ustxtxb_obs_2004_08_13_50_00043-00000_000.pdf

BY CHAR MILLIR Beef, continued from page 25 required to defend itself. Whereas all other proteins have a single unchanging structure, the prion can spontaneously mutate into different forms, thus affecting the disease’s incubation period and the type of lesions it makes upon the nervous system. It was, furthermore, an infectious agent that lacked nuclei, but could still “somehow” reproduce itself. And it could, as mentioned, be passed on hereditarily. “A whole body of dogma,” as a result of the prion, had to be brushed aside before scientists could continue to pursue a preventive solution or, at least, a temporary cure for TSE. Fortunately, when the cows started going mad, the prion had been fully accepted as a ruthless, mercurial, and persistent agent that followed its own set of twisted values. We still don’t know how cows contracted the disease that has come to be known as BSE. But when the English cows got sick, and when their neurons revealed those spongy holes, scientists and health officials had a very good idea of what they were up against. And they knew immediately that humans were at risk. There was, after all, every reason for BSE, should it be transmitted to humans, to manifest itself as CJD. Which leaves Maxime to answer one final question: How could it get to humans? Here’s where the story might start to feel familiar. Scientists published the first article on BSE in 1987. One year later they learned that it passed among cows through their feeda meat and bone meal mixture manufactured from cow carcasses. In 1996, the strong suspicion that beef eaten from an infected cow could cause CJD became stronger when 10 Britons contracted a new varierties remarkably similar to BSE. “[The] apparent fact that the BSE agent was the same as that of nvCJD,” writes Maxime, “led to the nearly inevitable conclusion that the latter human disease stemmed from the BSE epidemic, and more pre cisely from the consumption of meat or other products from contaminated cattle.” The terrifying causal link had been made. So that’s the science behind Mad Cow Disease. The most disturbing aspect of it all, however, is one that Maxime only touches upon by way of conclusion: Now that we know what causes nvCJD, our most pressing task is to regulate it. The United States, for its part, has talked a big talk on this score, banning outright feed made with bone meal. But the failure to test that Texas cow back in April reminds us that science, while beautifully illuminating the nature of this horrific disease, is also, as Edward Abbey once said, “the whore of industry.” Until we the general public learn more about the disease through important books like Maxime’s, we’ll be the ones getting screwed. Contributing writer James E. McWilliams lives in Austin. He remains a carnivore Fifty Years of the Texas Observer Edited by Char Miller Foreword by Molly Ivins “From Molly Ivins to Willie Morris, Jim Hightower to Larry McMurtry, no other against-the-grain publication in America has helped to nurture such a stellar array of writers.” Adam Hochschild Book Signings: Wednesday, Sept. 8 @ 7:3o PM, BookPeople in Austin Thursday, Sept. 9 @ 5 PM, The Twig Book Shop in San Antonio For updated event information, go to www.trinity.edu/tupress TRINITY UNIVERSITY PRESS -vvvvvv.trinity.edu/tupress Distributed by Publishers Group West 8/13/04 THE TEXAS OBSERVER 43