>If you give your animals distilled water, they will drink themselves into
>oblivion!  It is the minerals IN the water that satisfies thirst.
 
That must be the rationale behind the latest product from MF, Love Canal
Ferret Drink.  The bottle says "after this, your ferret will never drink
anything else."
 
>Not sure if albino fitch pelkts had any value so I can't answer on that.
 
Didn't European royalty and wealthy like to edge ceremonial grab with white
fur?  I always figured they used ermine, but I'm sure there were cheap knock
offs even then.
 
>Does anyone out in CA land have access to data or a sound estimate on how
>much money the State is now putting out to harass, investigate, jail, and
>publish anti-ferret literature.
 
If this tactic worked, the war on drugs would have been canned long ago.
Some things government takes on as a mission have no basis in economic
sense.  In '94 over 12 billion was expended in the US on drug law
enforcement directly and indirectly.  If somebody can show me how '95 had
less of a drug problem than '93 as a result, I'd appreciate it.
 
>Now, I have a question for the list.  ECE appears to be a mostly American
>and Canadian disease.  Another American/Canadian trait is low-bulk kibbled
>foods fed almost exclusively to the ferrets.  Has anyone feeding ferrets a
>high-bulk diet developed ECE, and if so, how bad was the occurance?  I have
>no data, but my gut tells me there could be a correlation.
 
A shocker, but I have to disagree with your premise.  First, ECE seems to
have started in the Eastern US and spread slowly, so the geographic
limitation may be more like the early days of AIDS, or (hopefully not) E.
Bola.  (Remember a few years ago that Canadian ferrets were touted as ECE
resistant?) Selective exposure at work.  That aside, let's examine the bulk
impacts.  As you've stated, bulk moves things along, so a potential
mechanism to explain a result you want is that the gut is purged of the
virus before it can take hold.  However, ECE goes from exposure to full
blown symptoms in 48 hours or so.  During that time you'd be talking a
relatively small difference in gut dwell time for a N.  Am.  kibble diet
compared to some higher bulk diet somewhere else.  Lets say an hour total,
maybe two to be really extreme.  There might be six meals in that period and
a compariable total in-gut time of 18 hours in one case and 16 in the other.
 
If your theory is that just the first meal difference in transit time is the
critical exposure, the percentage time difference again seems like it would
be too small to account for something with such a quick build time.
Possible, but unlikely given how a virus spreads.  Then you run into the
problem that ECE causes a symptom of rapid gut transit (from both ends
intitially) for a prolonged period in a very short time after the intial
exposure and that doesn't clear the disease.  So any impact of higher fiber
is simulated by the body's longterm reponse to the infection.  Again this
makes it seem as if the initial toehold of ECE virus is quicker than the
fiber mechanism could affect.  If you have some rationale beyond the
geographic correlation of dietary bulk and ECE incidence (for the benefit of
others - a correlation does not imply cause and effect), I'd like to hear it.
 
I can't see a mechanism that bulk would have enough impact on to cause a
difference in ECE with its short incubation period.  Nor can I see how pre
exposure differences in dietary bulk would cause a change in intestinal
tissue that would favor lower virus uptake.  If anything, it would make the
digestive work at the absorptive extreme.  For a bit I thought that maybe
the chronic Heliobacter might work, but this is so long term that again the
difference in gut transit is trivial compared to the total
exposure/incubation period.  At this point in time, if there is somebody
with a high bulk diet that hasn't had ECE, I'd write it off to lack of
exposure or some reason other than the bulk content in the food.  My
experience with my ferrets when they had ECE was that ECE symptoms were
varible even when diet was the same, and everything I read about TLE's
experience with a larger group shows the same to be true.  You could take
TLE's case as evidence that there is variation when the diet factor is
uniform.  What would adding an extra variable do answer the question looking
for the source of differences?  Evidence shows that there is varaition with
that one out.
 
I fear that the likely answers to this question are more likely to track the
cancer in foreign ferrets issue.  A while back it was widely held by some
that foreign ferrets got NO cancer, it was a US thing.  I've since seen
posts by some of these same people and others in other countries recently
asking about cancer treatment.  We've gone from a difference in kind to one
of degree, and with more sophisticated diagnosis, I bet the degree gap is
narrowed.  ECE is hard enough to diagnose in the US, in areas where it may
just be impacting, probably more so.  As with the incidence of cancer in
foreign ferrets, I'd bet it is diagnostic skill differences causing a
difference in reporting, not in incidence.  Give the area a few more years
for the spread and experience level to mature and I'd bet it tracks with
ours very well.  The US has more widescale experience with ferrets as house
pets and there is clearly a great deal of variation in diagnostic and
treatment skill here (in owners and vets).  If nothing else, this list has
shown me that.  In short, any evidence you'd get supporting your idea could
be attributed to several other sources more plausible than the bulk one.
 
   ( )--(a)
   (@=@=) \     Till next time.......Rudy the ferlosopher
   O__)  \ \___
      \   \
      /\ * )  \             (Hi, Houseboat lady)
[Posted in FML issue 1913]