Skip to Content

Weeding Out Bacteria

Australian seaweed may hold the key to slowing down drug-resistant bacteria, which have increasingly frustrated the medical profession.

Slimy plant life floating around the ocean may hold the key to slowing down the spread of certain infections, and could lead to a new strain of drugs that won’t be susceptible to antibiotic resistance, a problem the Centers for Disease Control calls one of its top concerns.

University of New South Wales researchers found that seaweed compounds, called furanones, can stop the bacteria that cause cholera by cutting off the communication systems enabling the disease to spread. The breakthrough has researchers speculating that furanones will likely also work against other bacteria, including those that cause staph infection, food poisoning and tuberculosis – which are increasingly becoming resistant to some antibiotics.

According to the CDC, every year nearly two million people in the United States get infections in the hospital, and 90,000 die. And 70 percent of the bacteria that cause these infections are resistant to at least one antibiotic.

But researchers say bacteria won’t have an incentive to develop mutations that will foil furanones because they dont actually kill bacteria, only block their communication with each other, which prevents them from growing strong enough to cause problems.

“The fact that the furanones do not kill the cells means that there is no disadvantage to the individual cell, but only to the (bacteria) community as a whole,”says Dr. Diane McDougald, a senior research associate at the University of New South Wales Centre for Marine Biofouling and Bio-innovation. “So the (selective) pressure to develop resistance is very low or not at all.”

Many bacteria rely on quorum sensing – a communication system that determines when enough bacteria is present to overwhelm the hosts immune system. The Australian seaweed, a red algal species found in Sydney’s Botany Bay, prevents bacteria from sensing a quorum, thereby stopping the formation of biofilms on leaves. That’s significant because in people, biofilms can cause resistant, chronic infections.

“It’s one of the better studies documenting the effects of a marine natural product on marine bacteria,”says Paul Jensen, an assistant research microbiologist at the Scripps Institution of Oceanography in La Jolla, California. “The testing of these compounds as antibiotics is a logical extension of this work.”

Some researchers believe bacteria might eventually outsmart any obstacle thrown their way, including compounds derived from furanones. If bacteria can detect an advantage, they might mutate in a way that allows them to circumvent the furanone signal jamming.

“(The furanone approach) depends on the assumption that there is truly no selective advantage of quorum-sensing proficiency in life and growth of the organisms,”says Susan Rosenberg, professor of molecular and human genetics and molecular virology and microbiology at Baylor University in Houston. “This might be so. But if there is a growth advantage for those capable of quorum sensing, then mutants that defy the blocker will be selected.”

But McDougald points out that in one million years of evolution, no bacteria have developed a resistance to furanones in the natural environment.

She and her colleagues will soon publish data that details the communication system they’ve discovered in bacteria. And they continue to study the furanones in mice and tissue culture. Preliminary results show that the compounds work against Pseudomonas aeruginosa, the major cause of death in cystic fibrosis patients.

The first products to come from the research will likely be used simply to coat medical supplies and devices. A biotech company, Biosignal, hopes to commercialize the technology and is developing contact lenses – human trials should begin in a year – as well as urinary catheters with the furanone attached to the surface to prevent infection.

“This technology will allow us to coat most any surface that is implanted into the body, artificial joints, heart valves etc.,”says McDougald. “These are a huge source of secondary infections due to bacteria attaching to the surfaces and growing.”

Another company, Quorex Pharmaceuticals, hopes to get a chunk of the $25 billion antibacterial market by exploiting furanones to develop infection-fighting drugs. Quorex’s website says its technology will speed up the drug discovery process, although it normally takes anywhere from five to 10 years to develop a new drug and get it through the regulatory process.

This is just the beginning, though, of what many researchers believe will be the harnessing of naturally-occurring defense mechanisms to fend of disease and infection. Already, other researchers in Eastern Europe and Russia have been using bacteria-eating viruses called phages in treatments.

Phage never caught on in the West, mainly because antibiotics were effective and phage therapy is extremely specific. One phage will eat only one strain of one type of bacteria, and it seems more likely than furanones to fall victim to antibiotic resistance.

Whatever the solution, new drugs will likely come from studies of how organisms fight bacteria in the environment, says Julia Kubanek, an assistant biology professor at Georgia Tech. McDougald and her colleagues discovered the furanone phenomenon when they noticed that a certain red sea algae in the bay escaped the creep of bacteria and barnacles.

“If the UNSW group had not been interested in how seaweeds ward off bacterial colonization, this discovery would not have occurred,” says Kubanek. “The insights that come from studying ecological processes are valuable to protection of human health and the environment.”

Keep Reading

Most Popular

It’s time to retire the term “user”

The proliferation of AI means we need a new word.

The problem with plug-in hybrids? Their drivers.

Plug-in hybrids are often sold as a transition to EVs, but new data from Europe shows we’re still underestimating the emissions they produce.

Sam Altman says helpful agents are poised to become AI’s killer function

Open AI’s CEO says we won’t need new hardware or lots more training data to get there.

An AI startup made a hyperrealistic deepfake of me that’s so good it’s scary

Synthesia's new technology is impressive but raises big questions about a world where we increasingly can’t tell what’s real.

Stay connected

Illustration by Rose Wong

Get the latest updates from
MIT Technology Review

Discover special offers, top stories, upcoming events, and more.

Thank you for submitting your email!

Explore more newsletters

It looks like something went wrong.

We’re having trouble saving your preferences. Try refreshing this page and updating them one more time. If you continue to get this message, reach out to us at with a list of newsletters you’d like to receive.