Small Animal
EDITORIAL
Advances in
Gastroenterology
M.D. Willard, DVM, MS
Texas A&M University
G
astrointestinal (GI) dis-
eases are among the
most common prob-
lems seen by veterinarians in
primary as well as referral prac-
tices, and these diseases can be
a major source of frustration.
The reasons for this stem in
part from the extreme difficulty
involved in trying to diagnose
the cause of vague signs that
wax and wane unpredictably. In
addition, these diseases some-
times do not respond as the
textbook or lecturer says they
should. Although the advent of
less invasive modes of eval-
uating the digestive tract (i.e.,
gastroduodenoscopy, colono-
ileoscopy, laparoscopy, ultra-
sonography) have helped allevi-
ate some of the frustrations
associated with GI diseases,
these techniques have, in my
opinion, caused a few new frus-
trations. Specifically, we are
now faced with the problem of
determining the clinical sig-
nificance of the results we pro-
duce.
Nowhere is this tension
more evident than with intesti-
nal biopsies, especially those
obtained endoscopically. I grant
that this is a personal soapbox;
I might be overstating what is
Small Animal Gastroenterology
actually a minor or infrequent
problem, but I don’t think so. I
am sympathetic to the numer-
ous groans that echo in the lec-
ture hall when I ask a group of
veterinarians, “What do you do
when the biopsy report states
that the dog or cat has mild to
severe, subacute to chronic,
lymphocytic-plasmacytic-
eosinophilic gastroenterocoli-
tis?” Why the groaning? First,
some veterinarians have told
me that it is difficult to submit a
sample of intestinal tissue to
the lab they use and not have it
read out as having lymphocyt-
ic-plasmacytic inflammation of
some type or another. Second,
the diagnosis does not neces-
sarily correlate with the re-
sponse to therapy.
There are probably several
reasons for these observations.
Stated bluntly, some (many?
few?) endoscopic intestinal
biopsy samples that are turned
in to veterinary diagnostic labo-
ratories are grossly inadequate.
There is sometimes too little
tissue present to make a mean-
ingful assessment. In some
cases the pathologist is expect-
ed to make a diagnosis after
viewing a bunch of villus tips.
Furthermore, the tissue is
sometimes riddled with arti-
facts. We as veterinary clini-
cians must realize that patholo-
gists are a bit like computers
(i.e., the old “trash in causes
The Compendium March 1997
trash out” syndrome), and
there is much more to provid-
ing them with adequate intesti-
nal tissue samples than ripping
some mucosa out of the patient
and scraping it into a vial of for-
malin. However, after the sam-
ples have been submitted, there
can at times be a puzzling lack
of agreement or consistency
among pathologists about what
constitutes a diagnosis of lym-
phocytic-plasmacytic enteritis
or colitis and how mild or se-
vere it is. Granted, sometimes
the diagnosis can be obscure
even to the most experienced,
accomplished pathologists sup-
plied with several generous, ar-
tifact-free tissue samples (e.g.,
distinguishing very well-differ-
entiated lymphoma from severe
lymphocytic enteritis). Howev-
er, some of the differences of
opinion I have encountered do
not involve such subtle ques-
tions but are more in the realm
of deciding whether the tissue
has moderately severe inflam-
matory disease or is normal.
This concern might not be
limited to clinical laborato-
ries. Examine the published
reports about these mal-
adies, and you may be left
wondering if a slide diag-
nosed as “moderate lympho-
cytic colitis” by one group
would be diagnosed similar-
ly by another group. I fre-
quently ask for recuts of the
histopathology slides of previ-
ously submitted specimens
when difficult cases are referred
to me or for cases for which I
am a consultant. The difference
between what two patholo-
gists (or sometimes groups of
pathologists) read out after
viewing the same slide is oc-
casionally unsettling. Is it any
wonder that a patient being
treated for “inflammatory bowel
disease” (which by definition is
an idiopathic disorder with po-
tentially numerous causes) may
not respond for various rea-
sons, including an incorrect di-
agnosis?
Some clinicians have been
left wondering how useful it is
to have these diagnoses. What
does this problem (or what I
see as a problem) mean for vet-
erinary gastroenterology? I sug-
gest that either we become
more accomplished in our tak-
ing, processing, and evaluating
of intestinal biopsy samples or
there will be a loss of credibility
that will be hard to regain.
The Compendium March 1997
Gastric Helicobacter infec-
tions are another area in which
I believe there is confusion.
Helicobacter pylori is the major
cause of ulcers and sponta-
neous gastritis in humans. It
took decades to recognize the
association of this bacterium
with gastritis and ulcers because
investigators knew that normal
people harbor the bacterium.
After the clinical importance
of human gastric helicobacte-
riosis was finally established,
attention quickly turned to ca-
nine and feline Helicobacter in-
fections. As with humans, there
are reports noting that clinically
normal dogs and cats can har-
bor Helicobacter species in
their stomachs, in some cases
with a concurrent histologic
gastritis. Discussions with col-
leagues invariably involve ex-
amples of vomiting animals
that did not respond to “any-
thing” until the Helicobacter in-
fection was resolved with ap-
propriate therapy. I also have
my share of such patients that
vomit relentlessly until treated
with some combination of
drugs that we expect will elimi-
nate Helicobacter species, and I
too have attributed clinical
response to elimination of the
bacteria. However, the drugs
that are used for helicobacterio-
sis may also have beneficial ef-
fects in treating other diseases.
When a patient “responds”
to some combination of
metronidazole, antibiotic,
antacid, bismuth, and/or su-
cralfate, how do we know
which, if any, of these drugs
the animal actually responded
to? For that matter, do we
know whether the Helicobacter
species commonly found in
dogs and cats need the same
drug combinations that hu-
mans seem to require? To fur-
ther muddy the waters, I vividly
recall one chronically vomiting
cat that I finally “cured” after
eliminating the gastric heli-
cobacteriosis. To my chagrin, I
later found out that the owner
never got around to adminis-
tering the drugs, and the
chronic vomiting stopped just
about the time I wanted the
owner to start the therapy.
As clinicians, we always like
to believe that a good response
is attributable to our therapeutic
intervention(s). Perhaps we
need to cultivate the virtue of
skepticism. I am not suggesting
that gastric helicobacteriosis is
unimportant in dogs and cats; I
believe it probably has an im-
portant place in our under-
standing of GI disease. I am
suggesting that when we are
faced with a biopsy report not-
ing the presence of gastric
spirochetes, we need to careful-
ly consider whether this finding
explains the cause of the ani-
mal’s clinical signs or whether
it is a convenient excuse for
telling the client that we have
found the problem and need
not look any further.
More confusing still is the is-
sue of whether canine and feline
helicobacterioses are public
health hazards. There are rea-
sonable reports of transmission
of Helicobacter species from an-
imals to humans. However, my
question is not whether it is
possible for a pet to be respon-
sible for a human infection, but
rather whether cats and dogs
pose a significant (i.e., common
or frequent) risk to humans. It is
interesting to note that physi-
cians are still not in agreement,
as far as I am aware, about how
most people become infected in
the first place. This is an impor-
tant question that awaits a
definitive answer.
Feline pancreatitis presents a
different dilemma than intesti-
nal biopsies or helicobacterio-
sis. I believe that this disease
can be one of the most difficult
entities with which veterinary
gastroenterologists must deal.
The old adage that “a cat is not
a small dog” applies here. The
clinical signs of pancreatitis
(e.g., vomiting, anterior abdom-
inal pain, typical changes on
imaging) can be obvious in
some cats. In others, however,
the signs are so vague that the
clinician never realizes that pan-
creatitis should be seriously
considered. Even if you decide
that pancreatitis is an important
diagnostic differential, confirm-
Small Animal
ing this diagnosis can be diffi-
cult, requiring ultrasonography
performed by an adept opera-
tor. Some animals might re-
quire pancreatic biopsy for di-
agnosis. The value of serologic
tests (e.g., TLI) is being investi-
gated, and these may prove to
be useful alternatives. After we
figure out how to diagnose this
disease accurately, it will be in-
teresting to determine just how
common and important it is. Fi-
nally, after a diagnosis is ob-
tained, the question of how to
treat the patient remains. We
need some answers to this one,
as soon as possible.
While there are currently
many other problems in veteri-
nary gastroenterology, these
are at the top of my list of ones
that I would like to see re-
solved. I realize that new prob-
lems will appear shortly after
(or even before) these are gone,
but we can cross those bridges
later. Right now, we have a
large enough river to occupy
our immediate attention.
ABOUT THE AUTHOR
Dr. Willard is with the De-
partment of Small Animal
Medicine and Surgery, Col-
lege of Veterinary Medicine,
Texas A&M University, Col-
lege Station, Texas. He is a
Diplomate of the American
College of Veterinary Inter-
nal Medicine.