of Clostridiums.
While any of the clostridiums are capable of producing gas gangrene
the most common (though uncommon in goats) is Malignant Edema
caused by Clostridium septicum. Other clostridials that
cause specific diseases include Clostridium tetani (tetanus),
C&D perfringens. etc.
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Here
in the southern most areas of Southern California and
parts of Arizona had problems with gangrene mastitis
as a direct result of severe copper deficiency in our
goats. Their copper deficient state resulted in acutely
compromised immune systems and poor production of anti-alpha
toxins that allowed udders infected with alpha toxin
producing bacteria to quickly lead to a gangrenous condition
of the udder tissues.
Gangrene
mastitis is not a particular "kind" of mastitis, but most
often the result of the most common mastitis' causing
bacteria, coagulase-positive Staphylococcus aureus. Staph
aureus can produce alpha toxin, a potent vasoconstrictor
that is thought to be involved in the pathogenesis of
gangrene mastitis. Other common pathogens are sometimes
involved, including coagulase-negative Staphylococci,
and any number of Gram-positive, Gram-negative, and coliforms
bugs. |
In
these immune deficient does the infection and progression to
gangrene happened far too quickly (in just hours) to do anything
about. Before we were even aware there was a problem the does
were acutely ill and the irreversible conditions that would
result in gangrene were already in progress. When toxin (spore)
producing bacteria are involved, killing the bacteria isn't
the end of the problem. Not only do the toxins remain, but the
dying bacteria release even more.
Photo
#2-
In this first freshening two year old the condition
developed in just hours while the doe was in labor.
Despite the owners early intervention the affected udder
half was lost.
A
yearling Alpine (photos #4
& 5 bottom of page)
was affected two weeks before freshening.
Photo #6 is a dry yearling.
My
own doe (photo #1),
was just off feed with no temp, a normal physical examination
and a negative CMT the a.m. before, she was the same
in the p.m. Despite the lack of positive findings I
started her on systemic oxytetracycline that evening
.... I found her down and near death very early the
next morning. She was under our vet's care, on IV's
and appropriate medications within an hour of our finding
her. Despite our best efforts the udder quickly turned
blue, then black, and she was milking blood (photo
#3) by the next morning.
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#2
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#1
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There
were something like 15-18 cases in one 18 month period,
in just our local circle. Different animals were treated
with different medications and protocols, it made
no difference, the affected udder tissue always sloughed
off. Fortunately, we didn't lose any of the animals,
but most of these does were does on our show strings,
integral parts of age and group classes, now reduced
to brood does.
(see note CH Eder's Jenalee)
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AN INTERESTING
NOTE: Linda Colquitt's (Eder's Toggs & Alpines) beautiful
CH Eder's
Jenalee had gangrene mastitis in 2002. The teat and most of the
affected side of the udder sloughed off (without chemical or surgical intervention).
Jenalee freshened with and raised triplets in 2003 and twins in 2004. She
had already earned her CH before the gangrene mastitis and in 2004 at the
age of 8 with only half an udder linear appraised 91 EEEE. |
