[Sukie note: a vet, Ben Otten, posed questions on
http://groups.yahoo.com/group/Ferret-Health-list
asking what assorted vets would do with a given suite of symptoms.  It's
one of those areas in which more is still being learned.  As a result, I
am providing his questions and the suite of replies, in order received,
for your consideration, and so that those with ferrets undergoing GI
difficulties can review options and know that there still is a lot of
share and a lot to learn.
 
In the case of our Scooter Dr. Mark Burgess' description fits like a
glove; others may fit different fits for different ferrets and different
situations.
 
Ferret medicine has come a huge way in the last 20 years; almost nothing
was then known; heck, it's only been 11 years since the work was completed
to have a rabies vaccine that meets the strict standards of the USDA, and
only 3 years since the CDC rabies-virus-shedding studies were completed
and the Compendium for Animal Rabies control changed to be more fair to
ferrets.
 
A lot has been done but a lot more need to be done; you can help that
effort with donations to those places that achieve such advances:
certain veterinary universities such as UGA and Dept. of Comparative
Med at MIT, a few clinics such as the AMC and Charles Weiss', the AFIP
(which is working on a tissue bank that can be used by researchers
anywhere to facilitate more effective work (Research for Ferrets, Dept.
of Telemedicine, Armed Forces Institute of Pathology, Washington DC
20306-6000; your check should be made out to the Registry of Veterinary
Pathology, and at the bottom should be marked "For Ferret Research"), and
the Morris Animal Foundation (specify "ferret" or "domestic ferret":
1-800-243-2345, 45 Inverness Dr. E., Englewood, CO 80112-5480).
 
I am sure that others will fill in contact info that I don't have handy
right now.  As you will note in the cross-posts there are more yet places
that can use funds to help improve ferret medical care.  This year Steve
and I can't give our usual figure (over $1,000) because income will soon
be going away; at least I can let you know about the need so that those
who want to see such improvements can give.]
 
Discussion opener from BAO:
 
> 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, bladder,
> prostate, intestines,  Questionable unusual feel to stomach.
> NON PAINFUL
>
> RADS: normal chest / normal heart.  Unusual charateristic to stomach -
> R/O pyloric obstruction - Possible loss of serosal detail in cranial
> abdomen 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 - your day off.
>
> DO YOU come in and cut the ferret or Do YOU put it on helicobacter
> therapy, 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 choose...
> 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
>    work)
> 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
>    stomach 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
>
> ANY SUGGESTIONS ??
>
> WHO WOULD HAVE CUT SOONER ?
>
> 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.
 
RH: That's a toughy.  Obviously with vomiting, etc, you cut.  A case like
the one you describe, I'd probably recommend surgery as the best option.
However - with relatively normal rads, a ferret who is not crashing, no
obvious FB palpable or visible... well, I've seen several of these get
better with aggressive fluid therapy and nutritional support, plus ulcer
treatment.  Bloodwork is always a really good idea, and I highly recommend
in-house labs if at all possible.  Obviously not possible in this
situation, though.  Pancreatitis - I've seen it too.  Once.  I don't tend
to worry about it too much in ferrets.
 
It sounds like you definitely took the best course of action given the
situation you had.  I am a little curious about using both Pepto and
Pepcid - I tend to use one or the other.
 
Dr. Ruth
*****************************************
Save lives - spay or neuter your pet.
  ----------
 
BW:
Ben - I think I would have advocated cutting over the weekend, for a
number of reasons.  To start, this animal has a history of FB ingestion -
two years doesn't mean much - I had a ferret who went years between
plastic bag FB - 1st a 1 year, 2nd at 2, and 3rd at 4.  History can be
very telling.
 
All of the symptoms are compatible with a foreign body - Helicobacter is
not going to cause minimal fecal output or straining, and only rarely
vomiting - if he is vomiting several times, or dry heaving, it doesn't
look good for Helicobacter.
 
Now, he may have passed the fb - these don't sound like people who would
pick through the stool in a bowl of water to see if it was passed - and
now he would be eating and pooping normally.
 
I guess if there is any backslide, I'd go to surgery with him.
 
It's often in how it is presented to the owner.  I actually have one of my
own that is doing some of the same stuff - dry heaves, poor stool, some
straining - not eating well, not putting out much.  No grinding, though.
I'm cutting him on Saturday.  Here's why: if I come up empty on a foreign
body or hairball or God forbid a mass, then I can take a couple of
biopsies of the intestine, and I'm out, I've done the most sophisticated
diagnostic test available, and I've collected the most diagnostic
evidence.  People get unnecessarily bummed out when an exploratory fails
to find a foreign body - it would be nice to in every case, but it doesn't
make the surgery a failure if there isn't one there.
 
As I've said many times, I'd much rather go in early on a good surgical
candidate than wait to try multiple empiric therapies until the surgery
becomes an emergency!
 
With kindest regards,
Bruce Williams
    -------
 
 ... From MB:
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 describe.
 
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
[Posted in FML issue 3610]