Message Number: YG8728 | New FHL Archives Search
Date: 2001-11-16 02:30:00 UTC
Subject: Re: Question: GI Dz in ferrets

--- In Ferret-Health-list@y..., toucanvet@a... wrote:
> Hi there fellow ferret listers + DVMS, and VMDs,
> I have a procedure question to pose to the vets,
> At what point do you opt for exploratory sx VS medical therapy
> with ferret GI dz?
> OK case in point:
> 5 yr. m/c ferret. has previous history as a young ferret of
multiple FB
> ingestion
> has not done that in over 2 years though.
> Owners don't always closely monitor ferret (they work)
> started with GI signs 5 days ago:
> vomiting, bruxism, diarrhea, inappatince, minimal fecal
production occ
> straining to deficate.
> +/- Weight loss T = 101.5 deg F Blood glucose = 95 PCV
= 45%
> TS = 5.5 mg/dl WBC = WNL No alopecia, 1 episode seasonal
loss 2 yrs
> ago.
> Palpation revels: small spleen, unremarkable liver, kidneys,
> prostate, intestines, Questionable unusual feel to stomach. NON
> RADS: normal chest / normal heart. Unusual charateristic to
stomach -
> R/O pyloric obstruction - Possible loss of serosal detail in cranial
> with possible free fluid ? Radiologist R/O Perferation. NO obvious
> visualization of Radiodense FB.
> OK HERES THE QUESTION: Chem panel norm. its Sat afternoon. - no E
clinics in
> area cut ferrets (illegal animals to own) - your day off.
> DO YOU come in and cut the ferret or Do YOU put it on helicobacter
> force feedings and wait the weekend.
> You elect for medical mgmnt since you could not talk any techs to
come in
> with you.
> Owner does not have money for Biaxin + Omeprazole so you
> 1. Amoxi BID
> 2. Pepto QID
> 3. Flagyl BID
> 4. Pepcid AC SID since you don't have chem yet about kidneys
> 5. Sucrulfate QID 20 min before pepcid (sucralfate binds to H ions
if you
> give h2 blocker first no H ions left to bind to - drug does not
> 6. A/d syringe feeding 60 cc BID
> and are relieved that its the owners giving it and not your hospital
> NOW its Wednesday - owners have not called - no news is GOOD NEWS
ferret is
> eating like a champ !!! and passing normal stool.
> WHAT NOW ????
> CUT or NOT and if so why ?
> I say CUT ---> here's why....
> 1. he had stomach ulcers not true FB - FB ferrets don't vomit - even
with a
> perf'd stomach.
> 2. May or may not have had secondary Helicobacter infection - I'm
not real
> sure about this
> he had not exposure to other ferrets in > 2 years and i
usually see
> this as a young guy disease
> 3. I think he has a Hairball FB causing a chronic irritation to his
> lining, setting up a gastritis and vomiting
> also acts like a partial ball valve to explain some GI signs
and diarhea.
> 4. Significant gastritis in ferrets may induce - PANCRETITIS - i
know I know
> ferrets don't get pancretitis -
> well to quote those famous CarTalk guys from Haavyard
Squaare -
> BULLL SH_____. I've seen it
> and i;ve seen pathological diagnosis of inflamed pancreases in
ferrets with
> severe gastritis.
> So maybe thats were the radiologist was getting the free fluid from.
> anyway.
> I have not done anything with this guy yet.
> I';m going to finish the helicobacter tx. 21 days and then cut him
if still
> wt loss. / thin
> Would you have cut on Friday without a chem profile - what if
vomiting was
> uremic?
> Do ferrets get elevations in Creatinine with Azotemia? Why or why
not ?
> why do old ferrets get hairball FBs and young ones don't?
> What do you use for Ulcers? / Helicobacter?
> does any one have a good source for small doses of biaxin - i can't
get the
> boss to
> splurge for $200 of drug.
> thanks for your patience and patients.
> --ben
> Benjamin A. Otten, DVM
> Practice Limited to Avian
> and Exotic Pets
> "There is a fountain that is not
> built by the hands of man"

Hi Ben,

I can probably answer all your questions, plus some you haven't
thought of... I'm not sure you'll agree with the answers, though.
I'll answer your questions in the order you asked them, and try to
organize my thoughts to fit the sequence. First question: do you come
in and cut the ferret or put it on helicobacter therapy? The answer
is, neither. The signs you describe definitely do not sound like an
emergency surgical patient... sick for 5 days and still looking
stable, pretty much rules out an intestinal foreign body, as does the
lack of gastric distension and still having stools. The combination
of vomition, bruxism, diarrhea and straining to defecate is highly
suggestive of enteric, not gastric disease (although I wouldn't be
surprised to see both... they usually go together). The most likely
cause of these signs, especially if acute in onset, is bacterial
overgrowth in the bowel and/or bacterial enteritis. Treatment with
antibiotics and supportive care usually resolves the signs, but not
the underlying pathology which led to the acute episode. Flagyl is
the best at rapidly resolving bacterial enteritis (green seedy to
watery stool) in these cases; amoxi can broaden the spectrum of
coverage a little. BAytril can be used in cases where flagyl creates
too much nausea response. Kaopectate and probiotics are also useful.
Antiemetics may be needed for oral therapy to succeed. I would not
cut this patient immediately because this patient is ill and needs
supportive care, and is not a surgical emergency. Once the patient
looks BETTER, however, I would cut him. The reason is this: you need
to identify the underlying pathology which led to the patient being
susceptible to bacterial enteritis; normal individuals don't typically
develop these signs.
What is the underlying pathology? You list some possibilities
under the section: "Cut or not and if so why?" I will comment on
those possibilities first, and then tell you what I think is really
going on with this little guy. Your first possibility you mentioned
was stomach ulcers... not the most likely scenario, as you had no
tarry stool, and you had diarrhea and straining. Foreign body is also
not likely, although foreign body cases CAN definitely vomit (I've
seen plenty) although they often do not. Helicobacter also isn't a
likely explanation, for the same reasons: your signs suggest
intestinal pathology, and all these problems listed are gastric. I
also have found Helicobacter to be heavily overdiagnosed, as it gets
the blame for a lot of gastrointestinal pathology that it simply isn't
responsible for. Biopsy is the only way to confirm that the bacteria
may be contributing to gastric pathology; studies have shown the
bacteria to be ubiquitous in the ferret population, and thus it likely
behaves as normal flora in many cases. It likely produces transient
gastritis in newly infected (ie young) animals, and then is suppressed
thereafter. Your ferret IS a likely carrier, because most ferrets
are, and he doesn't have to be exposed to a new young ferret to get
it. If he was never aggressively treated to eliminate the bacteria, he
probably is a carrier. The problem is in deciding if it truly is
causing pathology. In hundreds of gastrointestinal biopsies I have
done in the past decade, I can find no Helicobacter organisms in any
of my gastritis patients except a small focus at the pyloric area in
about 50% of the cases. The gastritis is often diffuse throughout the
stomach, and is accompanied by enteritis; Helicobacter doesn't explain
the pathology here. The most we could say, if the organism is
numerous, is that it may be contributing to some pathology in the
stomach, but I doubt it is the primary player in most gastritis cases
in adult ferrets. The papers establishing Helicobacter as a ferret
pathogen had some serious flaws, which makes it difficult to interpret
the papers' conclusions. In one of the more recent Helicobacter
papers (Fox et al) wherein they used Clarythromycin and Ranitidine +
bismuth to totally eliminate Helicobacter, they found that eliminating
the bacteria produced no reduction in the level of gastritis, again
bringing into question how important the bacteria are. I rarely
assume Helicobacter are a problem in an adult ferret without finding
significant numbers on gastric biopsy.
The next idea you discussed was a gastric foreign body, and again
it is very unlikely to cause the diarrhea, and straining to defecate
(a large intestinal sign). The "ball valve" effect doesn't make sense
when explaining intestinal signs; more likely you would simply get
gastritis signs which came and went sporadically. Many practitioners
have a tendency to concentrate on the stomach simply because there is
vomition; one needs to remember that enteritis or colitis often
produce nausea or vomition even in the abscence of gastric disease.
My experience with ferrets is that enteric, not gastric, disease is
the most frequent cause of acute nausea in a case such as you
The last point you make is to suggest that gastritis in ferrets
can cause pancreatitis. Well... sort of, but probably not the way you
mean it. I know why you probably think this; I will also disagree
with you partially. Lipase levels often elevate significantly in
ferrets with gastritis; this does NOT indicate pancreatitis, but
rather is lipase of gastric origin, and correlates well with
gastritis. Be careful when interpreting pathologists comments; the
"pancreatitis" they sometimes find is typically a mild to moderate
periductal lymphocytic infiltrate, which is a direct extension of
inflammation in the gut. However, it does not involve the pancreatic
parenchyma, does NOT produce clinical pancreatitis, and is an
incidental finding. Therefore in any meaningful clinical sense,
ferrets don't have pancreatitis with gastric disease. I've biopsied
cases like this for most of a decade, and the conclusions my
pathologist and I have reached are backed up by pretty extensive
histopathology. Incidentally, any practitioner's conclusions about GI
or other diseases, especially in exotic pets, are heavily dependent on
the quality of the pathologist you're using. I can't tell you how
many times I see misdiagnoses by pathologists. As practitioners we
have a tendency to treat pathology as the bible; in reality it is
heavily subjective and requires expertise with the species in
question. The best pathologist I've found with regards to exotic pet
species from ferrets to frogs, and especially with this ferret GI
stuff, is Mike Garner at N.W. ZooPath in the Seattle area. He and I
have worked out the bugs on ferret GI diseases for a decade now.
Now time for suggestions (your last section on the posting). I
would not have cut the patient because stabilization first made more
sense, and the patient responded to antibiotics exactly as I would
have predicted. The problem is, he's still ill, even if he looks
normal. The underlying pathology is probably lymphoplasmacytic
gastroenteritis, which my pathologist and I have been working with for
most of the 1990's. It is histologically indistinguishable from cat
IBD, and possible etiologies of course include food allergy, viral,
parasitic, etc. About 50% of cases I diagnose have NO clinical signs.
When signs occur, they may include chronically thin body build (ok
body fat but slight to severe muscle wasting), inconsistent stools
(including tarry or green or seedy stool), and occasional episodes of
sudden illness such as your case had. Secondary ascending hepatitis
(not pancreatitis) is a common finding (ALT over 200); the hepatitis
is usually lymphocytic portal hepatitis and often subclinical, but can
develop suppurative hepatitis which is acute and severe, with ALT over
400-600 in many cases. GGT is also a good indicator of biliary
pathology; levels over 5-6 are elevated (using Idexx vet labs). Ast
and AlkPhos are poor indicators for ferret hepatic disease and only
elevate in the most severe suppurative or neoplastic liver disease.
Screening for IBD in these guys can be done with serum chemistries
with surprisingly good results: lipase levels over 500 IU/L at Idexx
labs or over 1000 IU/L on a vet test in house machine are highly
suggestive of gastritis. Globulin levels over 3 g/dl indicate an
inflammatory response (most likely in the gut). Once stabilized, I
would recommend biopsies on every ferret with sporadic GI signs OR
elevation of lipase or globulin. Biopsies need to be surgical, not
endoscopic. You need to biopsy stomach (preferably close to pylorus),
and mid duodenum and mid jejunum; the pathology in these cases is
often worse in the intestines than the stomach. Also biopsy any
prominent lymph nodes, especially the gastric and peripancreatic
(duodenal) lymph nodes which are easy to access. You are looking for
hyperplasia and atypia in the nodes; untreated IBD leads to
progressive nodal hyperplasia and eventual neoplasia (lymphoma) in
many cases. IBD is the most common precursor to lymphoma in ferrets,
and proper recognition allows you to predict and prevent this
neoplasia, reducing lymphoma incidence dramatically. So biopsy,
biopsy, biopsy, but don't rush into it on a clinically ill patient.
Lymphoplasmacytic gastroenteritis is an important disease, in part
because it is so common (it even beats adrenal disease in incidence),
it is subtle but progressive, and it can kill via progressive wasting
disease when advanced, or via lymphoma development. Other diseases
such as Helicobacter, Aleutians, or ECE often get the blame, which has
further delayed recognition of this syndrome. This disease also leads
to other pathology, such as delayed gastric emptying due to chronic
gastritis... to answer your question about hairballs, I believe many
ferrets with trichobezoars (especially repeat episode cases) have
preexisting gastric disease which reduces motility and predisposes to
hair retention... that's why you see more hairballs in older ferrets:
they have sick g.i. tracts. This (IBD)disease syndrome also leads to
megaesophagous in ferrets (it's the primary reason ferrets get
esophageal disease). Understanding the esophageal pathology has
allowed us to control and cure virtually all of our megaesophagous
cases. Controlling gastric reflux and chemical esophagitis leads to
vastly improved esophageal function; my drug of choice for this (and
for ulcers) is Zantac, compounded into a 5 mg/cc suspension; dosing is
3.5mg/kg PO BID.
Treatment of IBD is usually longterm antiinflammatory meds; I
prefer Imuran to pred, because at the doses needed to be effective,
pred will eventually produce muscle atrophy, potbelly, rear end
weakness, etc. I know a few people who use pred with Imuran, but the
Imuran alone works well in most cases without the pred side effects,
so why use cortisone? Pred may also predispose to gastric ulcers, and
in cases with secondary hepatitis, the liver may become much worse
when pred is used. Imuran avoids all these problems and is very well
tolerated. Also try hypoallergenic diets; the most palatable for
ferrets seem to be Hill's Z/D and Walthams Duck & Rice; most ferrets
will eat one or the other. Some clients report improvement on these
diets; some IBD cases may be food allergy after all.
So I encourage you to treat these cases aggressively but logically;
don't cut on an emergency basis without solid evidence supporting
surgery, but DO cut to diagnose when the patient is stabilized. And
remember to include the lower gut in your thinking; the stomach is
somewhat overrated.
Last question of yours: does creatinine elevate in azotemia in
ferrets. It can, but usually not impressively. Often an advanced
renal patient has a huge BUN but low creatinine. Apparently failing
kidneys still eliminate creatinine well? Or ferrets don't generate
much creatinine? Part of the problem may be that the normal range
needs to be very low and strictly interpreted; even a minimal
elevation may be significant in a ferret even though it doesn't look
as impressive as in a cat renal patient.
Hope this is helpful! Any questions, drop me a note. Best wishes,
Mark Burgess DVM Southwest Animal Hospital/ Exotic Animal Practice