Like other golden ages, this one may be short-lived. Dangerous bacteria, most notably those that cause tuberculosis and gonorrhea, are now more difficult to control with antibiotics than they were ten or twenty years ago. Bacteria have been evolving defenses against antibiotics just as surely as they have been evolving defenses against our natural weaponry and that of fungi throughout their evolution- ary history. As Mitchell Cohen of the Centers for Disease Control and Prevention put it recently, “Such issues have raised the concern that we may be approaching the post-antimicrobial era.”
Indeed we may. Consider staphylococcal bacteria, the most com- mon cause of wound infection. In 1941, all such bacteria were vul- nerable to penicillin. By 1944, some strains had already evolved to make enzymes that could break down penicillin. Today, 95 percent of staphylococcus strains show some resistance to penicillin. In the 1950s, an artificial penicillin, methicillin, was developed that could kill these organisms, but the bacteria soon evolved ways around this as well, and still new drugs needed to be produced. The drug ciprofloxacin raised great hopes when it was introduced in the mid- 1980s, but 80 percent of staphylococcus strains in New York City are now resistant to it. In an Oregon Veterans’ Administration hospital, the rate of resistance went from less than 5 percent to over 80 percent in a single year.
In the 1960s, most cases of gonorrhea were easy to control with penicillin, and even the resistant strains responded to ampicillin. Now 75 percent of gonococcal strains make enzymes that inactivate ampicillin. Some of these changes were apparently a result of stan- dard chromosomal mutation and selection, but bacteria have another evolutionary trick. They are themselves infected by tiny rings of DNA called plasmids, which occasionally leave a part of their DNA behind as a new part of the bacterial genome. In 1976, it was discov- ered that the bacteria that cause gonorrhea had gotten the genes that code for penicillin-destroying enzymes via plasmids from Escherichia coli, bacteria that normally live in the human gut, so that now 90 per- cent of the gonorrheal bacteria in Thailand and the Philippines have become resistant. Similarly, the gene that caused antibiotic resistance in a strain of Salmonella flexneri that caused a 1983 outbreak of severe diarrhea on a Hopi Indian reservation was traced back to a woman who had been taking long-term antibiotics to suppress an E. coli uri- nary tract infection.