Free Happy Accidents: Serendipity in Major Medical Breakthroughs in the Twentieth Century by Morton A. Meyers

shown. Eventually the bacteria cause injury to the stomach lining through their toxic waste products and release of destructive enzymes, causing chronic inflammation. Some H. pylori even use a structure similar to a hypodermic needle to inject a particularly potent toxin into the stomach lining, boosting the associated inflammatory response. On top of all this, H. pylori infection stimulates the secretion of gastric acid. At that point, the bacteria's human host experiences symptoms of gastritis, and a peptic ulcer may eventually result from the inflammation of the stomach lining.
The crafty invader gets its supplies from the unfortunate besieged victim itself—specifically, the stomach tissue—using the inflammatory response as a means of obtaining a constant and reliable source of nutrients. Thus, micronutrients from the body's bloodstream seep across to feed and sustain the H. pylori population for years or decades. The bacteria possess yet another survival mechanism: In unfavorable environments, such as nutrient deprivation and antibiotic exposure, H. pylori may ball itself up and assume a rounded (coccoid) form for survival in a dormant state.
The gastritis induced directly results in structural and functional changes in the stomach and intestinal lining that can cause ulcer disease. It is now known that H. pylori infection accounts for 80 to 90 percent of gastric ulcers (the remainder being the consequence of high doses of aspirin or other nonsteroidal anti-inflammatory agents) and more than 95 percent of duodenal ulcers. Of even greater significance, it is the leading cause of stomach cancer.
    “T HIS G UY I S A M ADMAN ”
    Marshall's first formal sting of rejection by organized medicine's orthodoxy of belief in the causation and treatment of peptic ulcer disease was felt in January 1983 when he submitted a report for the meeting of the Australian Gastroenterology Society in which he contended that bacteria might be responsible for ulcers. Although fifty-nine of the sixty-seven submissions for this meeting were accepted, Marshall's was not. The society had neglected the wisdom of Claude Bernard, the nineteenth-century founder of experimental medicine, who famously said, “If an idea presents itself to us, we must not reject it simply because it does not agree with the logical deductions of a reigning theory.” 7 In a wry understatement Marshall noted, “It was clear I was thinking very differently from the gastroenterologists.”
    He was encouraged by a colleague to present his findings to a meeting in September in Brussels of infectious disease specialists gatheredto focus on campylobacter infections. This paradigmatic shift in drawing the attention not of gastroenterologists but of infectious disease specialists at an international workshop was the stepping-stone to eventual acceptance. Marshall presented evidence that he had found a new bacterium in the stomach and that it resembled the campylobacter species. This part of his presentation was accepted by the audience as clear and appropriate. 8 However, to Martin Blaser, an American physician expert in infectious diseases, Marshall's claim regarding the bacterial causation of peptic ulcers without the presentation of any scientific evidence was “the most preposterous thing I'd ever heard. I thought, this guy is a madman.” 9 In time, Blaser became a dedicated researcher in the field.
    Warren and Marshall's landmark study, “Unidentified curved bacilli on gastric epithelium in active chronic gastritis,” was published later that year in the Lancet, 10 in an unusual format: two separate letters. Warren's letter described work on the bacteria that he had conducted alone before collaboration with Marshall. Marshall's described their joint work. The two men published a joint report the following year indicating the bacterial cause of gastritis and of gastric and duodenal ulcers. 11 “I was certain,” Marshall said, “that it would immediately gain universal