Let's pretend the Intelligent Design hoax is real and that everything that happens in nature is by design.
I'm afraid we'll have to drop the nonsensical stuff about this designer being benevolent or even particularly anthropophilic though, because the facts just don't sustain that notion at all, even if we bend over backwards to accommodate the notion of Intelligent Design by ignoring so much evidence. Some mental acrobatics require a mental agility that results in too many strains and breakages for comfort.
Okay, so now we need to try to fit some real-world facts into our fantasy world with its magic invisible designer in which nothing happens except by this designer's design and omniscient intent. Let's try to fit the findings of this team who were investigating some bacteria who have developed resistance to our human-designed antibiotics into this Intelligent Design fantasy:
For those not familiar with the story so far: the Intelligent Designer designed lots of bacteria for making humans ill (as I said we have to abandon notions of benevolence) so human scientists tried to find substances to make us better or avoid becoming ill in the first place, and invented antibiotics.
But the Intelligent designer found a way to beat humans and redesigned some bacteria so they were resistant to these antibiotics, so humans had to invent so more. The Intelligent designer then made his bacteria resistant to those too. This went on for many years until we now have lots of bacteria that are resistant to lots of antibiotics and humans have run out of new antibiotics, so it looked like the Intelligent Designer had won and lots of humans were going to get sick and die again like they used to.
Now this team of researchers led by Eric Pamer from Memorial Sloan-Kettering Cancer Center, New York, USA, and colleagues have found what looks like a promising cure for even these triumphs of the Intelligent Designer's skill.
You have to eat faeces from healthy people. It seems this Intelligent Designer thing has an unhealthy fascination with coprophagia.
Antibiotic resistance among enterococci and γ-proteobacteria is an increasing problem in healthcare settings. Dense colonization of the gut by antibiotic-resistant bacteria facilitates their spread between patients and also leads to bloodstream and other systemic infections. Antibiotic-mediated destruction of the intestinal microbiota and consequent loss of colonization resistance are critical factors leading to persistence and spread of antibiotic-resistant bacteria. The mechanisms underlying microbiota-mediated colonization resistance remain incompletely defined and are likely distinct for different antibiotic-resistant bacterial species. It is unclear whether enterococci or γ-proteobacteria, upon expanding to high density in the gut, confer colonization resistance against competing bacterial species. Herein, we demonstrate that dense intestinal colonization with vancomycin-resistant Enterococcus faecium (VRE) does not reduce in vivo growth of carbapenem-resistant Klebsiella pneumoniae. Reciprocally, K. pneumoniae does not impair intestinal colonization by VRE. In contrast, transplantation of a diverse fecal microbiota eliminates both VRE and K. pneumoniae from the gut. Fluorescence in situ hybridization demonstrates that VRE and K. pneumoniae localize to the same regions in the colon but differ with respect to stimulation and invasion of the colonic mucus layer. While VRE and K. pneumoniae occupy the same three-dimensional space within the gut lumen, their independent growth and persistence in the gut suggests that they reside in distinct niches that satisfy their specific in vivo metabolic needs.
Intestinal colonization precedes the development of disseminated infections and bacteremia by the nosocomial pathogens vancomycin-resistant Enterococcus (VRE) and carbapenem-resistant Klebsiella pneumoniae.
Although antibiotic treatment renders mice susceptible to dense colonization by VRE or K. pneumoniae, it is unclear whether these microbes compete for space and resources in the gut. Our quantitative studies demonstrate that the density of intestinal colonization by either VRE or K. pneumoniae is unaffected by the presence of the other species, suggesting that they occupy separate niches. Using fluorescence in situ hybridization, we show that both bacterial species indeed occupy distinct niches but inhabit the same regions within the intestine. We find that K. pneumoniae, but not VRE, induces mucus production and invades the mucus layer adjacent to colonic epithelial cells, potentially leading to increased K. pneumoniae translocation to mesenteric lymph nodes. Despite their high colonization levels, both VRE and K. pneumoniae can be displaced from the intestinal lumen following transplantation of a healthy microbiota. Our study provides insight into the interactions between VRE and K. pneumoniae with each other and with their host.*
Caballero S, Carter R, Ke X, Sušac B, Leiner IM, Kim GJ, et al. (2015)
Distinct but Spatially Overlapping Intestinal Niches for Vancomycin-Resistant Enterococcus faecium and Carbapenem-Resistant Klebsiella pneumoniae.
PLoS Pathog 11(9): e1005132. doi:10.1371/journal.ppat.1005132
*Copyright: © 2015 Caballero et al. Reproduced under the terms of the Creative Commons Attribution License (CC BY 4.0).
It's been recognised for some time that a faecal transplant (basically, an enema made from a donor's faeces) from a healthy donor can give spectacular results in people suffering from infection with Clostridium difficile and has been shown to give protection from other multi-resistant organisms colonizing not just the intestinal tract but sites such as wound sites, etc.
Now the technique has been shown to work in mice infected with two multi-resistant bacteria simultaneously. While these two Intelligently Designed (we're still pretending, remember!) appear to be able to live in perfect harmony in the intestines, there is at least one, and possibly more than one, organism found in the normal, healthy intestinal biota which definitely won't tolerate these harmful pathogens. For humans, the question now is which bacteria are the ones responsible for this result and how do they do it.
The mystery for creationists is why the Intelligent Designer designed these harmful bacteria to make us ill, designed another bacteria to fight them and prevent them doing what they were designed to do, and ended up by requiring humans to eat other people's faeces to restore these 'friendly' bacteria to overcome its harmful ones, even inventing antibiotic-resistant bacteria to make it necessary.
Can anyone really discern any hint of intelligence in this designer? Does it have an obsession with coprophagia, maybe, or is it just doing this because it can, as some sort of ego thing?
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