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]