A progress update on the Intelligent Designer's campaign to make human and other animals get sick and die, using the bacterium Escherichia coli.
The story so far:
E. coli is the name of a highly diverse group of bacteria which displays far more genetic diversity than entire families of multicellular organisms with only about 20 percent of genes being common to all strains. Some authorities believe the taxon is overdue for revision and that some bacteria classified as Shigella should be reclassified as strains of E. coli while some E. coli, for example, the K-12 strain, should occupy a different taxon. Some strains have no flagellum, so lack motility.
E. coli is a normal part of the lower gut flora of warm–blooded organisms and may even be symbiotic in that it produces vitamin K2 and helps prevent the growth of pathogenic organisms. It can live and thrive in anaerobic, i.e., oxygen deficient, conditions but can also live aerobically in fresh faeces where it can increase rapidly for a few days in the presence of oxygen. In normal conditions in the gut it can replicate every 20 minutes. Replication is normally asexual but they can exchange genetic material by conjugation.
It is parasitised by bacteriophage viruses which can incorporate E. coli genes into their own genome then pass these on to other E. coli, so also facilitating horizontal gene transfer. It is believed that strain 0157:H7 acquired the Shiga toxin by horizontal gene transfer from a Shigella bacterium.
The Escherichia bacteria are related to Salmonella, the two groups having diverged about 100 million years ago as the mammals diverged from the reptiles and birds. Escherichia species live in the gut of mammals while Salmonella occupies the same niche in birds and reptiles.
Some strains of E. coli can become pathological, causing diarrhoea that is normally self-limiting in healthy adults but can be fatal to children, especially in the third–world. The strain 0157:H7, with its Shiga toxin can be fatal to the elderly and very young, and to people with reduced immunity.
Normally harmless strains of E. coli can become pathological when out of their normal gut environment. For example, if they enter the urinary tract they can cause urinary tract infections.
In 2011, the enterohemorrhagic E. coli strain O104:H4, believed to have been carried on Egyptian fenugreek seeds, caused a major outbreak starting in Germany and spreading to 15 other countries. In 1996, 20 people in Wishaw, Scotland, died as a result of food poisoning caused by E. coli 0157, traced to contaminated meat from a local butcher.
According to biochemist and leading Cdesign proponentsist, Michael J. Behe, an intelligent designer must have designed E. coli because, so he claims, the flagellum of E. coli, and in particular the proton motor that drives the flagellum, was personally designed by the Intelligent Designer (who, just like the Christian god, is supposedly the only entity capable of creating things).
Since the only discernible purpose for E. coli is to make more E. coli and to make humans and other animals sick and die, we have to assume this is what the Intelligent Designer designed it for, after all, the definition of design must include a purpose.
The logic is quote simple and something that no devout
- The Intelligent Designer is omniscient and omnipotent so knows exactly what it's designs will do when it created them.
- The Intelligent Designer designed E. coli.
- E. coli make humans and other animals sick.
- Therefore, the Intelligent Designer designed E. coli to make humans and other animals sick.
We are already aware that this designer has had to intervene to help E. coli overcome human medical science's attempt to protect humans from it with antibiotics, by redesigning it to be antibiotic resistent.
Now it has hit on another little scheme. It has found a way to get wild giraffes to carry and transmit antibiotic-resistent E. coli!
According to an American Society for Microbiology press release:
A team from the University of Minnesota has shown that antibiotic-resistant Escherichia coli bacteria in wild giraffes most likely come from anthropogenic sources, such as local cattle herds and humans. The research is published in Applied and Environmental Microbiology.
“We found that the majority of antibiotic resistance genes identified in giraffe E. coli had been previously identified in E. coli from both humans and domestic cattle in East Africa,” said corresponding author Elizabeth A. Miller, PhD, Postdoctoral Research Associate, College of Veterinary Medicine, University of Minnesota, St. Paul. There was little evidence that the bacteria were being transmitted between giraffes via social interactions, she said.
Surprisingly, giraffes three months of age or younger were more likely to harbor antibiotic resistant E. coli than other age groups. “This is particularly surprising as giraffe neonates nurse from their mothers exclusively and interact minimally with other group members, leading us to predict they would have low exposure to resistant bacteria and residual antibiotics in their environment,” said Dr. Miller. “These results suggest there may be competition between antibiotic resistant and susceptible E. coli strains in the giraffe neonatal gut, with resistant E. coli having a selective advantage.
Just why antibiotic resistant E. coli outcompete the susceptible strains is a matter of pure speculation at this point, said Dr. Miller. “One intriguing theory refers to iron acquisition genes that have been observed to occur on the same plasmid as resistance genes,” she said. “Bacteria with these extra iron acquisition genes might have a selective advantage in this iron-depleted environment, and any antibiotic resistance genes associated with the iron resistant genes would be carried along for the ride,” she said, noting that the theory had previously been suggested in a 2004 article in this journal.
The research is contributing to scientific understanding of how resistance genes are spread in natural ecosystems, said Dr. Miller. “This research also highlights the potential importance of host age as a predictor of harboring antibiotic-resistant bacteria—at least in giraffes. Further, the fact that resistant E. coli were more frequently identified in neonatal giraffes suggests that the neonate gut may represent a site of complex competition dynamics between microbe members. While similar age-related patterns have been observed in humans and some domesticated animals—especially cattle—to our knowledge, this study is the first to show this striking pattern in a wild mammal.”
Creationists must be very proud of the brilliance of their
</sarcasm>
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