Natural GMOs Part 88. The state of knowledge of antibiotic resistance and pathogenic E. coli in 1975.

In 1975 right at the start of the genetic engineering era, all of the genetic behaviour of gut germs that explains the evolution of the HUS German outbreak strain of E. coli was well established [by about 1957, years before genetic engineering in laboratories was ever used]. Evolution of new virulence capabilities in bacteria were clearly identified. For many years the plasmid mini-chromosomes involved in evolution of multiple drug resistance to antibiotics had been well understood and extensively analysed. The topic was the subject of an important book by Prof Stanley Falcow, entitled surprisingly enough Infectious Multiple Drug Resistance.

A recent claim by a writer the Natural News website that the German outbreak E. coli strain was deliberately engineered by drug companies to confer multi-drug resistance  on the germ,  and that the proof of this:

…is written right in the DNA of the bacteria. That’s forensic evidence, and what it reveals cannot be denied. This strain underwent repeated and prolonged exposure to eight different classes of antibiotics, and then it somehow managed to appear in the food supply. How do you get to that if not through a well-planned scheme carried out by rogue scientists? There is no such thing as “spontaneous mutation” into a strain that is resistant to the top eight classes of brand-name antibiotic drugs being sold by Big Pharma today. Such mutations have to be deliberate.

..would have been ludicrous in 1975, even in light of what was known then [as explained in more detail at the end of this post, and in even more detail here].. Given what we now know, it remains absolutely bizarre and absurd as an assertion. Any professionally trained microbiologist or geneticist would likely laugh at amazement at the chutzpah, the idiocy or the deception (its hard to tell which) that is exhibited in this mischievous claim.

It is extremly sad that the people of Germany and other countries nearby should be scared by this irresponsible deluded nonsense in such tragic times. They deserve an apology. It’s unfortunate also (but quite  understandable) that many people are not well enough educated about biology to easily work out for themselves the difference between crackpot biology and serious modern science.

If readers examines the full Natural News article within which this claim it made, they will find only references are to newspaper articles or other similar nonscientific sources of information. It is obvious to myself as a professional geneticist and teacher of genetics, that the person who wrote it has a totally inadequate education as far as biology is concerned, and it should be totally ignored as a source of meaningful comment on an extremely serious issue.

I would have made similar comments in 19975 when I first read Dr Falcow’s book, even though I had only then  been studying genetics for 9 years. The article tempts me to ask how much time the Nature News writer himself has devoted to critical scientific thought. [On page 2 of the book Falcow discusses reports by the Japanese scientist Kitamoto discussing multiple-drug resistance of Shigella bacteria in 1956.]

Resistance of E. coli  to multiple-antibiotics in 1975.
Just below I have provided one figure from the book of Stanley Falcow illustrating a typical plasmid or mini chromosome rearrangement deduced from studies available in 1975. The plasmid carries several different genes conferring resistance to different antibiotics and confers drug resistance on the germ that it happens to be living in. They perfectly illustrate events that Nature News thinks cannot happen without lab-engineering. They happened before genetic engineering was invented. They illustrate that E. coli can mate with another species and that plasmid mini-chromosomes can change in a new host.

C in the diagram stands for chloramphenicol resistance, S for streptomycin, Su for a sulfanilamide resistance genes. Note that the diagram represents the possible natural horizontal gene transfer of genes into another gut bacterial species called Proteus mirabilis from E. coli.

The text of the blurb of this book is also appended at the end of this post.

Note the clear-cut reference in the book blurb to plasmids that confer directly traits related to bacterial pathogenicity.

Chapter 11 is a whole chaper of the book devoted to plasmids which contribute to pathogenicity. It foreshadows all  the behaviour of the E. coli strains now wreaking havoc in Germany. It includes mention of plasmids Ent K88 and Hly from E. coli, all relevant to disease.

Book back cover.
Pion advanced biochemistry series
S.Falkow, Department of Microbiology, University of Washington, Seattle.

This volume is a documented guide to the study of infectious multiple-drug esistance (R) factors and other bacterial plasmids. The first three chapters review the properties of the classical R-factor and the bacteriophage lambda so that they may serve as the prototypes for the comparison of the broader spectrum of extrachromosomal elements that are found in Nature. From this base of information there follows an analysis in depth of the genetics, molecular nature, and replication of R-factors and other plasmids. Particular emphasis is placed on She more recent research developments, including the classification of R-factors by their incompatibility properties, electron microscope heteroduplex analysis, the use of restriction endonucleases for the dissection of the plasmid genome, and the use of R-factors and other plasmids for ‘cloning’ genetic material.

The ecology of R-factors and their implication to human and veterinary medicine is covered in considerable detail with emphasis on the critical areas of nosocomial infection, the use of antibiotics in animal feeds, the dissemination of R-factors in vivo, as well as the biochemical basis and origin of R-factor-mediated drug resistance. Although the R-factors are employed as the general model system, specific chapters also deal with the plasmids of the staphylococci and plasmids, such as Ent and K88, which are known to contribute directly to bacterial pathogenicity.

The book will be of prime interest to microbiologists, clinicians, research workers, and students in the fields of medicine, public health, veterinary medicine, -genetics, and molecular biology. It will also serve as a text for an introductory course on plasmids.

Published by Pion Limited, London UK 1975.

Update from the comments section to this post:

One example of well characterised gene movement related to germ virulence demonstrated and studied in 1966 — Long before laboratory genetic engineerin
g started:
Episome-Carried Surface Antigen K88 of Escherichia coli I. Transmission of the Determinant of the K88 Antigen and Influence on the Transfer of Chromosomal Markers

Ørskov, Ida (Statens Seruminstitut, Copenhagen, Denmark), and Frits Ørskov. Episome-carried surface antigen K88 of Escherichia coli. I. Transmission of the determinant of the K88 antigen and influence on the transfer of chromosomal markers. J. Bacteriol. 91:69–75. 1966.—The transmission of the determinant of the Escherichia coli K88 antigen in mixed cultures of E. coli strains is described. The K88 factor could not be transferred by filtrates, nor could responsible phages or colicines be detected. Acriflavine was shown to “cure” the bacteria for the K88 antigen. Generally, the strains having acquired the K88 antigen also acquired the ability to transfer chromosomal markers, but this ability was in some cases retained by segregants which had lost the K88 antigen. Introduction into an F+ strain caused reduction of the recombination frequency and disappearance of the f+ antigen. Not all wild-type strains with the K88 antigen are genetic donors of this antigen, at least not to a discernible degree. It was concluded that the K88 antigen determinant is carried by an episome.
J Bacteriol. 1966 January; 91(1): 69–75.
PMCID: PMC315911

Some more about the history of gene movement in bacteria.
Readers are challenging the facts about the existence of novel natural GMO germs such as pathogenic E. coli before the invention of genetic engineeering in the lab around 1975.

Gene movement in bacteria was discovered in 1946 by Lederberg and Tatum.

Resistance of Shigella (a bacterium closely related to E. coli) to sulphonamides drugs was discovered in Japan in 1952.  In 1956, Kitamoto in Japan  described a strain of Shigella that was resistant to streptomycin, tetracycline, chloramphenicol and sulphonamides, and by 1957 multiple-resistant strains of Shiglla were being isolated on a regular basis (Falcow, 1975).
Subsequently these multiple-drug resistances were all shown to be carried by mobile-genes and mini-chromosomes that move freely between bacterial species and which frequently rearrange naturally. These  genetic structures contain intricate devices that do natural genetic engineering (such as DNA integration catalyst enzymes, integrons, shufflons and the like). They existed before engineeering.
These natural genetic manipulation devices are highly developed in long-known pathogens such as Vibrio chlolerae. They existed before bacterial genetics in laboraries was ever thought of.

Cholera has killed millions of people since it emerged out of the filthy water and living conditions of Calcutta India in the early 1800s. Since then, there have been a total of eight cholera pandemics. A cholera pandemic is a cholera epidemic that can last many years or even a few decades at a time, and that spreads to many countries and across continents and oceans. The first cholera pandemic of 1817-1823 spread from India to Southeast Asia, Central Asia, the Middle East and Russia leaving hundreds of thousands of people dead in its wake. The recent cholera epidemic in Pohnpei, which was part of the eighth and current pandemic, added some more sad numbers to the tragic statistics of cholera. In this year, since January there have been cholera outbreaks in Peru, southern Africa and the Marshall Islands.

Shigella itself is essentially a pathogenic variant of E. coli.We would call it that if it were discovered today. Shigella infections are very nasty. Again, they were there long before laboratory based genetic engineering.

The Discovery of Shigella Bacteria

Shigella bacteria are named after Kiyoshi Shiga, a Japanese scientist who discovered Shigella dysenteriae type 1 in 1896 during a large epidemic of dysentery in Japan (Keusch & Acheson, 1996). Since that time, several types of Shigella bacteria have been discovered – S. dysenteriae, S. flexneri, S. boydii, and S. sonnei – all named after the lead workers who discovered them (Centers for Disease Control and Prevention [CDC], 2009a).

All these germs existed before the era of genetic engineering, and analysis of their genetics show they exchanges genes with other bacteria in the same ways as the German E. coli O104 appears to have done. None of this well-known history was discussed by Mae-Wan Ho in her Dream or Nightmare book where she presents a story that blames genetic engineering in the lab for evolution of new disease germ. It would have ruined the simplistic story line of her book, and there would have been fewer scared people in the world if she had told the full story. The genetics history is  part of standard college major courses in Microbiology. The Pundit know that because he has taught them for many years.

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