A Practical Medical Application of ID Theory (or, Darwinism as a Science-Stopper)
| December 9, 2007 | Posted by GilDodgen under Darwinism, Science |
In a previous UD thread, a dude named Poachy (where do these guys get these screen names?), with much sarcasm about a comment I made, proposed:
We need to start voting with our feet and eschew all but the medical advances that come from application of the ID paradigm.
Here’s a prediction and a potential medical application from ID theory: Design a chemical or protein which would require a triple CCC to defeat its toxic effects on a bacterium, and it will exhaust the probabilistic resources of blind-watchmaker mechanisms to counteract the toxic effects.
Such a success could and will only come from engineering and reverse-engineering efforts, not from Darwinian theory.
In the meantime, medical doctors should prescribe multiple antibiotics for all infections, since this will decrease the likelihood that infectious agents can develop resistance through stochastic processes. Had the nature of the limits of Darwinian processes been understood at the outset, the medical community would not have replaced one antibiotic with another in a serial fashion, but would have prescribed them in parallel.
This represents yet another catastrophic failure of Darwinian presumption, which is based on hopelessly out-of-date 19th century scientific naïveté.
90 Responses to A Practical Medical Application of ID Theory (or, Darwinism as a Science-Stopper)
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Corey,
I’m so sorry I missed your question on post #46:
Could you clarify what you mean when you say “bacteria. . . are apparently designed optimally.”
And then you give this following example to say that bacteria are not designed optimally:
For example, lets take the chemistry of the ?-lactamase that gives bacteria resistance to penicillins. It isn’t a damaged piece of the cellular machinery that stops penicillin from working, but rather it breaks the penicillin molecule down so that it can’t function. That is the bacteria doesn’t just throw out (or break) the piece of itself that penicillin is attacking. Using this enzyme it actually detoxifies the antibiotic.
This following site has your specific example listed:
http://www.answersingenesis.or.....lution.asp
Biologists mimic evolution in the lab?
of special note:
“This is evolution? The gene that produces ‘penicillin killer’ enzymes (TEM-1 ß-lactamase) easily mutates into different forms that break down a variety of antibiotic molecules. Hall was able to get eight bacterial cultures in his laboratory to ‘develop’ resistance to various antibiotics. In seven cases, bacteria in nature already had this resistance,”
Thus Corey it is not a novel molecular ability it is only the refining of a preexisting molecular ability that was present in the bacteria.
And to make matters worse for this “evolved” ability, once the antibiotic is removed from influencing the bacteria population, the “evolved bacteria population will soon be out-competed by its “parent” bacteria relatively quickly and return to a “normal” optimal population state.
As esteemed French scientist Pierre P. Grasse has stated “What is the use of their unceasing mutations, if they do not change? In sum, the mutations of bacteria are merely hereditary fluctuations around a median position; a swing to the right, a swing to the left, but no final evolutionary effect.” Needless to say, this limit to the variability of bacteria is extremely bad news for the naturalists.
This following site has some of the loss of functions listed for other bacteria/antibiotics
http://www.trueorigin.org/bacteria01.asp
of special note:
Antibiotic Phenotype Providing Resistance
Actinonin -Loss of enzyme activity
Ampicillin -SOS response halting cell division
Azithromycin -Loss of a regulatory protein
Chloramphenicol -Reduced formation of a porin or a regulatory protein
Ciprofloxacin -Loss of a porin or loss of a regulatory protein
Erythromycin -Reduced affinity to 23S rRNA or loss of a regulatory protein
Fluoroquinolones -Loss of affinity to gyrase
Imioenem -Reduced formation of a porin
Kanamycin -Reduced formation of a transport protein
Nalidixic Acid -Loss or inactivation of a regulatory protein
Rifampin -Loss of affinity to RNA polymerase
Streptomycin -Reduced affinity to 16S rRNA or reduction of transport activity
Tetracycline -Reduced formation of a porin or a regulatory protein
Zittermicin A -Loss of proton motive force
Hope I helped Corey.
Thanks for showing that part of the sentence twice, but we can see that he was saying that in this setting they were basically normal mice as far as their tests could tell.
If you’re interested in more of the implications of this study there was a good piece by Erika Check in Nature in September.
Corey,
Here is another quote from the scientists who conducted the study:
“The deletion of these elements likely has relatively mild effects on fitness that are gradually selected against over time — several or more generations from when they arise — but not on observable time scales.
Thus even the very scientists who conducted the study admit their test were not extensive.
We can speculate all we want, but the fact is that without extensive tests, conducted over several generations testing for offspring variability, as well as test testing for molecular robustness on the same time scale, establishing with 100% certainty that no fitness was lost at all in the deleted DNA mice, then the test is not substantial enough to establish a solid case for the radical front-loading mo^del and defeat the genetic entropy mo^del.
As with bacteria that show their true colors for genetic entropy when they are forced to change, I believe this mice will show their loss of information (Genetic Entropy) when forced to vary.
Depends on the organism and the clinical situation: if the organism is very susceptible to a low-toxicity antibiotic and the infection is not life or limb threatening one antibiotic is usually enough. If the infection is more serious, often two will still be used even after culture and sensitivities are back. A good example is MRSA, which my ID consultant always treats with two antibiotics.
This is correct. It usually takes at least 2-3 days for a culture to grow something identifiable, often longer. Sometimes you know there’s an infection but you can’t get a culture.
An example is a patient I’m consulting on right now who has pain in the hip and groin, an elevated white cell count and C-Reactive protein, and an MRI showing probable infection in the iliopsoas muscle, but with no abscess fluid to aspirate for culture.
Slicing the patient open just to get a piece of muscle to culture is not really practical or justifiable at this point so we’re just going to have to go with best guess. There is a history of a urinary tract infection with MRSA a few months ago so that is the most likely organism and so antibiotics will be aimed at that. If the person gets better we will never know what it really was. If not we will repeat the MRI and if there’s fluid we’ll try to get a needle into it for a culture specimen.
Thanks for taking the time to answer dacook.
I thought MRSA was resistant to multiple antibiotics. Is there something special (new) about the two antibiotics he uses to treat MRSA with?
That is pretty elegant. I hadn’t heard of that. I suspect the new Vanco will still be bad for ears and kidneys, however.
What would really be nice is if less toxic antibiotics like the Cephalosporins could also be modified to kill MRSA.
Dear Touchstone (or whoever you were here),
I apologize for any lapse of memory I had about the Fat Albert episode titled “The Hospital“. I was six years old when the episode in question first aired.
I also remember the Brady Bunch show airing an episode around that time on the exact same subject. It was probably a rerun when I first remember seeing it.
I remember these things even though I was fairly young at the time because I had chronic throat problems as a child, and my parents resisted contemporary medical advice to have me undergo a tonsillectomy. Being unable to afford the operation was a large contributing factor, I might add.
As for your accusation that I blame “the Devil” for this strangely recurring theme in family TV shows from 1971-1972, you can surely do better than stereotyping your opponents as Bible-thumping ignoramuses (though I shouldn’t expect you to do so). I don’t need to go to supernatural explanations when good old greed and Bernaysian brainwashing will suffice.
Also, in the little time I had to research it, I found at least one recent source (anecdotal, sure, but from an M.D.) about the frequency of and reasoning behind tonsillectomies in the 1970s.
Another much older medical source (from 1917, when Darwinists were a little less shy and politically correct) states in very bold terms the exact attitude I was alluding to.
Before you launch into another stereotypical attack, yes, I support surgery when it is necessary. Even things like arms and legs should be removed if their existence is killing the person attached to them. What I don’t support is writing off a body part as worthless and having it removed because of a little discomfort. Especially if it’s for profit’s sake.
MRSA is obnoxious because it is resistant to not only Methicillin and its cousins (Nafcillin, Oxacillin etc.) but to the whole class of Cephalosporins (Keflex, Ceclor et.al.)
The standard antibiotic used against MRSA is Vancomycin, which has been around a long time and is potentially quite toxic, has to be given IV (except for GI Clostridia which is another issue), has to be monitored and is risky and is just generally a pain to use if you don’t have to.
Even back when I was in medical school and MRSA was rare there was concern that it would acquire Vancomycin resistance from enterocci, which are common in the gut, and commonly resistant to Vanco. There now exist some strains of Staph resistant to Vancomycin. A Staph that learned to be resistant to both Vanco and Methicillin would really be a problem.
The antibiotic that’s usually used in addition to Vanco is actually a combination of Trimethoprim and Sulfamethoxazole (brand names Bactrim or Septra). This is also an old drug, which has been used for UTIs (urinary tract infections) for decades.
One of the reasons to use two Abx is a double attack to make sure the dang bug dies before it learns to be resistant to anything else, especially Vanco. Also to get it under control quicker than Vanco may be able to do alone before its toxicity kicks in.
Thanks Dacook,
I looked up Vancomycin and it appears scientists have been tweaking it, trying to make it resistant proof.
http://pubs.acs.org/cen/news/84/i07/8407notw8.html
Vancomycin Redesigned
of special note:
Vancomycin works as an antibiotic by binding to a peptidoglycan that is essential to the biosynthesis of bacterial cell walls. The most common form of resistance is due to a modification that changes a peptidoglycan amino acid from d-alanine to d-lactate. This mutation greatly reduces the affinity of vancomycin for the peptidoglycan, rendering it ineffective.
Crowley and Boger compensated with a comparably simple change to vancomycin. They synthesized an analog in which a carbonyl group positioned deep inside the vancomycin molecule has been converted to a methylene. This replacement enhances the compound’s binding affinity for the modified peptidoglycan in vancomycin-resistant bacteria yet preserves a substantial amount of the antibiotic’s affinity for the normal peptidoglycan in vancomycin-sensitive bacteria. The analog is thus 100-fold more active than vancomycin against vancomycin-resistant bacteria but only 3% as active as the against vancomycin-sensitive bacteria.
This is really exciting dacook in that they targeted the actual molecule that had mutated and compensated the binding for the mutation that prevented interaction with vancomycin. This is really taking the battle to the bug I would say!
bornagain77 (62): I will have to look deeper into this, and make sure I have all my bases covered…
From “Cichlids of the Rift Lakes” by Melanie L. J. Striassny and Axel Meyer, Scientific American, February 1999:
Thanks a lot J;
That study goes well with this study:
2006 The Royal Society
African cichlid fish: a system in adaptive radiation research
http://www.pubmedcentral.nih.g.....id=1635482
It seems that when these two studies are stripped of their evolutionary garbage, they will be a key piece of proof that will verify the ID/Genetic Entropy , maybe even enough proof to show that environmental cues are providing the primary mechanism for the rapid adaptive radiation from a parent species. As well, the rate of accumulated mutations (Genetic Entropy), if nailed down, could explain the much older lakes much larger divergence of genetic diversity, as well as explaining the lack of the ability of the “older” species in the older lake to radiate. (note; genetic diversity of the younger lakes cichlids is shown to be much less than the older lakes cichlids)
It may now even be possible to prove when the ID was implemented, whether at one time or whether at separate times for the cichlids and at what approximate time/times.
It looks like it will be a bit of a project, to get all the data straight from all the studies listed.
Just for the entertainment value, I checked out the Panda response to my post. I seem to have a penchant for arousing their ire and vitriol, and I can explain why.
If my UD posts were as scientifically and logically vacuous as the Pandas claim, no response would be required, but they seem to have a passion for devoting both tomes and insults to refuting my arguments. I am perpetually labeled as being completely ignorant about science (even though empirically verifiable science is what I do every day for a living). Yet, whenever I post an incisive comment about the empirical, observational, mathematical, or computational problems with blind-watchmaker Darwinism, the Pandas go into a feeding frenzy.
I’ve struck a nerve. The personal insults and claims that I know nothing about science are very telling.
dacook you ask,
What would really be nice is if less toxic antibiotics like the Cephalosporins could also be modified to kill MRSA.
Looks like someone has already thought the same thing dacook,
Action of New Cephalosporin Antibiotics Effective Against MRSA & VRSA
http://tahilla.typepad.com/mrs.....index.html
of special note:
Three cephalosporins (compounds 1–3) have been studied herein, which show antibacterial activities against MRSA, including the clinically important vancomycin-resistant strains….These cephalosporins exhibit substantially smaller dissociation constants for the preacylation complex compared with the case of typical cephalosporins, but their pseudo-second-order rate constants for encounter with PBP 2a (k2/Ks) are not very large (?200 M–1 s–1). It is documented herein that these cephalosporins facilitate a conformational change in PBP 2a, a process that is enhanced in the presence of a synthetic surrogate for cell wall, resulting in increases in the k2/Ks parameter and in more facile enzyme inhibition. These findings argue that the novel cephalosporins are able to co-opt interactions between PBP 2a and the cell wall in gaining access to the active site in the inhibition process, a set of events that leads to effective inhibition of PBP 2a and the attendant of the MRSA strains.
Do you think this may be of help for you dacook?
dacook you ask,
What would really be nice is if less toxic antibiotics like the Cephalosporins could also be modified to kill MRSA.
Looks like someone has already thought the same thing dacook,
Action of New Cephalosporin Antibiotics Effective Against MRSA & VRSA
http://tahilla.typepad.com/mrs.....index.html
of special note:
Three cephalosporins (compounds 1–3) have been studied herein, which show antibacterial activities against MRSA, including the clinically important vancomycin-resistant strains….These cephalosporins exhibit substantially smaller dissociation constants for the preacylation complex compared with the case of typical cephalosporins, but their pseudo-second-order rate constants for encounter with PBP 2a (k2/Ks) are not very large (?200 M–1 s–1). It is documented herein that these cephalosporins facilitate a conformational change in PBP 2a, a process that is enhanced in the presence of a synthetic surrogate for cell wall, resulting in increases in the k2/Ks parameter and in more facile enzyme inhibition. These findings argue that the novel cephalosporins are able to co-opt interactions between PBP 2a and the cell wall in gaining access to the active site in the inhibition process, a set of events that leads to effective inhibition of PBP 2a and the attendant of the MRSA strains.
Do you think this may be of help for you dacook?
dacook you ask,
What would really be nice is if less toxic antibiotics like the Cephalosporins could also be modified to kill MRSA.
Looks like someone has already thought the same thing dacook,
Action of New Cephalosporin Antibiotics Effective Against MRSA & VRSA
http://tahilla.typepad.com/mrs.....index.html
of special note:
Three cephalosporins (compounds 1–3) have been studied herein, which show antibacterial activities against MRSA, including the clinically important vancomycin-resistant strains….These cephalosporins exhibit substantially smaller dissociation constants for the preacylation complex compared with the case of typical cephalosporins, but their pseudo-second-order rate constants for encounter with PBP 2a (k2/Ks) are not very large (?200 M–1 s–1). It is documented herein that these cephalosporins facilitate a conformational change in PBP 2a, a process that is enhanced in the presence of a synthetic surrogate for cell wall, resulting in increases in the k2/Ks parameter and in more facile enzyme inhibition. These findings argue that the novel cephalosporins are able to co-opt interactions between PBP 2a and the cell wall in gaining access to the active site in the inhibition process, a set of events that leads to effective inhibition of PBP 2a and the attendant of the MRSA strains.
Do you think this may be of help for you dacook?
OOPS, sorry for the 3 time repeat Gil
Correction dacook,
the last sentence should read:
“,a set of events that leads to effective inhibition of PBP 2a and the attendant kil^ling of the MRSA strains.”
If my UD posts were as scientifically and logically vacuous as the Pandas claim, no response would be required, but they seem to have a passion for devoting both tomes and insults to refuting my arguments.
While I agree with the substance of your original post (I think we should put antibiotics in the water – let’s defeat the germs *before* they infect us).
I don’t agree with the statement you wrote above here. By that logic, we could just ignore everything the Darwinists say. If logic is wrong, we should point it out to people.
That said, I’m pretty sure the Panda people (where are they? are they science teachers?) would be wrong to criticize you. As you say, you’re a scientist. What the hell do they know? They’re probably just high school science teachers (and we all know how much an education degree is worth).
J,
In this following study they (the evolutionists) puzzle over several lines of evidence. Evidence which happens to fit the ID/Genetic Entropy mo^del very well, As well the environmental cues of the ID provide the missing primary driving mechanism at the genetic level for rapid speciation that is grossly and insufficiently explained by natural selection of neo-Darwinism.
http://golab.unl.edu/publicati.....s_JME.html
Of special note:
Neotropical (south american) cichlids might have experienced lower rates of extinction and speciation than their African counterparts, preserving primitive characteristics and thereby accumulating higher levels of genetic divergence in some of these lineages.
also of note;
However, this rapid speciation rate is not correlated with high genetic divergence, since African cichlids are known to exhibit an overall low amount of genetic variation (e.g., Meyer et al. 1990). Recently, Zardoya et al. (1996) found twice as much variation at a nuclear marker (TmoM27) among South American than African cichlids. Our path length analysis and relative rate tests confirm this finding based on nuclear DNA that, although considerably less speciose than their African counterparts, the Neotropical cichlids are extremely more variable at the molecular level. The rate of nucleotide divergence at the 16S mitochondrial fragment in Neotropical cichlids was significantly higher than in the African lineages (Fig. 4). However, the rate acceleration was only significantly higher among geophagines.
Hmm, Yet again no explanation from neo-Darwinism, indeed not even a viable mechnism, but it fits easily into our nascent mod^el.
I asked a physician and pathologist about this.
Multiple “shotgun doses” of antibiotics is not economically sound, or chemically efficient. Not efficient as the interactions of using several at once can be dangerous to some people, and not likely to do what you want in the first place, as even without dangerous mixes, one antibiotic can take over the task at hand and leave the others impotent.
Drug interaction is a nasty risk. Just ask your local pharmacist too.
ellazimm
I think that Intelligent Design proponents and Creationists should have an equil opportunity to defend themselves in tax funded public schools. ID proponents and creationists are quite right to ask evolutionists and comitted naturalists to support their statements in public schools by exposing students to opposing sides of the issue instead of using lies and unscientifically brainwashing them with one side and censoring all others using stolen tax dollars. ID proponents and creationists are quite right when they demand that students should be allowed to see the pros and cons of opposing sides and choose for themselves what to believe.
http://www.pandasthumb.org/arc.....he-nc.html
When the people at the pandas thumb stop resorting to using strawman and dishonestly taking people out of context then we’ll talk.
http://www.pandasthumb.org/arc.....he-nc.html
I still don’t get why evolutionists and/or committed naturalists insist on using such dishonest tactics to persuade others to believe their message? Why? Why is their first instinct to resort to dishonesty? Wy can’t they just be honest? You see, the honest thing to do would be allow students to be exposed to opposing sides of the issue. Instead, they resort to dishonestly taking people out of context. This is supposed to be scientific? Does science endorse this kind of dishonesty? It sure seems like many naturalists do.
George DW, @ 50
Re sickle cell anaemia, you wrote
I would say indicative of devolution, or loss of information, rather than adaptation. People with sickle cell anaemia have abnormal haemoglobin (HbS) that sticks together under conditions of low oxygen concentration or dehydration. This deforms the red cell and makes its surface rigid. Apart from making the cell useless for oxygen transport it also makes it hard for cells to pass through fine capillaries so they get blocked and the tissue downstream dies.
The disease is a problem for malaria parasites because they can’t colonise sickled red cells. It is a worse problem for homozygous carriers of the mutation who are sick, off an on, for all of their short lives. See the Wikipedia article.
Others, re design of antibiotics,
I’m rather impressed with the design of the drug known as “Augmentin”. It’s a combination of clavulanic acid and amoxycillin. The clavulinic acid binds irreversibly to the beta-lactamase enzymes that inactivate other penicillin-derived antibiotics and this allows the amoxycillin to do its job.
Also I don’t think we should be surprised that something as fundamental to bacterial survival as their cell walls would be protected by (I believe, designed) mechanisms of some sort. How we use antibiotics comes down to stewardship with the problem being that we, being greedy, are quite bad at that.
Janice you stated:
“The clavulinic acid binds irreversibly to the beta-lactamase enzymes that inactivate other penicillin-derived antibiotics and this allows the amoxycillin to do its job.”
I have to say I am really impressed with this. This is really taking the fight to the bug!
Do you know of any sites that give a little background on how the antibiotic was developed and who was responsible for developing such a wonderful and specific response to bacterial resistance?
This is interesting Janice and Dacook;
Princeton scientists break cholera’s lines of communication
http://www.eurekalert.org/pub_.....111407.php
Breakthrough research suggests a way to fight bacteria without Antibiotics
http://isuman.blogspot.com/200.....ay-to.html
I wonder if this technique could be used as a “stand alone” method for fighting all types of bacterial infections or if it could at least be used in conjunction with current treatments to make them more effective in fighting infection?
bornagain77:
That’s interesting stuff you’ve found. I’ll have to look at it in more detail, especially about the Cephalosporins.
It will be a challenge to test those against MRSA because they are notorious for looking like they’re killing the bacteria in vitro but then not working in vivo.
My patient with the presumed MRSA is improving on Vanco and Levaquin.
I’m really beginning to think these cichlids should become the poster child for the front loaded portion of the ID theory:
Multiple Genes Permit Closely Related Fish Species To Mix And Match Their Color Vision
http://www.sciencedaily.com/re.....072648.htm
of special note:
In the new work, the researchers performed physiological and molecular genetic analyses of color vision in cichlid fish from Lake Malawi and demonstrated that differences in color vision between closely related species arise from individual species’ using different subsets of distinct visual pigments. The scientists showed that although an unexpectedly large group of these visual pigments are available to all the species, each expresses the pigments selectively, and in an individual way, resulting in differences in how the visual world is sensed.
The researchers identified a total of seven “cone” (color-sensing) visual pigments underlying color vision in these cichlids. They have measured the sensitivities of the cones to different wavelengths of light and isolated the seven genes that give rise to the pigment proteins. The seven cone types have maximum sensitivities ranging from the red end of the spectrum right through to the ultraviolet–light outside the range of human sensitivity. The researchers showed that in order to tune its color vision, each cichlid species primarily expresses three of the seven cone pigment genes encoded by their genomes.
It is not clear why such closely related cichlid species have evolved such different visual sensitivities,
I don’t know what they think but this example is screaming front loading to me.
The cichlid “speciation” data clearly implies a few things:
- As admitted in the Sci Am article, it’s obviously not due to the typical Darwinian random variation + natural selection scheme.
- It doesn’t qualify as true speciation as everyone understands it — it’s simply variation. (The genetic variability in hundreds of cichlid “species” is less than that of the (single) human species.)
- The variability appears to be due to activation of genetic “programs” that are already present in the genomes of the cichlids. (Apparently, the cichlids have a branching genome, with heritable switches that can be set to steer development along certain genetic pathways, depending upon the environment.)
I agree that cichlids epitomize the concept of front loading. The question (beyond the scope of ID theory, per se) is how the front loaded information got into them. Were the first front-loaded cichlid gametes fabricated by an intelligent agent and set loose into the lakes of Gondwanaland? Or did the information in their genomes evolve over time?
There is, as you know, no evidence that Darwinian evolution is feasible. (There has never been a demonstration that nonteleological evolution results in any kind of functioning, so it’s silly for anyone to propose that as an explanation of how the cichlids came to “feed on other fish or on eggs and larvae, to nip off fins, scrape algae, tear off scales, crush mollusks or any of myriad other functions.”) But teleological evolution — in a system designed for evolution, and with a driving purpose built in — has been shown viable by (intelligently designed) evolutionary computation.
If the information did evolve (teleologically), then the next question is: How did numerous such “programs” wind up in a single genome? Logically, it would seem that there are only the following possibilities:
- The programs evolved independently, in different lineages, and were brought together through recombination(?), without obliterating the (temporarily) unused programs — somehow.
- The pathways evolved serially in one lineage, without obliterating the previously evolved programs — somehow.
- A combination of these two occurred.
J,
As you know the evidence for cichlids is just starting to come in. So we have much left to learn. Yet we already know several things are likely.
The older lakes will have several sub-species of cichlids that have lost the functionality of their unused cones as they became more “reproductively isolated” through time. This will be due to the principle of Genetic Entropy. Much like the cave dwelling spiders, scorpions etc..etc.. have lost their ability to see.
We already know that the older lakes cichlids have more genetic diversity than the younger lakes. We also know the younger lakes’ cichlids radiated from a more “ancient” lineage of cichlids.
This all conforms to ID/Genetic Entropy. Thus we can predict that the greater genetic diversity is due to the fact that the deleterious mutational load has built up in the older lakes sub-species at a substantial (and constant?) rate.
We can do repeatable experiments that come directly from the ID/Genetic Entropy mo^del, Using consistent environmental cues, The parent species will have a greater propensity for consistent adaptive radiation. Thus ruling out any “random” variation producing the consistent adaptive radiation and validating the Front-Loaded portion of ID.
Intense genetic study of cichlids may even find markers that tell us many useful genetic markers for when the genome is vibrant and when it has been subject to Genetic Entropy.
dacook #87,
“That’s interesting stuff you’ve found. I’ll have to look at it in more detail, especially about the Cephalosporins.
“It will be a challenge to test those against MRSA because they are notorious for looking like they’re the bacteria in vitro but then not working in vivo.
My patient with the presumed MRSA is improving on Vanco and Levaquin.”
Please let me know if you find anything interesting, I would really like to know if this line of research is panning out.
As well, I am glad your patient is responding well to treatment.