I know you've already got a lot to worry about, what with the North Pole being 20 degrees hotter than it's supposed to be, and the polar bear that went and crushed all our hearts this week, but don't forget to feel concerned about the looming antibiotic resistance crisis sometimes. 

If things keep going as they are, antibiotic-resistant superbugs are expected to kill 10 million people by 2050, and so far, we have no solution. But researchers have found that we could actually fight fire with fire - a predatory bacterium has been shown to kill antibiotic-resistant bugs.

The bacterium in question is called Bdellovibrio bacteriovorus, and it's known as a predatory bacterium, because it seeks out and consumes its own kind. 

A team from Imperial College London and the University of Nottingham in the UK decided to pit it against an antibiotic-resistant strain of the human pathogen Shigella flexneri - a common cause of food poisoning.

Shigella bacteria are responsible for making 160 million people sick each year (diarrhoea is its speciality), and more than 1 million people die each year from infection, mostly because of contaminated food.

There is currently no vaccine to prevent Shigella infection, and in many cases, antibiotics will not help - most patients are told to just wait it out until the infection resolves itself in five to seven days. 

It's a formidable foe - but not for Bdellovibrio, it seems.

When the researchers combined the two types of bacteria in the lab, Bdellovibrio caused the population of antibiotic-resistant Shigella to decline 4,000-fold. 

Next they infected live zebrafish larvae with Shigella, and gave them a shot of Bdellovibrio. Rates of survival for the larvae were around 60 percent.

For the control group that didn't get a shot of Bdellovibrio, only 25 percent of them lived long enough to reach the third day of infection.

The bacteria are so effective because they eat the Shigella bacteria from the inside out, growing large and swollen before bursting out of their dead host's shell. 

So far, the researchers have found no evidence of unwanted side effects from infecting the larvae with Bdellovibrio, and the same could be true for us, James Gallagher reports for the BBC, because previous research has found Bdellovibrio bacteria occurring naturally in healthy humans.

"This study really shows what a unique and interesting bacterium Bdellovibrio is, as it presents this amazing natural synergy with the immune system and persists just long enough to kill prey bacteria before being naturally cleared," says one of the team, Serge Mostowy from Imperial College London.

While the introduced population of Bdellovibrio appeared to give the zebrafish larvae some level of protection even if they'd had their immune system compromised as part of the experiment, the researchers say the strongest response seems to come from the predatory bacteria working in tandem with the host's own white blood cells.

"The predatory action of the Bdellovibrio breaks the Shigella-pathogen cells, and this stimulates the white blood cells; redoubling their 'efforts' against the pathogen and leading to increased survival of the zebrafish 'patients'," says one of the researchers, Liz Sockett from the University of Nottingham.

Of course, zebrafish aren't humans, and humans aren't zebrafish, so until similar results are demonstrated in humans, we can't get too excited. But the researchers say this is a promising sign that the answer to the antibiotic resistance crisis could be the very thing we're trying to fight.

"It may be unusual to use a bacterium to get rid of another, but in the light of the looming threat from drug resistant infections the potential of beneficial bacteria-animal interactions should not be overlooked," Michael Chew from the Wellcome Trust in the UK, who wasn't involved in the research, said in a press statement.

"We are increasingly relying on last line antibiotics, and this innovative study demonstrates how predatory bacteria could be an important additional tool to drugs in the fight against resistance."

The research has been published in Cell Biology.