PBS reports on the death of a Nevada woman who had a bacterial infection resistant to all known antibiotics (they tried 26). Microbes, it seems, are evolving resistance faster than humans can devise new antibiotics.
The report from the Centers for Disease Control is here; the bit below is an extract from the PBS article:
Public health officials from Nevada are reporting on a case of a woman who died in Reno in September from an incurable infection. Testing showed the superbug that had spread throughout her system could fend off 26 different antibiotics.
“It was tested against everything that’s available in the United States … and was not effective,” said Dr. Alexander Kallen, a medical officer in the Centers for Disease Control and Prevention’s division of health care quality promotion.
The case involved a woman who had spent considerable time in India, where multi-drug-resistant bacteria are more common than they are in the U.S. She had broken her right femur — the big bone in the thigh — while in India a couple of years back. She later developed a bone infection in her femur and her hip and was hospitalized a number of times in India in the two years that followed. Her last admission to a hospital in India was in June of last year.
The unnamed woman — described as a resident of Washoe County who was in her 70s — went into hospital in Reno for care in mid-August, where it was discovered she was infected with what is called a CRE — carbapenem-resistant enterobacteriaceae. That’s a general name to describe bacteria that commonly live in the gut that have developed resistance to the class of antibiotics called carbapenems — an important last-line of defense used when other antibiotics fail. CDC Director Dr. Tom Frieden has called CREs “nightmare bacteria” because of the danger they pose for spreading antibiotic resistance.
In the woman’s case, the specific bacteria attacking her was called Klebsiella pneumoniae, a bug that often causes of urinary tract infections.
Here, from Wikipedia, is K. pneumoniae growing on an agar plate;
And here’s a video about the superbug:
One thing I think could have been usefully added to the PBS piece—and to the video above—was that this is a case of evolution in action. They don’t even mention that “antibiotic resistance” is simply the result of natural selection: those bacteria who can survive an antibiotic are those that leave offspring, and those offspring carry the genes for antibiotic resistance. Many people harbor the misconception that “antibiotic resistance” somehow involves the infected human acclimating to the antibiotic, when it fact it’s the bacterium undergoing natural selection in the body.
Second, it’s always puzzled me that when bacteria resistant to antibiotics become resistant to a new antibiotic, they doesn’t lose resistance to the old ones. In many cases in evolution, there are “costs to resistance”: it takes special enzymes or physiological changes in a bacterium to fend off antibiotics, and those would reduce its reproduction in the absence of the antibiotic. (These are also called “tradeoffs”.) For example, if you adapt fruit flies to a medium that’s high in salt, they will adapt to it, but then if you put them back on normal medium, they’ll lose the salt tolerance. That’s because the salt tolerance involves adaptations that, in the absence of the salt, reduce your reproduction compared to non-tolerant individuals.
This doesn’t appear to be happening in bacteria: they seem to have an infinite ability to acquire resistance to one antibiotic after another, without losing resistance to the antibiotics they previously encountered but are no longer exposed to. That’s what makes the whole problem so hard, because otherwise we could just go back and try old antibiotics, not used for years, on bugs that have acquired resistance to new ones.
Why is there no “cost to resistance” in bacteria? I’m not sure, but I suspect some readers will know. My own guess is that the resistance is often due not to simple mutations in the bacterium’s own circular chromosome, but is carried in plasmids—bits of circular DNA that can be exchanged among bacteria, and that carry the genes for antibiotic resistance. Once you acquire a plasmid that confers resistance, it may simply be hard to get rid of it, for it’s just sitting there in your cell and either may not incur a reproductive cost (though I’d think it would, by slowing down reproduction). Alternatively, there may not be “mutant” bacteria that somehow lack the plasmids.
Still, the video above indicates that some antibiotic resistance comes from mutations in the bacterial DNA itself; and that implies that if you stopped using that antibiotic, the bacteria would, due to the cost of resistance, revert to being sensitive again after a period of time when it’s not exposed to the antibiotic. (That reversion to sensitivity is itself produced by natural selection; individuals with resistance are at a reproductive disadvantage in the absence of the antibiotic.)
If you know that answer to this puzzle, weigh in below.
h/t: Mark N.
