Small Things Considered reports on a scientific finding that shows that antibiotic resistance in bacteria strains taken from soil samples is fairly common. Even though in some of these samples, they would be unlikely to have come into contact with man-made antibiotics. Testing 18 antibiotics from man-made and natural sources against 11 different samples, researchers did not find any sample that didn’t have bacteria that could metabolize at least 1 antibiotic.
Its an interesting find, which has implications for medicine and health, but is it surprising? I would tend to disagree. Given the rate that bacteria can evolve antibiotic resistance, it stands to reason that there should bacteria exist in nature that can metabolize them.
I quote Paul Orwin who left a comment in the above blog post:
I thought it was fairly clear that in the environment, there are lots of bacteria making antibiotics, and others that can break them down and/or resist them… I can’t see any way that this doesn’t affect clinical use of antibiotics. First, we know that there is plenty of movement of bacteria between soil and host organisms. Second, we know there is plenty of gene transfer going on in both environments. Therefore, there is a very high probability that within a soil microbial population, there is a potential pathogen (Burk and Pseudo being pretty strong contenders) that eats antibiotics for breakfast.
Pay special attention to where the creationist lies about how fossils are dated, while standing in front of a placard describing about how it actually works.
I feel sorry for these kids that are getting brainwashed. I can only hope that they, like the museum curator, will one day be able to draw their own conclusions based on empirical evidence.
This could provide a new area of evolutionary microbiology. Apparently, Campylobacter jejuni and Campylobacter coli trade so much genetic material via horizontal transfer, that the two species are merging.
So I’m giving a journal club presentation in about an hour (as of 6, when I started this) and I figured I’d write a quick blog post about it.
The urinary tract is a multi-organ system that opens to the external environment and, as a result is prone to infections from various pathogens. Approximately 50% of women will get at least one urinary tract infection (UTI) in their lifetime. Uropathogenic Escherichia coli (UPEC) is responsible for 80% of community acquired UTIs, so it is an important pathogen to study.
There are essentially four stages in the current UTI model. Attachment of UPEC to the walls of the urinary tract, invasion of host epithelial cells, replication within those cells, and exfoliation of the epithelial cells concurrunt with bacterial efflux.
My presentation is primarily concerned with the first stage of this process, namely attachment or adherence. UPEC adhesion to the cell wall is absolutely required for initiation of infection, which makes adhesins molecules attractive candidates to study, for the ultimate purpose of vaccine creation. In addition to initiating infection, adherence prevents mictruition, or the ‘washing out’ of UPEC by urine flow throughout the urinary tract. Another important factor is that these adhesin proteins can act as surface antigens and be recognized by the host immune system.
Evading immune response would then become a primary ‘goal’ of UPEC, from selection pressures from the immune system. There are several homologous types of adhesins, and each has various roles in the infection process. In a multi organ system, a bacteria may want to express different adhesins at different times. This would help the organism adapt to microenvironments and conserve resources by limiting coexpression. In addition this could help UPEC evade host immune response by ‘hiding’ key surface antigens. This is known as phase variation.
I’m primarily concerned with a specific adhesin known as pyelonephritis-associated pili (Pap). These pili bind to uroepithelial cells and are responsible for symptomatic UTIs. The expression is controlled by a single operon (promoter, operator, structural gene sequences). UPEC contain several homologous copies of this operon, which have variation in their function.
So, we know that phase variation can control the expression of analogous adhesins, because the gene expression is regulated by different mechanisms. But, homologous copies of the pap operon are controlled by the same mechanism, even though they can have slightly different functions. How can a bacterium control the expression of these different pap operons?
The answer lies in the their very sequence variation. Sequence variation in the genes that encode their epigenetic regulators is selected for. These variation changes the functioning of the epigenetic proteins so that the expression can be modulated or the gene activators turned off. The expression of some copies of the operon are favored, and this is selected for by the host immune system.
References:
Makrina Totsika, Scott A. Beatson, Nicola Holden, David L. Gally (2008) Regulatory interplay between pap operons in uropathogenic Escherichia coli , Molecular Microbiology 67 (5) , 996–1011
My father was diagnosed with early stage Lyme disease this morning, so in honor of him I want to talk a little bit about Borelia burgdorferi.
Lyme disease was described a few decades before the cause was known. The present form became studied after outbreaks occured in the area around Lyme, Connecticut, giving the disease its popular name.
B. burgdorferi is a spirochete bacteria, meaning that it has a helical coiled shape. It was first identified by Jorge Benanch, of the State University of New York at Stony Brook, who developed the first critical ELISA antibody test that could test for the presence of the bacteria. Dr. Benanch just so happens to also be the boss of my department and his wife was one of my high school biology teachers (now there’s something wikipedia can’t tell you). Soon after it was isolated by Willy Burgdorferi, for whom the bug was named.
The life cycle of Borrelia is interesting because they require ticks for transmission and mammals to feed on. Tick larvae become infected with Borrelia during the larvae or nymph stage when they feed on white-footed mice. Borrelia remains in the tick as it advances in its life cycle to adult. The adult ticks then feed on small mammals or humans, transmitting the spirochete where (in humans and dogs) it can become pathogenic. However adult ticks preferentially feed on white-tailed deer (no immediate relation to white-footed mouse) and is the source of the name ‘deer tick.’ The adult tick has to feed on deer blood for at least three days in order to be able to reproduce. Borrelia is nonpathogenic to deer.
This is an interesting commensal/parasitic relationship between these three organisms. The ticks rely on deer and Borrelia relies on the ticks. They are barely aware of the others existence, yet they have evolved together in a unique sort of hierarchy.
Taking Swansont’s lead, I’m declaring an annual Talk Like a Biologist Day. As far as I know, there is no such day already, so I’m going to take the initiative in saying that there needs be one. The date is as yet to be determined, but some possibilities are April 22nd (Earth Day) and July 18th (birthday of Robert Hooke, discoverer of the cell). Leave a comment if you like one of these two dates, or you would like to propose a different one. This is a collaborative work in progress, so don’t be shy.
So in order to talk like a biologist, you’ll need to become familiar with the jargon and how to use it in every day situations. Allow me to provide some examples and feel free to add your own.
Is something distracting you from getting your work done on time? Don’t worry, it’s not your fault, it’s just due to an “allosteric interaction.”
Any type of regular route is a “pathway.”
Don’t talk about how someone looks, but you should discuss their “phenotype.”
Tough day at the office? If you snap at your co-workers, blame it on negative “environmental stimuli”
If something is happening here, it’s “autonomic.” Far away is “somatic.”
Murdered your child in a fit of frustration? Don’t worry, just pass it off as “strategic infanticide.”
Don’t pick out your outfit this evening, “apply selection pressures” to your wardrobe.
You’re not over the hill, you’re just in the ’stationary phase’ of your growth.
Trying to leave work early? Tell your boss that due to the “high concentration” of employees, you’re “diffusing” out of the building and that attempting to stay would be “energetically unfavorable.”
Put “saccharides” in your coffee.
Try to “replicate your design information” with your significant other tonight.
While your at it, assure them that s/he has your “striated involuntary cardiac muscle tissue.’
Don’t touch anything today, but “probe” with your “receptors.”
Refer to household pets by using their binomial nomenclature, and don’t forget to refer to yourself as a “taxonomist.”
If you happen to be stacking objects today, make sure everyone knows that its a “nested hierarchy.”
Don’t forget to take it easy today. On Talk Like a Biologist Day, its important to “maintain homeostasis.”
Original ideas that categorized filamentous bacteria as the stressed and dying members of a population are apparently wrong. This is not a terribly unusual finding since scientists are always correcting ideas; assigning roles to presumably defunct systems and finding mechanisms for what were thought to be random processes.
Filamentation in bacteria occur when the cell continues to grow after its chromosomes have been copied, but the cell doesn’t divide. Filamentous cells are characterized by their elongated shape, which can be 10-50 times longer than normal. Certain bacteria have genes that encode proteins which can make alterations to cell length for the purpose of becoming filamentous, but random mutations can cause deletions in components controlling cell division with a similar affect.
My last few entries have relied on a specific idea that, given a group of non-kin cooperating individuals, the ability to cheaply coerce cheaters is unique to humans. This idea may be the strongest evidence we have for the evolution of human social and sexual behavior., according to this paper, by Dr. Paul M. Bingham.
When multiple remote killing animals kill or threaten simultaneously, they achieve an unexpectedly large decrease in the cost or risk of enforcing individual self-interest. This requirement for simultaneity means that this strategy is viable only when the common, congruent, and thus, cooperative self interests of large numbers of individuals are engaged.
Parabasis talks about a theories that evolutionary biologists have come up with to explain determined altruism.
Parabasis on the ‘Potlatch Effect’:
… you’re trying to destroy your enemies by engaging in a competition to outspend each other, using charity as the means to the end of their bankruptcy.
I share his skepticism of this theory. It does a messy job of explaining human behavior within the context of culture, because it seems to ignore ultimate causation of human culture.
“Global warming is going to get really bad in 30 or 40 years, mass starvation, the whole bit.”
“So? I won’t be alive for that. I’m already 72 years old.”
“but… you should care about your fellow man even if it doesn’t benefit you!”
“That’s a false emotional impression, left over from our ancient herd instinct. Surely you’re not saying that it’s ‘better’ to care about your fellow man than not to.”
“Of course I am! People will die if you don’t!”
“So you say it’s better that people live than die? Why?”
“It just is!”
I was shocked and disappointed. He believed in this invisible, unmeasurable force called “better” as much as he believed in man’s equally-unmeasurable ability to discern and act on the “better” thing and that “it just is” right do that “better” thing when given the chance. He believed in things science can’t quantify.
Wong comes up with some interesting ideas about determinism and the subjectivity of what we think of as fact. He points out that even ideas in which humans can find common ground are still not necessarily universal Truths. Commentary about what is ‘right’, ‘wrong’, ‘good’ or ‘bad’ about genocide or climate change are just as arbitrary as saying that ‘pizza is the best food.’
He says that these ideas are vestigial relics of our evolutionary history, from a time when people lived in herds and relied on each other for their direct survival.
However, these types of behaviors are not ‘vestigial’ and are just as applicable as our hunter/gathering days.
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