This is a topic I have been wondering about for only a few years,
I guess, from reading abstracts and studies, but an article in the
June 2012 issue of Scientific American compiled enough additional
information that I had not read that when combining it in my head
with what I'd already read a number of questions arise. Those who
have that issue of Sci Am or have read it in their libraries will
notice that I have added some info from past reading, too, in
this post.

"What is a microbiome?" you ask. Still others ask, "What is a caecum?"

With a few exceptions until recently it was thought that most bacteria
in and on the body were pathogenic invaders to be dealt with. Not so.
Some are, yes. Many others are commensal which means that they perform
useful functions to help preserve our health. Some can be commensal or
can be pathogenic depending on certain circumstances or population
levels.

Two of the exceptions knowns about for some time were bacteria to help
break down certain ranges of vegetable origin foods types, and that
Vitamin B12 is created by commensal bacteria.

More later on some specifics but lets go now to ferrets and to caecums.

For a long time it was thought that animals with rapid transit times
through the GI tract has few intestinal bacteria, but now from human
work it is known that so many types of gastrointestinal bacteria need
specialized conditions that it becomes impossible to find them under
normal testing conditions or to culture them under normal culturing
conditions. What is done these days for such tender anaerobic GI
bacteria is that their genetic signatures are looked for rather than
looking for the bacteria themselves. In humans at least it turns out
that there are a heck of a lot of them normally and many of them may
well perform functions useful for health.

The caecum is the appendix. Remember when that was thought to be
without a function? Not so. It is now known that the caecum provides
a safe-house for intestinal bacteria turning diarrheal diseases. The
ones that hide away there repopulate the intestine afterward.

Some animals do not have a caecum. Ferrets are like that. That brings
up three questions:
1. If there are important and health related bacteria found in the GI
tract of ferrets when a researcher looks for hard-to-find kinds using
the hunt for their genetic signatures rather than the full bacteria,
then how are those bacteria naturally replenished if a diarrheal
disease occurs? Which bacteria are they, if there? Do polecats
reacquire them from other polecats or themselves by rather probing
grooming or do they have other sources, perhaps things in their diet or
perhaps things periodically in their diet, or do they spread onward
from other locations like the mouth after diarrhea to replenish the
population if one is normally there?
2. Given how long humans and pet ferrets have been living together, are
pet ferrets inclined to have share and successfully use some of our GI
bacteria or ones common in our diet (like ones in yogurt with active
cultures which many people have found useful in small amounts when
ferrets get diarrhea)? Studies have found some pet species of bacteria
in and on us, so...
3. If so for number 2, then does a change in the intestinal biome mean
that at least some pet ferrets have the means to successfully be more
omnivorous than wild polecats?

Okay, most of the work on microbiomes so far has been done on humans,
but notice some hints that some aspects of this, including some
Helicobacter pylori work, may point to a need for further
investigations in ferrets.

How many bacteria are in or on humans in the studies? Well, all told
they would weight a few pounds, but because bacteria are so much
smaller than our cells in numbers our normal populations of bacteria
probably outnumber our own body cells by as as many as ten to one, and
the specific gene numbers of the genetic material in the one thousand
or so types we humans are thought to normally have in and on ourselves
likely outnumber our own genes by over a hundred times.

The newborn originally has no bacteria, but passing through the birth
canal adds a number which start the healthy commensal relationships
going. Others are added later. (So, individuals with natural births may
begin with a health advantage over those born by cesarean.) Why don't
our bodies destroy them? It appears that useful bacteria can teach
the body to not over-respond. That protects those bacteria, but that
education might also reduce rates of immune disease in the hosts, which
protects the animals (including humans) in which those bacteria live.
In humans Bacteroides fragilis is especially good at this function to
educate the T Cells of the immune system to not over-respond, but like
H. pylori that bacterium is becoming more scarce due to life style and
medical choices. Earliest in life after birth is a great time to add
some of the GI bacteria, too. For the first few days the stomach is not
very acidic. That allows the body to not break down the immune cells
the mother provides in the colostrum she delivers before the breasts
switch over to milk (which are just digested later in development) but
it also may allow some of the commensal (useful) bacteria to take hold.

H. pylori: fighting it, using it:

Ferrets have Helicobacter mustelae, something we all know well since at
times it can cause ulcers in ferrets, and because the work on ferrets
is what led to discovering the species we humans have.

Did you know that in studies on treating H. pylori in humans giving
probiotic bacteria along with treatment makes the treatment far more
successful? I posted to the FHL recently about that, I think.

On the other side of the coin, did you know that there are at least
two ways that H. pylori, in the right numbers and in the healthy
conditions, is useful for our health?

In past studies humans with low or missing populations of H. pylori
are more inclined to have acid reflux and as a result to have the
esophageal problems associated with acid reflux.

More recent work indicates that this species of Helicobacter for
humans. In those of us without the bacterium there is a lack of
production of ghrelin which is one of the hormones that prevent us from
feeling hungry inappropriately. That means hunger when there should not
be hunger, so both discomfort and overweight with all of its associated
health problems can happen (and some researchers think that the low
numbers of children with H. pylori along with bad diet and lack of
exercise might play a part in the childhood obesity epidemic which is
spelling shortened lives and even high rates of childhood obesity and
circulatory disease).

Is there new work on how H. pylori can be involved in the creation of
ulcers? Yes. It appears that if the stomach becomes too acid certain
strains of H. pylori helps control that (and as a result reduces the
risk of reflux). Those strains contain a specific gene which allows
them to do this using specific proteins those bacteria make to signal
for less acid production, but those variants are not tolerated by all
people and are to blame for ulcers.

Is something similar going on in ferrets? Does Helicobacter mustelae
perform useful functions in ferrets, being commensal as well as
possible pathogen?

Sukie (not a vet)

Recommended ferret health links:
http://pets.groups.yahoo.com/group/ferrethealth/
http://ferrethealth.org/archive/
http://www.miamiferret.org/
http://www.ferrethealth.msu.edu/
http://www.ferretcongress.org/
http://www.trifl.org/index.shtml
http://homepage.mac.com/sukie/sukiesferretlinks.html
all ferret topics:
http://listserv.ferretmailinglist.org/archives/ferret-search.html

[Posted in FML 7436]