Why You Need to Worry About NDM-1: Not a ‘Superbug,’ But Still a Threat

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Antibiotic-resistant bugs have been around almost as long as antibiotics, and health officials have long warned about the looming danger of superstrains — bacteria that are impervious to all of our available antibiotic medications.

But now they’re really worried, because microbes seem to have found a clever and potentially lasting way of evading our best drug defenses: NDM-1, a genetic mutation that allows bacteria to make an enzyme that chews up antibiotics. It’s not actually a superbug — more like a supergene. (More on Time.com: Drug-Resistant Superbug Shows Up in Three U.S. States)

The enzyme made by bugs with NDM-1 easily dispatches the last-resort antibiotics known as carbapenems, which were designed to combat such potentially toxic bacterial byproducts. What’s more, the mutation is easily passed between different species of microbes, like a secret survival code. So far, three such species have picked up the NDM-1 alteration in the U.S., including E. coli, K. pneumoniae, and E. cloacae.

“This is a really big problem and is spreading more rapidly than I thought it would,” says Dr. Louis Rice, chairman of the department of medicine at Brown University’s Alpert School of Medicine and an expert of antibiotic resistance.

The NDM-1 mutation originated in hospitals in New Delhi. Other similar genetic alterations that help bacteria produce the same enzyme have been popping up not just in India but in Pakistan as well. The U.S. cases of NDM-1 involved patients who had received medical care in India. (More on Time.com: New Weird Source of Antimicrobial Drugs: Cockroach Brains?)

Hospitals in developing countries are especially fertile environments for drug resistance, says Rice, since doctors tend to overprescribe antibiotics and patients often take them improperly — that provides the perfect selective pressure for bacteria to develop resistance. Increasingly, he says, drug-resistant bacteria are relying on enzymes that can neutralize the antibiotics, or on molecular pumps that can eject the drugs from the microbe.

A bug like pseudomonas, which is the most common infection among those hospitalized for more than a week, relies on at least a dozen different pumps to rid itself of antibiotics. Attempting to deactivate these pumps may be problematic since healthy human cells rely on similar mechanisms to keep remove toxic agents.

The emergence of resistance mutations such as NDM-1 is a warning sign that we are losing the battle of the bugs, say infectious disease experts. If the microbes are resistant to the carbapenems, says Arjun Srinivasan, a medical epidemiologist at the Centers for Disease Control and Prevention, “we really don’t have ideal antibiotic therapies for these bacteria.”

In fact, says Rice, “it’s not that unusual in the modern hospital to be looking at a patient who is seriously infected and say, ‘I don’t have an antibiotic that I know will work.’”

That’s particularly scary for cancer patients who depend on antibiotics to keep them free of infections when their immune systems are wiped out by chemotherapy treatment, or for transplant patients who take powerful drugs to suppress their immune systems to prevent them from rejecting donated tissues. In those cases, doctors are turning to older agents, such as coliston, which were abandoned because they proved too toxic. But in desperation, these drugs are being dusted off again. (More on Time.com: Want Good Health? There Are 10 Apps for That)

“It’s vital that we focus on new antibiotics,” says Srinivasan. “Even in the best case scenario, we are a decade away from having an antibiotic that is really new that we can use widely in patients.”

Until then, he says, the best defense against the inevitable microbial onslaught is more vigilance in the way we dispense and use antibiotics. Making it difficult for bacteria to develop resistance, by limiting use of antibiotics to only when it is necessary and then advising patients to take them properly, is the only weapon we have at the moment. “If we don’t do something to improve the way we use antibiotics,” he says, “even if we get a new drug, we will lose that one too.”

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