The Man Who Turned Antibiotics Into Animal Feed–Part 3
Posted by Richard Conniff on March 10, 2014
The introduction of penicillin during World War II was the great world-changing product of that genius, and it prevented tens of thousands of deaths from infected wounds among Allied troops. After the war, the astonishing promise of the antibiotic era set off a scramble for other bacteria-killing drugs. Benjamin Duggar, a botanist who worked mainly on plant diseases caused by fungi, had joined Lederle as a full-time consultant after reaching mandatory retirement age at the University of Wisconsin. Duggar was soon assigned to the search for new antibiotics, which were now making their mark as wonder drugs in civilian health care, too. Duggar’s long interest in fungi soon paid off. “It was a few months later,” Jukes recalled, “that he wrote me that they were having good results, so much so that his assistants and others were ‘stealing’ portions of the crude extracts to cure their colds.” (The idea then was that antibiotics could cure anything, even perhaps cancer.)
Duggar was working with a fungus he had collected from the soil at an experimental agronomy plot belonging to the University of Missouri in Columbus. In culture, the fungus not only demonstrated powerful antibiotic effects, but also produced a yellow pigment for which Duggar named it Streptomyces auriofaciens, or “the gold-bearing streptomyces.”
The name had an apt double meaning. When the president of the company showed off a vial of the stuff to his research committee, he boasted that it “would make a million dollars for Lederle.” This would turn out to be a wild underestimate. By the end of 1948, the antibiotic was being marketed as Aureomycin. It was the first of the tetracycline antibiotics, a genuine miracle drug, effective against a much broader spectrum of disease-causing microbes than the other leading antibiotics, penicillin and streptomycin. Doctors found it particularly useful, The New York Times soon reported, against whooping cough, Rocky Mountain spotted fever, eye infections, typhus, amoebic dysentery, and both streptococcus and staphylococcus infections.
That December, Jukes received a sample to test on chickens. The poultry industry had lately begun to feed its birds soybean meal as a cheaper substitute for fishmeal. But the chickens weren’t thriving. Soybeans lacked an essential ingredient, the elusive “animal protein factor” or “anti-pernicious anemia factor” that we now know to be the essential vitamin B12. In humans, pernicious anemia had until recently been routinely fatal; it had killed Alexander Graham Bell, Annie Oakley, and Madame Curie, among many others. Then, in the 1920s, researchers found a lifesaving cure in the form of raw liver. But eating a half-pound of raw liver daily was almost worse than the disease.
A concentrated liver extract became available in the 1940s. Soon after, competing researchers at Glaxo in England and Merck in Rahway, New Jersey, finally identified the life-saving ingredient. The animal protein factor thereafter became known as vitamin B12. Merck didn’t say so at the time, but it had managed to extract B12 from the fungus Streptomyces griseus, meaning that it could now mass-produce the precious “animal protein factor” in huge fermentation vats.
Lederle must have felt the competitive pressure. It was also searching for a microbial source of animal protein factor, Jukes later wrote, because researchers there had independently concluded that it was a product not just of animal meat, as the name suggested, but also of microorganisms in an animal’s gut, since it was present in their manure. Jukes and a colleague, Robert Stokstad, were experimenting with hens given just enough feed to allow their eggs to hatch. The resulting “depleted” chicks were generally doomed to die within two weeks unless they got more of the critical animal protein factor.
Some of the chicks received diets supplemented with animal protein factor, in the form of liver extract, and some received an Aureomycin supplement, on a hunch that the fungus it came from might also produce the animal protein factor. Soon after their experiments began, though, the researchers realised that they had stumbled upon something unexpected. The chicks being fed the Aureomycin brew were growing even faster than chicks supplemented with animal protein factor alone. It seemed to supply the animal protein factor, plus something extra: “an unidentified growth factor that made the chicks grow more rapidly than did a complete diet”. (University of Wisconsin researchers had in fact demonstrated a similar effect with other antibiotics several years earlier, but without any commercial consequence.)
Looking back almost 35 years later, Jukes wrote, “If such a discovery were made … in 1985, there would be round after round of committee meetings, and plans would be made to cope with various US Food and Drug Administration (FDA) roadblocks. Long-term and short-term toxicity tests would be started. Metabolites and residues would be isolated and identified. Above all, the product would be tested for carcinogenicity. Finally, the FDA would refuse permission to market it.
“None of these things took place in 1949.” Instead, the company informed Jukes that his animal feed lab “could have no more of the product because it was needed for the extraction of the antibiotic for use in human medicine”. It was just about the last time for many decades that human medical need for antibiotics would take priority over livestock and drug industry profits.