The little organisms are being used by the bacterium. They can live in some of the most inhospitable places on our planet, such as arid deserts and toxic acidic lakes.

The venom of snakes and spiders is a new habitat for the hardy little microbes. Scientists assumed that venoms with antimicrobial compounds were sterile environments in which no microbes could thrive.

The discovery means that anyone who is bitten by a snake or spider may need to be treated for an infectious disease.

We found that all the venomous snakes and spiders that we tested had some type of genetic material in their venom.

If a doctor gave you the wrong antibiotics, it would make matters worse.

We have thought for a long time that venom must be sterile. Up to three-quarters of snake-bite victims develop infections in the bite wounds, which are usually caused by a secondary infection frombacteria that live in the mouth of the snake, left behind in the poop of its prey.

Recent studies have shown that the mouths of non-venomous snakes were more sterile than those of venomous snakes, and that thebacteria found therein are likely native.

Moschos and his colleagues wanted to know if venom and venom glands were the source of the additionalbacteria and how they adapted to live in a hostile environment.

The venom and envenomation apparatus of five snake species were studied.

They isolated and examined the microbes from two spider species, Indian ornamental Poecilotheria regalis and Brazilian salmon pink bird-eating tarantula Lasiodora parahybana.

Some of the microbes in the snake mouths were likely oral or environmental, but some were found in both the venom and venom glands, including Enterococcus faecalis, a common bacterium found in the gut of humans.

The team could compare it to E. faecalis samples found in hospitals.

When we looked at their genes, we found that they were resistant to the venom. The venom is so thick that it's like a cocktail of antibiotics, and you would have thought thebacteria wouldn't stand a chance. Moschos says that they had done it twice, using the same mechanisms.

The resistance of E. faecalis was directly tested and compared to a classic hospital isolates, which did not tolerate the venom at all.

This should be unsurprising given how quickly a colony can develop antibiotic resistance and how long it has been doing so. The results suggest that treating the bites by venomous animals may not be as simple as treating the secondary infections.

These changes may give us a new tool to understand antibiotic resistance, and how to circumvent it in other circumstances.

Steve Trim of Venomtech says that by exploring the resistance mechanisms that help thesebacteria survive, we can find entirely new ways of attacking multi-drug resistance.

The research has been published.