STD Awareness: Ceftriaxone-Resistant Gonorrhea

Nestled in the throat of a Japanese woman was a collection of clones that scientists abducted from their temporary habitat and christened H041 — a humdrum moniker for a strain of bacteria that would burn headlines in medical journals. Though the bacteria never caused symptoms in their host, they lingered in her throat from at least January until April of 2009, when a swab finally tested negative. Rather than succumbing to repeated bombardment by an antibiotic called ceftriaxone, the infection probably just went away on its own — as oral gonorrhea infections tend to do.


Resistance to ceftriaxone, our last good gonorrhea drug, has been reported in Japan, Australia, Sweden, France, and Spain.


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.” 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. Resistance to cefixime was first documented in 1999, leaving ceftriaxone as our best remaining option, and the CDC’s first choice for treating gonorrhea. There are no good alternatives to ceftriaxone remaining, which is why reports of ceftriaxone-resistant gonorrhea are so deeply troubling.

What made H041 special was that it was the first extensively drug-resistant strain of Neisseria gonorrhoeae, the bacteria that cause gonorrhea. With an unusually high level of resistance to ceftriaxone — four to eight times higher than the previous record holder — the strain was also resistant to a slew of other antibiotics: penicillin and its relatives, fluoroquinolones, macrolides, tetracycline, trimethoprim-sulfamethoxazole, chloramphenicol, nitrofurantoin, cefpodoxime, cefixime, ciprofloxacin, and levofloxacin — and had reduced susceptibility to azithromycin to boot.

Another thing that made H041 special — as special as clones can be, anyway — is that it never reappeared. After its discovery, researchers in Kyoto and Osaka intensified their surveillance, trying to uncover it again and track its spread through the population. However, their search for H041 turned up empty handed. But other ceftriaxone-resistant strains have been documented around the world. Continue reading

STD Awareness: Antibiotic-Resistant Gonorrhea

Under the microscope, Neisseria gonorrhoeae infects larger human cells (click to enlarge). The bacteria resemble tiny pairs of coffee beans. Image: Dr. Norman Jacobs, CDC

Under the microscope, Neisseria gonorrhoeae infects larger human cells (click to enlarge). The bacteria resemble tiny pairs of coffee beans. Image: Dr. Norman Jacobs, CDC

Writing about sexually transmitted diseases (STDs), one must walk the line between warning readers of risks and engaging in full-fledged alarmism. So it’s a bit disconcerting that researchers writing in the New England Journal of Medicine last month declared that it’s “time to sound the alarm”: The emergence of completely antibiotic-resistant gonorrhea is becoming more of a realistic threat and less of a theoretical possibility. The bacteria that cause gonorrhea are evolving faster than we can develop effective antibiotics against them, and a return to the era of untreatable gonorrhea could see a rise in the particularly nasty complications that arise from a long-term gonorrheal infection, such as pelvic inflammatory disease and epididymitis.


There are genes that confer resistance to every single antibiotic we use to cure gonorrhea. If they all combine within one organism, we might have a superbug on our hands.


Neisseria gonorrhoeae is a species of tricky bacteria that cause gonorrhea, which can infect the mouth, throat, rectum, urethra, cervix, and even eyes. These bacteria have vexed us for thousands of years, having evolved many strategies for entrenching themselves in our bodies. They can alter the proteins that adorn their surfaces, rendering our immune systems incapable of recognizing them. They can form colonies in which they work together to manipulate our cell surfaces with their retracting appendages until they’re allowed entry inside, where they can surreptitiously multiply.

You’ve probably heard of MRSA, which is pronounced “mersa” and stands for methicillin-resistant Staphylococcus aureus — a strain of bacteria that has acquired resistance to methicillin, as well as pretty much every other antibiotic to boot. MRSA is an example of evolution by natural selection — what didn’t kill its ancestors made them stronger, spawning a drug-resistant strain.

Why are we talking about MRSA in a post about STDs? It’s not just because MRSA has apparently found a way to be transmitted sexually, but also because it helps make the concept of antibiotic-resistant gonorrhea more accessible. It wasn’t until less than a century ago that we finally developed a magic-bullet treatment for gonorrhea, and for a handful of decades it was quickly and easily treated with a dose of penicillin. Enter evolution by natural selection. Continue reading