http://www.enn.com/today.html?id=11465

I don’t know if this affects other readers, but I unconsciously index stories visually and seeing the same photo on a later story confused my mental timeline quite a bit.

It’s surprising to me, but I was completely disoriented when I saw that familiar photo of cells. I didn’t know what day it was or where in your string of RSS articles I was suddenly transported, but I knew that photo was familiar and the fact that it was familiar was what was disorienting.

Just FYI, another of those annoying “user interface” issues to think about. I wouldn’t think to annoy you with this, except that I absolutely love your blog and figure that you care about such things.

The article you have cited is well worth reading, and I will be adding it to my collection. My primary interest is in how things evolve – and this is definitely down my alley.

Incidentally, I have also posted “links” on Tara Smith’s blog since she is also writing pieces on this subject.

Please see:

http://scienceblogs.com/aetiology/2006/09/the_e_coli_mystery_deepens.php

I myself will be keeping an eye on both blogs as there is bound to be some interesting material of significance which goes well beyond the current outbreak.

The evolution of O157:H7 is pretty interesting I think, and some recent work is starting to reveal the genetic basis of the evolved pathogenic phenotype:

http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=1064018

Escherichia coli O157:H7 is not the E. Coli i know and love.

Nevertheless, obviously we are having problems with the misuse of antibiotics which is resulting in strains of bacteria which are resistant to antibiotics and the genes for such resistance are being transmitted by other phages. This is why putting antibiotics into cattle carcasses is a bad idea and why putting it into feed is probably a bad idea as well. In essence, bacteria have established a kind of small-world network reminiscent of the “Six Degrees to Kevin Bacon,” in which it takes relatively few steps to get from any one part of the network to any other – given the structure of the network and use of centralized hubs. In some case, the phages which infect different species of bacteria are even able to reach across biome boundaries – from the ocean into the soil.

It would appear that one of those hubs may be in the soil itself. Of course, this sort of network isn’t something which has sprung up only since the introduction of antibiotics by humans. It has been there for a very long time, providing phages with hosts to infect and bacteria with genes with which to adapt to a changing world. Interestingly enough, we are also sometimes finding that bacteria are resistant to some antibiotics before they ever reach the market. It appears that some strains of bacteria will produce antibiotics for use against other strains of bacteria which will respond by developing resistance. Thus when we introduce an antibiotic which is sufficiently similar to antibiotics already in use in nature, some bacteria may already be resistant.

Incidentally, understanding this provides us with a certain edge. Some companies creating new antibiotics will test them against the strains of bacteria found in soil to see whether they already have a degree of resistance. If they do, the company will know to hold off on mass-production until they come up with something else.

One more point which may be of some interest: many of the genes and pathways of pathogenicity which the bacteria use against their multicellular hosts also seem to have been around for a very long time. In some cases, they are using essentially the same mechanisms against us as they were using against our single-celled ancestors and continue to use against single-celled eukaryotes today.

The phage lysis response is classic temperate phage behavior. The lysis/lysogeny switch (best studied in lambda) is triggered by DNA damage or increased activity of DNA repair enzymes.

Exotoxins of Staphylococcus aureus
CLINICAL MICROBIOLOGY REVIEWS, Jan. 2000, p. 16

I spoke too soon. I just checked the talk origins thread, and “Jerry Sparks” has identified the filthy cause of the squirrel’s condition.
http://botfly.ifas.ufl.edu/abotfly/overview.htm

Again, my apologies to Carl for cluttering his blog.

Oh, I know, and my sincerest apologies.
… but for the moment at least, I would prefer to focus on something I find far more cheery, like phages, e coli, or for that matter, the bubonic plague.

That’s why I posted. I feared something like that had crept up in my front yard, and might have a scientist identify the condition, as many do frequent this blog. I was unsure who to contact, that could answer… As for your outside reference, I had not even considered, scienceblogs.com does have numerous science experts working with them, perhaps there is one available that can identify diseases or ailments in animals, in the future.

Again, the squirrel took me by surprise, and my apologies for panicking.

The squirrel was a bit off topic, although not necessarily that far off, but the passages from the Bible is much more of a reach. What you are bringing up is simply the traditional problem of evil – which more a problem in theology than biology. With respect to the creationists, it is not their belief in Christianity which is a problem, but rather their extremist views which they would seek to impose upon the rest of society, eventually as part of a theocracy. For those who have any doubts in this regard, I would recommend looking up the Reconstructionists/Dominionists – and remind them that Howard Ahmanson (probably the largest benefactor of the Discovery Institute) was a board member of the Chalcedon Foundation – a leading organization within this movement.

For more on the Reconstructionists, there was a fairly recent post (a few weeks back) on ScienceBlogs a few weeks back which could serve as an introduction:

Dispatches from the Culture Wars: A Weak Defense of Reconstructionism
Category: Theocracy
Posted on: August 23, 2006 9:24 AM, by Ed Brayton
http://scienceblogs.com/dispatches/2006/08/a_weak_defense_of_reconstructi.php

… but for the moment at least, I would prefer to focus on something I find far more cheery, like phages, e coli, or for that matter, the bubonic plague.

I tried the talk origins group to identify what was wrong with the squirrel, and “Klaus” responded, “It looks like a grey squirrel that survived a serious injury… massive scar tissue on its back.” in alt.med.veterinary, Susan responded about a pet fox which was attacked, “She lost all fur in that spot forever and it had the same appearance of your squirrels problem. Those nodules remind me of when I cut my wrist on an aquarium. The wound healed but a nasty, painful nodule formed due to the trauma… a friend with open heart surgery had the same nodules running up and down the incision area. Could the squirrel have been attacked (cat, hawk, whatever)..? Not a clue but that would be the most likely area a predator would grab.”

It’s probably an old nasty injury as they both suggested.

This presents a question for Creationists,
Lk:12:24: Consider the ravens: for they neither sow nor reap; which neither have storehouse nor barn; and God feedeth them: how much more are ye better than the fowls?
Lk:12:7: But even the very hairs of your head are all numbered. Fear not therefore: ye are of more value than many sparrows.

The young lions roar after their prey, and seek their meat from the Lord…[What if that "meat" is a Christian in a Roman arena? ? Skip Church]…Oh Lord, how manifold are thy works! In wisdom hast thou made them all…both small and great beasts… These all wait upon thee; that thou may give them their meat in due season.
- Psalm 104

Speaking of how well “the Lord” “satisfies the desire of every living thing,” let’s take “the young ravens which cry” as a prime example. A recent study showed that one-third of adult birds and four-fifths of their offspring die of starvation every year (David Lack, “Of Birds and Men,” New Scientist, Jan., 1996). Not surprising, since birds have to eat from one-quarter to one-half their body weight daily, so starvation is a common killer of birds.
-Skip

This creator has time to count hairs, and “feed the ravens”, part of the time. But no time to heal their wounds. No, the creator is too busy “intelligently designing” bigger and better tooth and claw and the arms race goes on … “better to see you with, better to hear you with, better to EAT YOU with.”

Carl, my apologies again for my tactless interuption

An Extracellular Darwinian Experiment with a Self-Duplicating Nucleic Acid Molecule
D. R. Mills, R. L. Peterson, and S. Spiegelman
Communicated May 18, 1967
PNAS 1967; 58: 217-224.
http://www.pnas.org/cgi/reprint/58/1/217

Evidence for De Novo Production of Self-Replicating and Environmentally
Adapted RNA Structures by Bacteriophage Q3 Replicase
Manfred Sumper and Rudiger Luce
Proc. Nat. Acad. Sci. USA
Vol. 72, No. 1, pp. 162-166, January 1975
Communicated by Manfred Eigen, October 11, 1974
http://www.pnas.org/cgi/reprint/72/1/162

Enjoy!

PS I sent in links some other more directly relevant articles, but the blog mistook them for spam and is holding them for the moment.

Reviews
Ecological fitness, genomic islands and bacterial pathogenicity
A Darwinian view of the evolution of microbes
J�rg Hackera and Elisabeth Carniel
EMBO reports 2, 5, 376-381 (2001)
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1083891

From the article:

“Fitness islands can be subdivided into different subsets, depending on the life-style of the microbe (its niche) (Figure 3), rather than on the intrinsic composition of the islands. Fitness islands that help microorganisms to live in the environment or to persist as saprophytes in a host may be considered ‘ecological islands’ and ‘saprophytic islands’, respectively. Other bacteria reside temporarily or permanently in a host (another microorganism, a plant or an animal), where they either provide some benefits to the host-organism (symbiont) or cause damage to it (pathogen). Accordingly, a ‘symbiosis island’ is a specific type of fitness island that helps bacteria to positively interact with their hosts, while a fitness island that participates directly or indirectly in the induction of lesions is a true pathogenicity island.”

Evolving Insights: Symbiosis Islands and Horizontal Gene Transfer
Turlough M. Finan
J Bacteriol. 2002 June; 184(11): 2855-2856.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=135049

Then here are two more reviews, the first of which is a real classic on the modularity of phages…

Evolutionary relationships among diverse bacteriophages and prophages: All the world’s a phage
Roger W. Hendrix, et al.
PNAS | March 2, 1999 | Vol. 96, no. 5 | 2192-2197
http://www.pnas.org/cgi/content/full/96/5/2192

Phages and the Evolution of Bacterial Pathogens: from Genomic Rearrangements to Lysogenic Conversion
Harald Br�ssow, Carlos Canchaya, and Wolf-Dietrich Hardt
Microbiology and Molecular Biology Reviews, September 2004, p. 560-602, Vol. 68, No. 3
http://mmbr.asm.org/cgi/content/full/68/3/560

Tim–The phages in O157:H7 are particularly weird, since they carry the toxin genes. That’s why you can’t give antibiotics for this strain. The phages sense the stress and break out, producing toxins.

I find it interesting that the phages become lytic (destroying the bacteria, and thereby spreading their virons to other bacteria) when it would seem that they are normally temperate, particularly as there still exists in many circles the view that viruses (and therefore phages) aren’t really alive since they have no innate metabolism. With respect to the gene for iron uptake, this is of course part of a pathogenicity island, but within a different ecological niche (outside of the prokaryote’s current host or within a different prokaryote) would simply be a metabolic island.

Here is one older technical article which deals with this sort of thing that I ran across within the past few weeks (for those who are interested):

A Genomic Island, Termed High-Pathogenicity Island, Is Present in Certain Non-O157 Shiga Toxin-Producing Escherichia coli Clonal Lineages
H. Karch, et al.
Infection and Immunity, November 1999, p. 5994-6001, Vol. 67, No. 11
http://iai.asm.org/cgi/content/full/67/11/5994

“The genomic islands may contribute to the fitness (fitness islands) or metabolic flexibility (metabolic islands) of the organisms, or they may increase their pathogenic potential (PAIs). The particular function of an island will thus depend strongly on the genetic background of the individual strains. Further experiments are necessary in order to define the exact role of the HPI element in the life cycle of STEC strains.”

Carl, this is a beautiful essay, that describes O157:H7 very nicely. The issue of species in bacteria is a tough one; Shigella is considered by classical microbiologists as a separate species, but is very, very close to E. coli metabolically, physiologically, and genomically. O157:H7 and K12 are at least as different as either one and Shigella, at least in some ways. We tend to use old metabolic keystones to type bacterial strains and species, and old habits die hard…

I believe the genes used by E. coli to form the Type III pathway have been shown to have originated from Yersinia pestis (bubonic plague), at least their sequence similarity is high enough to support this hypothesis. Thus, E. coli acquired these genes ‘across the species barrier’.