Super Bugs: The Horrific Consequences of Bacterial Sex

Superbugs are not a new problem. The first superbugs were discovered nearly sixty years ago, in the aftermath of dysentery epidemics in postwar Japan. Europe and America were slow to embrace the implications of this discovery. Pharmaceutical companies in America, Great Britain, and Europe were too busy marketing new antibiotics to heed the warnings of Japanese researchers. Only in recent years have health officials realized the dangers of multiple-antibiotic resistant pathogens.

Even today most people assume that the evolution of drug-resistant bacteria is a predictable process involving spontaneous mutations and selection in the presence of the anti-bacterial drug. “In actuality,” wrote Tsutomo Watanabe, in 1967, “a more ominous phenomenom is at work. It is called infectious drug resistance, whereby resistance to a number of drugs are transferred together and at one stroke.”

The Japanese researchers found that R-factors, (R for resistance)mobile pieces of DNA containing resistance genes, spread from harmless bacteria to pathogenic bacteria. And this promiscuous process of bacterial sex, between different species, occurred within the patients’ own intestines. Resident E. coli transferred R-factors—containing resistance genes to four different anti-bacterial drugs—over to Shigella pathogens, the bacteria that causes dysentery.

In the early 1960s, Naomi Datta, a British researcher working at Hammersmith Hospital in London, was the first western scientist to document transfer of resistance between different species of bacteria. But, because she was woman and published her findings in a relatively obscure journal, her findings went unrecognized for years.

Mary Nugent, Hilary Richards, Naomi Datta, and Max Datta.1980 Cold Spring Harbor Symposium on “Movable Genetic Elements.” Photograph taken by Esther Lederberg.

Instead, Western medicine and industry gave more attention to the invention of the first designer drug, Methicillin. Methicillin was designed to prevent resistance to Penicillin. After World War II, Penicillin was widely available, and probably over-used. As early as 1942, two of the researchers who developed penicillin into a therapy also discovered “Penicillin-ase”, the bacterial enzyme that inactivates Penicillin.

This should not be surprising, if one steps back and considers where antibiotics come from: bacteria and fungi that live in the soil, competing among themselves for the available decaying organic matter (remember, the major roles of fungi and bacteria in the biosphere is to recycle decaying stuff). So the Penicillium fungus secretes Penicillin into the soil to inhibit the growth of competing bacteria. But the bacteria counter with penicillin-resistant enzymes that inactivated the penicillin. Germs invented germ warfare, with weapons created millions of years before humans started using antibiotics as medicines.

And so the inevitable emergence of Penicillin-resistant pathogens encouraged the pharmaceutical industry to develop Methicillin in 1959. Julian Davies,  who has devoted most of his six-decade career to the study of antibiotic resistance, wrote in 2010, “The landmark discovery and introduction of methicillin (the first designer antiresistance antibiotic) in 1959 were thought to be a sure defense against the penicillinases, but the appearance of methicillin-resistant S. aureus (MRSA) within just 3 years led inexorably to other multiantibiotic resistant varients, and the acronym now denotes multidrug-resistant S. aureus.

Julian Davis Heefron 6-80
Fred Heefron and Julian Davies, 1980.

Looking back on the golden age of antibiotics, Professor Davies commented, “Antibiotics have always been considered one of the wonder discoveries of the 20th century. This is true, but the real wonder in the rise of antibiotic resistance in hospitals, communities, and the environment concomitant with their use.”

The profligate overuse of antibiotics by physicians and farmers has certainly helped the emergence of superbugs. But it is the bugs who have us way outgunned. Davies concluded,

“The extraordinary genetic capacities of microbes have benefitted from the overuse of antibiotics to exploit every source of resistance genes and every means of horizontal gene transmission to develop multiple mechanisms of resistance for each and every antibiotic introduced into practice clinically, agriculturally, or otherwise.”

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