F Rosa Rubicondior: Malevolent Design News - The Superbug, Clostridium Difficile (C. Diff), May Be Developing Resistance to Vancomycin - Design or Evolution?

Friday 26 April 2024

Malevolent Design News - The Superbug, Clostridium Difficile (C. Diff), May Be Developing Resistance to Vancomycin - Design or Evolution?


Treatment for Deadly Superbug C. diff May Be Weakening - University of Houston

The latest rabbit hole Michael J Behe has driven the creation cult into is the daft notion of 'Genetic Entropy'. This was introduced following the failure of the Discovery Institute to trick the courts in the USA into declaring that 'Intelligent [sic] Design' is real science and so should be foist on impressionable children in science class at taxpayers’ expense.

The notion of 'Genetic Entropy' plays on what used to be presented as an anti-evolution argument - the Second Law of Thermodynamics, which says that a closed system tends to disorder (increased entropy), so evolution can't increase order and complexity. This ignores the fact that Earth is not a closed system, of course, and relies on the scientific illiteracy of its target marks. And it looks nice and sciencey - something that creationists all crave while purporting to reject science.

So, Genetic Entropy starts off with the assumption that every species was created perfect and then, because Adam and Eve allowed 'Sin' to enter the world, these 'perfect' genes have been getting progressively less perfect. Now, this isn't Bible literalism, obviously, because that would make 'Genetic Entropy' religion, not science! Got it!

I posted this in an Evolution Vs Creation Facebook group. Creationists appear to be pretending not to have seen it.

The problem then is, how can increasing 'entropy' lead to greater fitness in a given environment? It can't of course because unlike the random process of mutation, there is no selective element which can produce more descendants from a worse genome, and unless it is getting worse, in what possible sense of the word can it be getting less perfect?

So, faced with something like increasing bacterial resistance to antibiotics, creationists in Michael J Behe's latest rabbit hole have only two ways to go. They can't argue that increased entropy is leading to an improved genome (from the perspective of the bacterium) because that would mean 'genetic entropy' is leading towards greater perfection. That then leaves them with the unenviable choice of design or evolution, and for design, read 'malevolence' because increasing antibiotic resistance increases the ability of the bacterium to make us sick, and any omniscient designer would know that.

IOW, Michael J Behe's attempt to resuscitate the Discovery Institute's flagging 'Wedge Strategy' has resulted in his fundamentalist cult having to choose between the twin 'evils' of blasphemy or evolution!

The latest twist in the evolutionary arms race between bacteria and human medical science is in the increasing weakness of the antibiotic of choice for Clostridium difficile (C. diff), vancomycin, against which C. diff appears to be developing resistance. This was discovered by researchers at the University of Houston College of Pharmacy, Texas, USA, who have just published their findings in the Journal Clinical Infectious Diseases, sadly behind a paywall with only the abstract available. However, their work is described in a University of Houston news release:
The antibiotic vancomycin, recommended as first-line treatment for infection caused by the deadly superbug C. difficile (C. diff), may not be living up to its promise, according to new research from the University of Houston College of Pharmacy. C. diff infection is the leading cause of death due to gastroenteritis in the U.S. It causes gastrointestinal symptoms ranging from diarrhea and abdominal pain to toxic megacolon, sepsis and death.

Based on 2018 clinical practice guidelines, the use of oral vancomycin has increased by 54% in the past six years, but the clinical cure rates have decreased from nearly 100% in the early 2000’s to around 70% in contemporary clinical trials.

Anne J. Gonzales-Luna, research assistant professor in the Department of Pharmacy Practice and Translational Research, UH College of Pharmacy, reports the weakening of vancomycin, the top antibiotic to combat the superbug C diff.

Despite the increasing prevalence of data showing reduced effectiveness of vancomycin, there is a significant lack of understanding regarding whether antimicrobial resistance to these strains may affect the clinical response to vancomycin therapy. In fact, the prevailing view has been that antibiotic resistance to these strains are unlikely to impact clinical outcomes, given the high concentrations of vancomycin in stools.

Research assistant professor Anne J. Gonzales-Luna, Co-corresponding author
Department of Pharmacy Practice and Translational Research
University of Houston College of Pharmacy, Houston, Tx, USA
But the team arrived at a different conclusion after sifting through research included in a multicenter study, which included adults treated with oral vancomycin between 2016-2021 for C. diff infection.

We found reduced vancomycin susceptibility in C. difficile was associated with lower 30-day sustained clinical response and lower 14-day initial cure rates in the studied patient cohort.

Research assistant professor Anne J. Gonzales-Luna.
The finding is cause for concern.

It’s an alarming development in the field of C. diff as there are only two recommended antibiotics. If antimicrobial resistance increases in both antibiotics, it will complicate the management of C. diff infection leading us back to a pre-antibiotic era.

Professor Kevin W. Garey, co-author
Department of Pharmacy Practice and Translational Research
University of Houston College of Pharmacy, Houston, Tx, USA
Others on the research team include Taryn A. Eubank from UH and Chetna Dureja and Julian G Hurdle from Texas A&M Health Science Center in Houston.
Abstract

Background
Epidemiologic studies have shown decreasing vancomycin susceptibility among clinical Clostridioides difficile isolates, but the impact on patient outcomes is unknown. We hypothesized that reduced vancomycin susceptibility would be associated with decreased rates of sustained clinical response (SCR).

Methods
This multicenter cohort study included adults with C. difficile infection (CDI) treated with oral vancomycin between 2016 and 2021. Clostridioides difficile isolates underwent agar dilution vancomycin susceptibility testing, ribotyping, and Sanger sequencing of the vancomycin resistance vanR gene. Reduced susceptibility was defined as vancomycin minimum inhibitory concentration (MIC) >2 μg/mL. The primary outcome was 30-day SCR; secondary outcomes were 14-day initial cure, 30-day recurrence, and 30-day mortality. Exploratory analysis assessed the association between the VanR Thr115Ala polymorphism, susceptibility, and outcomes.

Results
A high proportion (34% [102/300]) of C. difficile isolates exhibited reduced vancomycin susceptibility (range, 0.5–16 μg/mL; MIC50/90 = 2/4 μg/mL). Ribotype 027 accounted for the highest proportion (77.4% [41/53]) of isolates with reduced vancomycin susceptibility. Overall, 83% (249) of patients achieved 30-day SCR. Reduced vancomycin susceptibility was associated with lower rates of 30-day SCR (76% [78/102]) than vancomycin-susceptible strains (86% [171/198]; P = .031). A significantly lower rate of 14-day initial cure was also observed among individuals infected with strains with reduced vancomycin susceptibility (89% vs 96%; P = .04). Reduced susceptibility remained an independent predictor of 30-day SCR in multivariable modeling (odds ratio, 0.52 [95% confidence interval, .28–.97]; P = .04).

Conclusions
Reduced vancomycin susceptibility in C. difficile was associated with decreased odds of 30-day SCR and lower 14-day initial cure rates in the studied patient cohort.

Taryn A Eubank, Chetna Dureja, Kevin W Garey, Julian G Hurdle, Anne J Gonzales-Luna
Reduced Vancomycin Susceptibility in Clostridioides difficile Is Associated With Lower Rates of Initial Cure and Sustained Clinical Response
Clinical Infectious Diseases, 2024;, ciae087, https://doi.org/10.1093/cid/ciae087

© 2024 Oxford University Press.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.
The problem for creationists then, since we can rule out 'Genetic Entropy' as there is no mechanism whereby increased vancomycin resistance in C. diff would be inherited if it made C. diff less perfectly adapted than its predecessor, is: is this malevolent design (which keeps creationism's putative designer in the process) or evolution by a natural process in which no intelligence is involved?

I would suggest there is only one sane answer to this problem, regardless of what mummy and daddy believe, or what an imaginary mind-reading thug in the sky might do if you follow the logic.

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1 comment :

  1. Michael J. Behe continues to invoke the false belief of Original Sin of Adam and Eve which is a myth, and continues to insist that deadly microbes such as Clostridium were intelligently designed. The inevitable result of this theory is that the creator is malevolent, malicious, cruel, sadistic, evil. Why would anyone want to believe that? He has so much in common with Calvinists. Michael J Behe makes God responsible for Natural evil and the suffering and death that goes with it. This totally takes away God's omnibenevolence and takes away God's love and mercy. This doesn't bother him as he shamelessly continues insisting that horrible diseases were intelligently designed by God. That's the God of Michael J Behe and that's the repulsive, hypocritical Calvinist God. It's certainly not the loving all good, loving, merciful* omnibenevolent God taught to us in church. Michael J Behe and Calvinists worship an evil deity and don't realize it. They are unable to see the evil of their beliefs. Too bad.

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