Ever since the discovery of effective antibacterial therapies less than a century ago, humans have been able to easily cure gonorrhea, the sexually transmitted scourge that laid waste to fallopian tubes and robbed newborns of vision. Most of us in the developed world have forgotten that this disease was once a leading cause of infertility in women and blindness in babies — and still is in much of the developing world.
Unfortunately, gonococci — the species of bacteria that cause gonorrhea — have been evolving resistance to every antibiotic we’ve thrown at them, including sulfonamides, penicillins, tetracyclines, macrolides, fluoroquinolones, and narrow-spectrum cephalosporins. We have one remaining first-line gonorrhea treatment left: extended-spectrum cephalosporins, which include cefixime, which is taken orally, and ceftriaxone, which is administered as a shot — and resistance is emerging to those drugs, as well.
Gonococci don’t swap potato salad recipes at family reunions — they swap genetic material!
The emergence of antibiotic-resistant gonorrhea is considered one of the most pressing problems in infectious disease — just two years ago, the Centers for Disease Control and Prevention named it an “urgent threat,” and indeed, gonorrhea seems to be evolving resistance to drugs at quite a rapid clip. Gonococci can acquire resistance to antibiotics in three ways.
First, a genetic mutation can endow bacteria with special antibiotic-fighting powers, making it harder for a drug like penicillin to attach to their cells and destroy them. Such a mutant is more likely to gain evolutionary traction if it finds itself in an antibiotic-drenched environment in which resistance to that drug allows it to “outcompete” other bacteria. Indeed, antibiotic resistance was first documented in the 1940s, just years after sulfonamides and penicillin were introduced as the first effective cures for gonorrhea. Continue reading