The Coming Plague

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Authors: Laurie Garrett
near-fanatic enthusiasm for antibiotics there were reports, from the first days of their clinical use, of the existence of bacteria that were resistant to the chemicals. Doctors soon saw patients who couldn’t be healed, and laboratory scientists were able to fill petri dishes to the brim with vast colonies of Staphylococcus or Streptococcus that thrived in solutions rich in penicillin, tetracycline, or any other antibiotic they chose to study.
    In 1952 a young University of Wisconsin microbiologist named Joshua Lederberg and his wife, Esther, proved that these bacteria’s ability to outwit
antibiotics was due to special characteristics found in their DNA. Some bacteria, they concluded, were genetically resistant to penicillin or other drugs, and had possessed that trait for aeons; certainly well before Homo sapiens discovered antibiotics. 14 In years to come, the Lederbergs’ hypothesis that resistance to antibiotics was inherent in some bacterial species would prove to be true.
    The Lederbergs had stumbled into the world of bacterial evolution. If millions of bacteria must compete among one another in endless turf battles, jockeying for position inside the human gut or on the warm, moist skin of an armpit, it made sense that they would have evolved chemical weapons with which to wipe out competitors. Furthermore, yeast—the molds and soil organisms that were the natural sources of the world’s then burgeoning antibiotic pharmaceutics—had evolved the ability to manufacture the same chemicals for similar ecological reasons.
    It stood to reason that populations of organisms could survive only if some individual members of the colony possessed genetically coded R (resistance) Factors, conferring the ability to withstand such chemical assaults.
    The Lederbergs discovered tests that could identify streptomycin-resistant Escherichia coli intestinal bacteria before the organisms were exposed to antibiotics. They also showed that the use of antibiotics in colonies of bacteria in which even less than 1 percent of the organisms were genetically resistant could have tragic results. The antibiotics would kill off the 99 percent of the bacteria that were susceptible, leaving a vast nutrient-filled petri dish free of competitors for the surviving resistant bacteria. Like weeds that suddenly invaded an untended open field, the resistant bacteria rapidly multiplied and spread out, filling the petri dish within a matter of days with a uniformly antibiotic-resistant population of bacteria.
    Clinically this meant that the wise physician should hit an infected patient hard, with very high doses of antibiotics that would almost immediately kill off the entire susceptible population, leaving the immune system with the relatively minor task of wiping out the remaining resistant bacteria. For particularly dangerous infections, it seemed advisable to initially use two or three different types of antibiotics, on the theory that even if some bacteria had R Factors for one type of antibiotic, it was unlikely a bacterium would have R Factors for several widely divergent antibiotics.
    If many young scientists of the mid-1960s considered bacteriology passe—a field commonly referred to as “a science in which all the big questions have been answered”—the study of parasitology was thought to be positively prehistoric.
    A parasite, properly defined, is “one who eats beside or at the table of another, a toady; in biology, a plant or animal that lives on or within another organism, from which it derives sustenance or protection without making compensation.” 15 Strictly speaking, then, all infectious microbes could be labeled parasites, from viruses to large ringworms.

    But historically, the sciences of virology, bacteriology, and parasitology have evolved quite separately, with few scientists—other than “disease cowboys” like Johnson and MacKenzie—trained or even interested in bridging

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