My SciBling Mike the Mad Biologist, who is an expert on antibiotic resistance, has an interesting post about an "epidemic" of commensal E. coli. It seems (if I understand his post correctly) that there is not the genetic range of E. coli lineages in humans as in animals. About 20% of our gut E. coli comes from one of three clones. There is no apparent reason for this as the E. coli don't seem to have any features that make one better off than another. I have nothing to add to the basic observation, but I thought I'd use it to review some elementary microbiology, since we talk a lot about infectious disease here.
It's a matter of both fact and interest that all life seems to harbor other life. In fact all living animals are used as habitats for other organisms. Even protozoa and bacteria have their own parasites and invaders. And with evolution even more habitats have been created (if I may be so bold as to use the words "evolution" and "created" in the same sentence on ScienceBlogs). In fact warm-blooded, complex organisms like us provide some of the most nutritious, favorable and diverse environmental niches for other tiny creatures (microorganisms), and thus we have become heavily colonized. There are three broad ways organisms living closely together can relate to each other, called mutualism, commensalism and parasitism.
Mutualism is a relationship that provides reciprocal benefits to both species. It may even be necessary for one or both members. We are colonized by many microorganisms that synthesize amino acids essential for our life, in return for which we provide them a home. Parasitism resides at the opposite end of the spectrum. A parasite lives at the expense of its host. It is a relationship that benefits only one of the partners, harming the other one. The advantage to the parasite is it gets energy and nutrients at no cost and can therefore devote more energy and nutrients to its own reproduction. Viruses are exclusively parasitic. Lying between mutualism and parasitism is commensalism (literally, eats at the same table).
Commensals use the host's body as a home and they are usually harmless (if they become harmful, they are considered parasites, not commensals). Since they may incidentally produce metabolites useful to the host or make the host most vulnerable to parasites, there is a hazy line between mutualism on one side, and, parasitism, on the other. Our skin, lungs and intestines -- all parts "open" to the external world -- are home to myriads of commensal microbial species. We usually refer to them as our "normal flora." But these flora are only "normal" as long as they are commensals. If they start to hurt us they become parasites, the agents of disease.
This last point underlines something important. What we call a "disease organism" is really nothing of the kind. Being a disease organism refers to more than the organism alone but extends to the relationship of the organism to its host. Disease is a parasitic relationship and the same organism can be part of the normal flora in one person and a disease organism in another (e.g., in an immunocompromised person, where it would be called an opportunistic infection).
We are not born into original commensal sin. Prior to birth we are essentially sterile, free of microorganisms (at least that's the way I learned it; I'll bet someone is going to call me on this in the comments. That would be good. I'll learn something). When the newborn passes through the birth canal the skin becomes colonized and during the next few days so are the upper respiratory and gastrointestinal tracts. By the time we are adults we are colonized by an estimated 10
Among these colonizers is an organism in our gut called E. coli (full name Escherichia coli, named after a German pediatrician who first studied it in the 19th century, although he didn't discover it). It is a common organism in the environment and in the gut of all warm-blooded animals. Indeed its presence in a water sample is taken as presumptive evidence that the supply has been contaminated by the feces of a warmblooded animal and may therefore also be contaminated with other organisms that cause disease, like the agent of typhoid). E. coli isn't the most abundant organism in our intestines (I've seen estimates it is less than 5% of fecal matter) but it is one of the easiest to culture and has been studied for a long time. There are also E. coli variants that are not so nice to us as the usual commensal form and cause disease, usually diarrhea.
And it is this example of our normal flora that Mike the Mad Biologist was discussing in his post.
Go read it. He knows a lot more about these bugs than I do. And read the comments for the corrections I expect are already winging their way through hyperspace.
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Just to add, the estimated number of microorganisms in the human GI tract is between 1 and 10 trillion (10^9 - 10^10). They make up the largest proportion of the commensal species that we harbor.
Actually, the number is about 10^9 - 10^10 PER GRAM of colonic fluid (essentially feces) It varies quite a bit from the stomach through the small intestine. That's a lot of bugs! E.coli is easy to culture, but there are actually a lot more Bacteroidetes and Firmicutes in the gut than Enterobacteraceae (E. coli and relatives). Nice post - lots of work right now trying to figure out what all of these guys do (see Jeff Gordon's and Dave Relman's work on the roles of gut commensals in obesity and gut archaea in disease, respectively)
Paul: I've heard most of the spp. in the gut are difficult to culture (and yet to be identified) anaerobes. Is that true?
When I was a kid, we spent summers in a village on the shore of Lake Ontario that had no sewer system whatsoever. When the water level was low, we kids would stand on the dock and time the interval between the flush inside the building and the resulting flow from the pipe under the dock into the harbor.
Being kids, we often fell (or jumped) off of docks or out of boats into the harbor itself. Often the public beach to the east of the mouth of the harbor would be closed due to E. coli. I was told that E. coli itself wasn't dangerous, but it was an indication that other fecal-borne diseases might be present.
When people started dying from E. coli in meat, I wondered how I survived my childhood. I now understand that the lethal strain of E. coli is a relatively new development, one that was perhaps made possible by poor sanitation in cattle feedlots and the widespread use of antibiotics in livestock rearing. It makes sense to me, but I'm wondering if the connection between factory livestock and lethal E. coli has been researched or proven.
Susan: There are at least four enterotoxigenic or enteropathogenic mechanisms whereby certain strains of E. coli can cause disease. These strains have genetic information in them not possessed by ordinary strains. Most E. coli is a common and harmless commensal but some can attach to and ulcerate the gut wall or elaborate a toxin that causes diarrhea. The toxin can also initiate multi organ system damage and it is this kind of strain (as in O157H7, the "Jack in the Box" agent) that is especially dangerous (leading to hemolytic uremic syndrome in children). I haven't looked at the factory farm connection, but the organism can find its way to us by contaminating produce that has been contaminated by the gigantic amount of waste from these confined feedlot operations.
Revere: That's basically true. The density is derived from cell counts and 16S type culture independent analysis. However, anaerobe culture isn't that hard, so many have been grown in labs. It is a very interesting complex ecosystem. there are a number of disease issues packed into this topic, including chronic diseases and acute gastroenteritis.
Paul - you're right. I misremembered my numbers. The best estimates say that the gut contains 10^13 -10^14 microorganisms. Anyone know of estimates on how many more have colonized our skin, respiratory tract, etc.?
I've read that, by count, 90% of the cells in what I thnik of as 'my body' are not human - they're fungi, bacteria and other microorganisms. Human cells are mostly big but we're outnumbered in our own body.
Perhaps strong believers in democracy should reconsider before taking antibiotics or systemic funcicides - they might be more harm than good to the majority of cells present.
I know you're busy, Revere(s), but I have a question about e. coli 0157:H7 that I thought you might be able to answer.
I've been reading (and really enjoying) The Omnivore's Dilemma by Michael Pollan, which examines our food industry. He states that cows' rumens are normally pH neutral, but that feeding cows corn turns their rumens acidic, which leads to health problems like acidosis for the cows (p. 78). He goes on to state that turning cows rumens acidic also causes their microbes to evolve into ones that can survive that acidic environment, and hence our own acidic stomachs, leading to strains that cause illness and death in humans (p. 82).
He also notes antibiotic resistance due to the routine use of antibiotics in cattle, but this was the first I'd heard that the feed of cattle contributes to the problem of dangerous strains of e. coli (which get excreted in their manure, get on their skins, and thus in meat). Is he correct, do our stomach acids kill some strains?
Btw, he also says that one researcher has found you can reduce E. coli 0157:H7 in cattle up to 80% if you feed them grass for a few days before slaughter (presumably because it returns their rumens to a more neutral pH), but that this isn't considered practical by the industry (p. 82).
Caia: Don't know the answer to your question off the top of my head. My impression was that the corn feeding leads to the use of antibiotics but the main problem was on the resistance promoting side, not the survival of pathogens like O157. If I have time I'll look into it, as it is interesting. I have 3 manuscripts to review, a paper due next week, a journal to edit and a doctoral student who wants to defend in 4 weeks, my course to get ready for the fall, so I am up to my eyebrows. Then there's the blog . . .
Yes, according to Pollan, the antibiotics and other drugs are necessitated by the corn, but to hear him tell it, it sounds like the corn also has an effect on its own.
I only asked because I thought you might know off the top of your head, and say Pollan was flat wrong, which would obviously make me regard him a little more skeptically otherwise. Since you're not saying that, I'll continue to regard him as a reliable source. Please don't feel obligated to look anything up on my account.
You have enough to do, and we all (except maybe the trolls) appreciate all you do here.
caia: It was an interesting question. FWIW Pollan seems to me to be a journalist who does his homework.