The first work was a neat bit of lateral thinking. In people who have
fewer heart attacks and strokes there are often higher levels of
lycopene and betacarotene in the body fat, but adding those to the
diet does not serve to confer those specific protections in study
(though some other studies find that for certain other things higher
antioxidant intakes are helpful). So, the researchers got thinking
about what else could cause higher levels of those antioxidants in the
body. Well, one thing is being able to better provide the antioxidant
in the body. Low, and behold, the intestinal bacteria that are better
at creating these antioxidants are also higher in people who have
reduced stroke and heart attack risk AND they also are less likely to
make inflammatory compounds and more likely to make anti-inflammatory
compounds. The work is in the Dec 4th "Nature Communications" and
available for free here:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3538954/

The bacteria associated with lowered risk and with the gut bacteria
that reduced inflammation compared to other predominant groupings had
greater proportions of Eubacterium, Roseburia, Bacteroides, and tended
to have more Clostridium. These bacteria produce more butyrate,
lycopene, and betacarotene. Inflammation is connected to a host of
other illnesses beyond vascular ones.

The bacteria w rates higher in the populations w vascular disease
include Ruminococcus and Collinsella -- with the name of the first
suggestive of ruminants so I wonder if it is more common in things
like beef mince -- and these bacteria are more likely to produce
peptidoglycan which is inflammatory.

Microbiomes are acquired in several ways. Some can come from the
environment, some from what is ingested, some from vaginal secretions
acquired during birth, some from breast milk, etc.

http://womenshealth.gov/news/HealthDay/EN/2013/Jan/08/672247.html
is on breast milk which has been found to contain over 700 types of
bacteria. Quotes below originate from a news release by the Spanish
Foundation of Science and Technology and then in a piece from the U.S.
Office on Women's Health.

"... a mother's hormonal state at the time of birth may affect the
diversity of bacteria species in her breast milk, according to the
study by Raul Cabrera-Rubio and colleagues, which was published in
the American Journal of Clinical Nutrition."

"Breast milk plays an important role in determining the composition of
the bacterial community in a child's digestive system, noted a news
release from the Spanish Foundation of Science and Technology.

The study authors are now trying to determine if bacteria in breast
milk help babies digest the milk or if they play a role in immune
system development. The investigators said their research could lead
to improved child nutrition.

"If the breast milk bacteria discovered in this study were important
for the development of the immune system, its addition to infant
formula could decrease the risk of allergies, asthma and autoimmune
diseases," they wrote."

Now, most humans have an appendix and the appendix turns out to not
really be the vestigial organ that people thought it was when I was
young. Instead, even though it no longer plays a role in digestion for
humans it DOES shelter gut bacteria so that after severe diarrheal
diseases the intestines return more rapidly to full function due to
repopulating from the appendix.

Ferrets do not have an appendix. That leads to the question of whether
it might be easier to switch the proportions of their intestinal
microbiomes by causing a loss and then providing replacements while
focusing on bacteria that provide more anti-inflammatory compounds,
since there not be the chance of the bacteria being out-competed by
previous colonies that retained populations in the appendix. (May also
work better for people who have lost theirs if the concept holds water
in practice.)

Personal genetics might also affect which bacteria survive the best,
though, so some individuals of any species might not be as good hosts
for what may be the better choices. One thing that suggests this might
be the case is that in studies of why there is so often the combination
of cardiovascular disease and gingivitis it has turned up that in
people that the genetics of the affected individuals can tend to make
both more possible.

That in turn leads to the question of whether epigenetics might have
an effect (since this turns on and off certain genes) and epigenetics
itself can be changed by the environment (or by the environment of
parents or grandparents in studies of the children and grandchildren
of people who suffered malnutrition and of ones where smoking had been
in the family).

So, maybe the bacteria might be able to create epigenetic changes
which might turn on of off certain genes, therefore making their own
environment more comfy for them but not for competing bacteria.

To date there is a lack of microbiome work specifically on ferrets so
while the same general principals may apply, the species of bacteria
and other microbes may differ and hence levels of things like
inflammatory compounds may differ. Just:

QUOTES

Methods Mol Biol. 2012;921:175-88.
Gastric Helicobacter spp. in animal models: pathogenesis and modulation
by extragastric coinfections.
Rogers AB.
Source
Lineberger Comprehensive Cancer Center and Department of Pathology and
Laboratory Medicine, University of North Carolina, Chapel Hill, NC,
USA.

Abstract
Animal models are used to study complex host, microbial, and
environmental influences associated with gastric Helicobacter
infection. Evidence that gastric helicobacters are pathogenic in
animals first came from ferrets. Felids, nonhuman primates, and many
other species also harbor stomach helicobacters. Today, mice are
preferred by most researchers for scientific investigation because of
cost-efficiencies, rapid reproduction, choice of laboratory reagents,
and availability of genetically engineered models. Infection with
Helicobacter felis or H. pylori Sydney strain-1 in appropriate mouse
strains produces disease with remarkable similarities to H. pylori in
humans. Due to recent advances in genetic engineering, in vivo imaging,
and system-wide genomics and proteomics, these models will become
even more widespread in the future. Recently, it has been shown that
extragastric infections can dramatically affect the severity of disease
induced by gastric Helicobacter spp. through heterologous immunity.
These models provide proof-of-principle for the "African enigma"
wherein gastric cancer is underrepresented in low-lying tropical
countries with concurrently high H. pylori and internal parasite
prevalence. Helicobacter gastritis and carcinogenesis in mouse models
may be augmented or ameliorated by other infectious agents depending on
the character of the invoked immune response. Knowledge gained from the
HumanMicrobiome Project and other investigations is certain to shed new
light on the influence of extragastric bacterial, viral, fungal, and
parasitic coinfections on H. pylori-associated peptic ulcer disease
and gastric adenocarcinoma.

PMID: 23015504 [PubMed - in process]

Clin Microbiol Rev. 2011 Apr;24(2):231-46. doi: 10.1128/CMR.00041-10.
Microbiology of animal bite wound infections.
Abrahamian FM, Goldstein EJ.
Source
David Geffen School of Medicine at UCLA, Los Angeles, California, USA.

Abstract
The microbiology of animal bite wound infections in humans is often
polymicrobial, with a broad mixture of aerobic and anaerobic
microorganisms. Bacteria recovered from infected bite wounds are most
often reflective of the oral flora of the biting animal, which can also
be influenced by the microbiome of their ingested prey and other foods.
Bacteria may also originate from the victim's own skin or the physical
environment at the time of injury. Our review has focused on bite wound
infections in humans from dogs, cats, and a variety of other animals
such as monkeys, bears, pigs, ferrets, horses, sheep, Tasmanian devils,
snakes, Komodo dragons, monitor lizards, iguanas,
alligators/crocodiles, rats, guinea pigs, hamsters, prairie dogs,
swans, and sharks. The medical literature in this area has been made
up mostly of small case series or case reports. Very few studies have
been systematic and are often limited to dog or cat bite injuries.
Limitations of studies include a lack of established or inconsistent
criteria for an infected wound and a failure to utilize optimal
techniques in pathogen isolation, especially for anaerobic organisms.
There is also a lack of an understanding of the pathogenic significance
of all cultured organisms. Gathering information and conducting
research in a more systematic and methodical fashion through an
organized research network, including zoos, veterinary practices, and
rural clinics and hospitals, are needed to better define the
microbiology of animal bite wound infections in humans.

PMID: 21482724 [PubMed - indexed for MEDLINE] PMCID: PMC3122494 Free
PMC Article

END QUOTES (and BTW, the microbiology of those bite wounds may have
info on the oral bacteria of the animals, too)

There are many microbiomes on beings in many places, from mouths, to
guts, to skins, to nasal membranes, and more (and plants also have
their microbiomes). In fact, by cell numbers we humans are more our
microbiomes than only ourselves which leads to the necessity to think
of any living being as actually an interactive community and how that
community can be perhaps adjusted for maximal health.

Sukie (not a vet) Ferrets make the world a game.

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

"All hail the procrastinators for they shall rule the world tomorrow."
(2010, Steve Crandall)

A nation is as free as the least within it.

[Posted in FML 7674]