WAY BACK in the dark ages,
when I first got out of veterinary school, I came across things
I had never heard of. Maybe my classmates and I had been taught
them in school and I just had not been listening, but I think we
simply were not told about many of them. One of our teachers had
explained that our diploma was a license to learn, and I learned
something nearly every day.
One of the conditions I am
sure we were not told about was Theiler’s disease, also known as
serum hepatitis.
I had been out of school
only a few months when I was called to look at a backyard pony
that I was told was acting crazy. When I arrived at the farm, I
was told the little guy was normally quiet and gentle. What I
saw was a four-legged hellion. He was running in an uncontrolled
manner, bellowing, and bouncing off trees. I did not know what
his owner wanted me to do because the pony could not be caught
or even approached. I was told that he had been acting this way
for several days.
But then the pony made
things easy, if not desirable: He dropped dead. The postmortem
report said "Serum hepatitis (Theiler’s disease)." This was new
to me--as had been a lot of things since graduation. I went to
my textbooks and looked it up.
Serum hepatitis
Serum hepatitis, or
Theiler’s disease, is a subacute hepatic necrosis (liver death)
resulting in liver failure and acute encephalopathy (brain
damage) in horses. Usually, the affected horse has received an
injection of tetanus antitoxin one to three months prior to the
onset of clinical signs. (I subsequently learned that the pony I
was called to treat had received tetanus antitoxin several weeks
after cutting a fetlock.)
Occasionally, cases of
serum hepatitis have been reported in horses that had never
received tetanus antitoxin but had been in contact with horses
that had received it. I am at a total loss to explain why that
happens.
Clinical signs
The usual signs are central
nervous system problems, jaundice, and discolored (reddish brown
to brown) urine. Central nervous system problems might be
manifested either as in the case of the unfortunate pony or as
depression. Ataxia (stumbling or unsteady gait) is common and
blindness might occur. The affected horse’s eyes are dilated.
Diagnosis
Diagnosis is made on
history--tetanus antitoxin administered within the previous 12
to 14 weeks--clinical signs, and laboratory test results
indicating liver damage or failure.
Laboratory tests that
detect liver problems measure serum or plasma levels of certain
enzymes. Gamma- glutamyl transaminopeptidase (GGT) is always
elevated in cases of serum hepatitis. Aspartate amino
transferase (AST) also is elevated but decreases in a few days
if the horse is to recover, so it should be measured two or
three times over a period of five to seven days. Sorbitol
dehydrogenase (SDH) initially is increased but decreases rapidly
in improving horses.
Total bilirubin is elevated
and this is the cause of the discolored urine. Prothrombin time
(PT) is very high. (My spellchecker is panting.)
A definitive diagnosis may
be made by liver biopsy, but with the history, clinical signs,
and laboratory results, a biopsy is not necessary. (If it looks
like a duck, walks like a duck, and quacks like a duck, you do
not need to toss it in the water to see if it swims.)
Treatment
Supportive therapy is the
main thing to do:
Prognosis
The prognosis is always
guarded, but affected horses that continue to eat usually
survive. Decrease in levels of prothrombin time and SDH,
accompanied by an improving appetite, are good indicators of a
horse that will pull through. One that is exhibiting severe
central nervous system problems that cannot be controlled by
sedation has a poor prognosis.
Recovery will occur in one
to two weeks in most horses that show signs of pulling through,
and there are rarely any residual problems.
Prevention
To prevent the possibility
of serum hepatitis in your horses, maintain a proper tetanus
vaccination program consisting of an initial series of two
tetanus toxoid injections one month apart, followed by annual
boosters.
If a broken skin lesion
occurs more than three months after a booster is given, boost
again with tetanus toxoid. Use tetanus antitoxin only if a horse
contracts tetanus or if the tetanus toxoid vaccination history
is not known in a horse that has a lesion.
Other cases
Fortunately, no one sees
many cases of serum hepatitis. After the case involving the
pony--when I did not know what serum hepatitis was and could not
have done anything about it even if I had known--I saw only two
more cases.
The next case I saw was not
long after the first one and it, too, involved a pony. This
filly was depressed and did nothing but stand in one spot. She
had received tetanus antitoxin one month before, after
graveling. Her gums and sclera were bright yellow (jaundiced),
indicative of liver problems.
With much pushing and
pulling, we managed to get her into a stall. She drank and ate a
little when water and feed were offered. All of her liver
enzymes were elevated but, with the treatment described above,
she was nearly normal within ten days and went on to fully
recover.
The other case--the last I
have seen to date--was a long time later and perhaps ten or 12
years ago. Another veterinarian had sutured a racemare after a
wound and gave her tetanus antitoxin at that time. The mare
became depressed about two months later, when the veterinarian
was out of town, so I was called to examine her.
Fortunately, her trainer
kept excellent records, and he had recorded "TAT" in her file to
indicate she had received tetanus antitoxin. She, too, was
jaundiced and her liver enzymes were high, as was her
prothrombin time. Both AST and prothrombin time counts were slow
to decrease, but both started to go down in about a week.
Supportive therapy sustained the mare, although she did not eat
well for several more weeks. She eventually came around, but her
racing days were over. She was sent to the farm to become a
broodmare.
Brent Kelley, D.V.M., is a practicing veterinarian living in
Paris, Kentucky.
