Message Number: YG14166 | New FHL Archives Search
From: Bob C
Date: 2002-06-25 07:17:00 UTC
Subject: Bob C: Some Thoughts to Ponder

Here is one for the vets on the list to ponder—as I have been doing for
the last weeks. Perhaps some sort of discourse can be stimulated to
take place….

I’ve been in California for the last two weeks, visiting my mom who has
been in intensive care. She is still there, but stable, so I came home
to catch up on a thousand-plus emails and work. While that isn’t
important to anyone but myself, it did give me a chance to read some
stuff I had on my lists of “to read” material. I finally finished a
long-winded discourse on the canine distemper-rinderpest-measles
triplex, yet another excellent book on evolutionary medicine, and quite
a few early ferreting books, including a few photocopied chapters that
dealt with ferrets taken from some extremely old veterinary tomes. Here
are a few of my observations:

In modern ferret-oriented veterinary literature, the death rate in
ferrets suffering canine distemper is 100%. This is not totally
accurate, for I know of at least 3 confirmed cases, including one here
in Columbia MO, where a ferret survived the disease, but for our
purposes, we can assume 100% is fairly accurate.

However, a century ago, most ferret literature reported some ferrets
could survive canine distemper. Without a doubt, many (or most) of
those early reports must have been wrong, and what was cured must have
been some other disease, such as influenza, or a bacterial disease that
mimicked distemper symptoms. But, some are NOT in doubt, including one
report from 1770. The descriptions of the disease, the close
association with dogs, the severity of the disease, and the low survival
rate are convincing enough to convince me that a century or more ago,
domesticated ferrets survived distemper in greater rates than found
currently. Maybe not a lot, but some.

I would be skeptical of suggestions that canine distemper was evolving
stronger strains, or the strain currently in the USA was a type of super
breed compared to earlier strains. While such suggestions have
possibility, viral diseases tend to become LESS of a bother over time.
The reason is that the nastiest strains tend to kill the host before the
virus has time to effectively reproduce, while at the same time, the
hosts with the least resistance to the disease tend to die the quickest.
The end result is that deadly diseases tend to become less deadly over
time, while at the same time hosts are becoming more resistant.
granted, there are some viral diseases that don't follow the pattern,
but most of them don't cause immediate death (= death within a month).

Still, without some other explanation, perhaps this co-evolution between
hosts and diseases isn’t taking place, or so slowly that the rate of
change has yet to be recognized. But, what if the difference was
something in the environment, rather than the actual disease? So, I
looked for major differences between the historic and modern groups,
thinking such a comparison could shed some light on the subject. I
realized three major differences: dietary, neutering, and geographical
movement.

[Note: historic reports did suggest younger ferrets survived canine
distemper better, which might suggest the mother passed along some
immunity, perhaps through her milk. I don’t think this is the case. If
a disease has a 100% death rate, mothers would die PRIOR to being able
to pass maternal immunity; after all, dead mothers can’t pass on
anything. Besides, if mother’s milk was the answer then, it would also
be the case now, and it isn’t.]

Geographical movement first. Canine distemper is such a hot disease
that it tends to kill all it infects, burning itself out on a local
scale before it really has time to pass geographic and climatic
barriers. Assuming modern strains are more-or-less equal to historic
strains in terms of lethality, about the best you can hope for is a sort
of parity; the death rates between both populations, historic and
modern, should be about equal. Since it is not, we recognize
geographical movement wouldn’t explain why so many historical reports
exist claiming ferrets were fully cured from canine distemper. Movement
has nothing to do with it at all.

Neutering could be a major factor in that the immune system is, forgive
the pun, intimately associated with the reproductive system. It is
possible that historic ferrets, uniformly fully functional in the sex
department, had some advantage granted to their immune system as the
result of hormonal normalcy. I would believe it except that canine
distemper decimates modern ferret farms, including breeding stock, which
is the major reason why they will not allow outsiders, nor dogs, near
their facilities. There doesn’t seem to be a clear association with
canine distemper resistance and the reproductive hormones.

So that leaves diet. The earliest reference I have regarding what to
feed domesticated ferrets is a Latin translation of a German text dated
to circa 1570s. The diet? Milk and bread, with meat added several
times a week. This basic diet was standard, with little exception,
until as late as the 1940s. Sounds horrible, doesn’t it? Actually,
it's not so bad. In terms of carbohydrates, proteins and fats, it isn’t
much different compared to modern kibble. But, it IS vastly different
in one respect; the milk used was not that Pasteurized, homogenized,
de-fatted stuff that looks blue in warm lighting. It was whole milk,
cream and all—a completely different monster.

Why is this important? Because whole milk contains a tremendous amount
of fat-soluble vitamins, including Vitamin A. After cod liver oil, milk
butter-fat is one of the richest non-fortified, easy to obtain foods
containing Vitamin A available.

Ferrets have a very hard time absorbing fats because they have such a
short bowel transit time. I can’t tell you how many fats pass through,
but the amount must be tremendous. How do I know? Because ferrets also
have an extremely high fat requirement in their diet. If you make the
fair assumption that ferrets have the same basic digestive physiology as
found in other carnivores, when why the disproportionate amount of fat
required in their diet? The answer is easy; fat is hard for ANY mammal
to digest, and for animals, like the ferret, with short bowels and rapid
transit times, it is especially hard to get enough fats. Either you
have to slow things down, or you simply eat more of what you have a hard
time absorbing. That is, you increase your intake of dietary fats,
which is exactly what we see in our ferrets.

The dry, extruded foods given to our ferrets has a high percentage of
fat, especially the more costly foods like Totally Ferret. BUT, and
this 'but' is much larger than my own, those fats are given at the same
time as carbohydrates, which actually reduces fat absorbability. If
those carbohydrates include cellulose, fat absorbability drops even
more. So even if they are eating about the same amount of fat as a
ferret eating whole animals, in comparison, LESS fat is actually
absorbed by a ferret eating a dry, extruded food.

So why is this a problem? Certainly, the energy derived from
carbohydrates meets the ferret’s needs, and the lost energy from fats
piling up in the corners is not really missed. The problem is, Vitamin
A is transported by fats, which makes sense considering it is a
fat-soluble vitamin. The absorption of Vitamin A is correlated to the
overall absorption of fats in the diet; absorb more fats, and absorb
more Vitamin A. I hypothesize that ferrets on a dry diet, especially
those not being fed vitamin supplements on a regular basis, run
chronically low levels of fat-soluble vitamins, and in particular (for
the topic at hand), low levels of Vitamin A. Notice I said, "chronically
low." That in NO way means I am suggesting normal, healthy ferrets on a
kibble diet has Vitamin A deficiencies. But it may be low enough so that
it becomes critically low in ferrets under physical stress, such as from
a disease, reproduction, or growth.

Deficiencies of Vitamin A include night blindness and other vision
problems, growth stunting, increased incidence of cataracts, and a
depressed immune system. Depressed immune systems can lead to increased
rates of bacterial and viral disease, as well as increased rates of
certain types of cancers. Evidence in humans suggests AIDS patients
with low Vitamin A levels die sooner than those with normal levels of
the vitamin.

But what about canine distemper? As already mentioned, C.D. is part of
a triplex of closely related diseases: rinderpest, canine distemper, and
measles. Rinderpest primarily attacks hoofed ungulates, such as cattle,
deer, and sheep. Canine distemper attacks carnivores, such as dogs,
wolves, coyotes, and fox, although it will also kill mustelids of all
types, raccoons, hyenas, and recently, cheetahs and African lions.
Measles is, of course, a human disease. And, that is where this thought
experiment is leading.

Children with measles who have low levels of Vitamin A have poorer
prognoses than those with normal or slightly elevated levels of the
vitamin. The tie is so close, that it is recommended that children with
severe measles infections be given Vitamin A supplements (among other
vitamins). It is probably safe to assume, given the extremely close
relationship between measles and canine distemper, that Vitamin A levels
would be important to ferrets as well.

Remember the whole milk and bread diet? Whole milk contains a
tremendous amount of butterfat, which, in turn, carries a tremendous
amount of Vitamin A (one of the highest natural sources). That whole
milk diet (not the milk, but the included fat-soluble vitamins), maybe,
perhaps, MIGHT have slightly helped those ferrets in the past combat
mild cases of canine distemper. The boost the vitamin gives to the
immune system MIGHT have slightly lowered some cancer rates. Low levels
of Vitamin A MIGHT contribute to the high incidence of cataracts in
ferrets. And PERHAPS ferrets with compromised immune systems fair
better, for some small bit of time, when they eat a diet higher in
fat-soluble vitamins, such as what they get consuming Bob’s Chicken Gravy.

I don’t know if ANY of this is true; these observations maybe nothing
more than the mental wanderings of a stressed son who sat at his
mother's bedside for far too long. I am not even sure that those old
records are all that accurate. Considering the potential toxicity of
fat-soluble vitamins, I wouldn’t recommend any rapid or drastic changes,
such as pouring liquid vitamins down the throats of ferrets. Still, it
is something to think about and discuss. And I hope we discuss this
topic, intelligently, at length.

Before you ask, I DON’T KNOW what a proper dose of Vitamin A would be
for a ferret. As far as I can tell, no one knows. It IS something that
demands careful exploration. What we know about the dietary
requirements of ferrets is tiny compared to what we don’t know. I am
convinced some of these ideas, regardless of their actual merit, have
value as a topic of discussion. Do ferrets on a dry, extruded diet
actually suffer from Vitamin A deficiencies? If healthy, probably not.
I think the real concern about vitamin levels should be given those
ferrets that are marginally healthy, or under prolonged stress.

So here is the big question (and please answer intelligently, not just
for the sake of bashing). Does anyone think that the modern diets fed
to ferrets has resulted in negative consequences? Come on vets; you
represent the intellectual elite of the ferret community. You should
answer as well.

Comments?

Bob C