The statements reported in that interview are at odds with the facts.
*"For Marshall and Warren’s proposal to gain scientific and clinical momentum, several requirements had to be met: others had to confirm both the bacteriologic and clinical findings; stronger evidence than mere “bystander” status for an etiologic (causative) role of the bacteria in PUD had to be offered and replicated; diagnostic methods less cumbersome and expensive than endoscopy, biopsy, and culture—the methods used by Warren and Marshall—had to be developed; and antibacterial treatment had to be shown to be more useful—i.e., as safe as but more effective than—standard treatments. The last requirement was not trivial, as I will discuss. All these steps would take time.
One might expect that if scientific medicine had dogmatically rejected Warren and Marshall’s hypothesis, there would be scant references to their reports for the several years after the initial publications. The opposite is the case: the biomedical world was abuzz with Campylobacter pylori from the start, as is demonstrated in the figure. It shows the number of papers listed on PubMed, the online database of the National Library of Medicine, as a function of the calendar year throughout the 1980s and early 1990s. The rate of increase after 1983 is nearly exponential. Anyone who doubts the infatuation that medicine had with C. pylori at the time can surf to PubMed and, using the same search criteria that I used to generate the data for the figure, peruse thousands of abstracts.
Within a couple of years of the original report, numerous groups searched for, and most found, the same organism. Bacteriologists were giddy over the discovery of a new species. By 1987—virtually overnight, on the timescale of medical science—reports from all over the world, including Africa, the Soviet Union, China, Peru, and elsewhere, had confirmed the finding of this bacterium in association with gastritis and, to a lesser extent, ulcers. Simpler and less invasive diagnostic methods were devised (Graham et al. 1987; Evans et al. 1989). The possibility of pyloric campylobacter being the cause of gastritis or ulcers was exciting and vigorously discussed, even as it was acknowledged by all, including Marshall and Warren, to require more evidence. Here is a typical opinion, in this instance from the Netherlands: “There is an explosion of interest in the role of Campylobacter pylori as a cause of active chronic gastritis. . . . To what extent this intriguing microorganism is causally related to peptic ulcer disease remains to be elucidated, but all the evidence which is available so far supports a pathogenetically important role” (Tytgat and Rauws 1987).
The New England Journal of Medicine, the most widely read medical journal in the world, offered this editorial: “Further unfolding of the details [of the possible etiologic role of C. pylori in peptic ulcer disease] will be enhanced by the development of an animal model, by epidemiologic studies, and by identification of the source and the virulence properties of specific serotypes of C. pylori. The prospects are exciting, intriguing, and promising” (Hornick 1987)."*
So, far from ridiculing and ignoring Marshall’s work, the medical/scientific community rapidly entered into the investigations needed to confirm his hypothesis, develop better diagnostic methods and validate treatment.
It should also be noted that the demonstration of H. pylori’s role in causing gastric ulcers did not harm gastroenterologists’ income (despite the Marshall interview suggesting that these docs pooh-poohed him for financial reasons). Endoscopy has boomed both for upper and lower G.I. problems, and while other diagnostic tests are widely used for H. pylori, I still get many gastric biopsies obtained in part for confirmation of H. pylori infection.