Part 10: Endgame Summary
Chapter Thirty-Four
By World War I, American medicine had been transformed. Still, the number of men and women conducting sound research in the field was small. The group was interconnected and everyone knew each other. Although the group had its “rivalries and dislikes,” it was “almost a brotherhood”—a brotherhood in a more literal sense, too, as there were very few women.
During the pandemic, “all of these scientists had worked frenetically,” often accepting conclusions based on evidence that would be unsatisfactory in normal circumstances. By the end of the pandemic, “they had lost their illusions.” Although they had been humbled by influenza, they did not stop the long search for answers.
In October 1918, leading scientists met at an influenza commission. Although the sessions only seemed to confirm how little they knew, the scientists did agree on the essential approach required. First, they needed to explore “the epidemiology of the disease. Second, they need to follow “clues in the laboratory.” Subsequent commission meetings ensured that different studies would “complement, and not overlap” with others.
As scientists around the world remained focused on the disease, they accumulated more knowledge of it. They concluded that the virus that spread in the spring of 1918 was the same virus that had erupted in the fall. They recognized that those living with more space, and those that had gotten the most rest, had experienced higher survival rates. However, “nearly everything else about the disease remained unsettled.”
In laboratories, “the fog remained dense.” Despite the resources being poured into research, the pathogen was unknown. As years passed, many scientists stopped studying the virus, and among those that remained, disputes arose. A central dispute formed with “William Park and Anna Williams on one side, Paul Lewis and many of those at the Rockefeller Institute on the other.” Amongst the scientists at the Rockefeller Institute, Oswald Avery “would make the most profound discovery of them all.”
Chapter Thirty-Five
At the beginning of the epidemic, even the most accomplished scientists “had mixed results” looking for Pfeiffer’s B. influenzae. After adjusting techniques and finding the bacillus more frequently, many scientists began to consider it to be the cause. These included Park, Williams, Lewis, and Wollstein.
If a scientist was unable to find B. influenzae, their competence was questioned. As a result, “bacteriologists began to find what they were looking for.” It was still puzzling, however; sometimes B. influenzae was not found at all, and very rarely it was found alone.
There was increasing doubt about “what finding [B. influenzae] proved.” By early 1919, Park and Williams no longer believed influenza bacillus was the pathogen. Like several others, they suspected that the disease was caused by a filterable virus.
Most of the scientists at the Rockefeller Institute, however, remained convinced that B. influenzae was the cause. By the end of the 1920s, many scientists still favored the bacteria as the likely cause of influenza.
At the Rockefeller Institute, Avery spent years studying B. influenzae. As the scientific community shifted its focus away from the bacteria, however, Avery returned to his study of pneumococcus.
Over the course of years, Avery’s singular focus on pneumococcus narrowed further and further. He began to investigate the coating around the bacteria, noting that encapsulated pneumococci seemed protected from the immune system. Bacteria without the coating, however, was “easily destroyed.”
Along with the biochemist Michael Heidelberger, Avery proved in 1923 that the capsules—composed of carbohydrate—triggered an immune response. In 1928, a British scientist proved that pneumococci could change: pneumococci without capsules could acquire them.
While this discovery at first seemed to make Avery’s work...
(This entire section contains 1184 words.)
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“meaningless,” Avery shifted his direction. He sought to “understand how one kind of pneumococcus was transformed into another.” While other scientists lost interest, Avery continued down his line of inquiry for years. His work of digging into one problem seemed to yield nothing. From 1934 to 1941, he published nothing.
While he had nothing to report, Avery’s search began to gain momentum. He became excited; he had “confidence that he would reach his destination.” He had isolated the substance that allowed pneumococci to transform. To determine what the substance was, he worked at “eliminating one possibility after another.”
Finally, he published findings that would prove pivotal to the field of biology. He had discovered that it was DNA that allowed the pneumococci to transform and that “DNA carried genetic information.”
While Avery himself never won the Nobel Prize, his discovery paved the way for other scientists to explore molecular biology.
Chapter Thirty-Six
Throughout the pandemic and for several years afterward, Paul Lewis led the Henry Phipps Institute at the University of Pennsylvania. Although Lewis had initially doubted that B. influenzae caused the disease, once he accepted it as the likely pathogen, he held onto his view despite the fresh doubts raised by other scientists.
At Phipps, Lewis became frustrated by the work of raising money to fund the institute. He became “restless,” his unhappiness exacerbated by tensions in his marriage. In 1922, he accepted a position at the University of Iowa. In 1923, he quit, “walking away from position, prestige, and money.”
Simon Flexner, one of Lewis’s mentors, offered him a position at the Rockefeller Institute’s Division of Animal Pathology. Although Lewis “produced nothing” in his first year, Flexner and Welch still saw immense potential in him.
Despite Lewis’s exceptional intelligence and the help of the talented scientist Richard Shope, his “work did not go well.” His superiors became concerned—not by Lewis’s failures, but by “the manner in which he was failing.” His setbacks confounded him, and he was unable to use them to move forward towards new knowledge. Lewis tried to prove himself, but he “was simply foundering.” Flexner advised Lewis to move on from his study of tuberculosis, warning that it was a “barren subject.”
Meanwhile, Richard Shope began to investigate the influenza that had spread amongst pigs during the pandemic. With Lewis’s help, he isolated “a bacillus virtually identical to B. influenzae and named it B. influenzae suis.”
In 1928, Flexner had a “blunt” conversation with Lewis. While Flexner still saw potential for Lewis to become an influential medical researcher and educator, he did not believe Lewis was “the investigator type.” The University of Iowa continued to pursue Lewis, and Flexner strongly encouraged him to take their offer. Lewis refused.
In May 1928 a fellow Rockefeller Institute scientist died while studying yellow fever in Ghana. Lewis volunteered to continue the study, despite his wife’s opposition. In June 1929, Lewis died of yellow fever in Brazil. His death was puzzling, and some even believed it was a suicide.
In 1931, Richard Shope published his discovery of the virus he found in pigs, which turned out to be directly related to the 1918 virus. In 1933, British scientists found the human pathogen. Had Lewis lived, he would have been part of Shope’s ground-breaking work, finally achieving the success he sought. While William Park pursued science “as a means to a larger end” and Avery was “driven and obsessive,” Paul Lewis “was a romantic.” In the end, “his failure to win what he loved killed him.”
