Snake and spider venom is not as sterile as we thought

(ORDO NEWS) — Bacteria are resourceful little organisms. They can live in the strangest and most inhospitable places on our planet – arid deserts, toxic acid lakes, even deep in the earth’s crust under the ocean floor.

But scientists have just discovered a new, very unexpected habitat for hardy little microbes: the venom of snakes and spiders. This is contrary to what we thought we knew: such poisons contain antimicrobial compounds, which scientists assumed meant it was a sterile environment in which microbes could not thrive.

The discovery to the contrary means that the bacteria that cause infections may be present in the venom before the victim is bitten, meaning that anyone bitten by a snake or spider may need treatment for the infection.

“We found that all the venomous snakes and spiders we tested had bacterial DNA in their venom,” said molecular biologist Stergios Moshos of Northumbria University in the UK.

“Conventional diagnostic tools failed to correctly identify these bacteria – if you were infected with them, your doctor would end up giving you the wrong antibiotics, which could make things worse.”

Although we have long believed that venom should be sterile, infected bites are not. Up to three-quarters of snakebite victims get infections in bite wounds; this is usually attributed to a secondary infection from bacteria living in the snake’s mouth and remaining in the poop of its prey.

However, recent studies have shown that the mouths of non-venomous snakes are more sterile than the mouths of venomous snakes, which is odd given the antimicrobial compounds found in the venom, and that the bacteria found in it are most likely native rather than colonized by prey microbiota.

Moshos and his colleagues wanted to know if venom and poison glands could be a source of additional bacteria, and if so, how microbes adapted to live in an extremely hostile environment.

They sampled the venom and venom glands of five snake species: the plump viper Bitis arietans, the black-necked cobra Naja nigricollis, the common lancelet Bothrops atrox, the western diamondback rattlesnake Crotalus atrox, and the coastal taipan Oxyuranus scutellatus.

They also sampled two species of spider – the Indian ornamental Poecilotheria regalis and the Brazilian salmon-pink tarantula Lasiodora parahybana – and set about isolating and studying the microbes from the venom.

Some of the microbes in snake mouths were likely oral or environmental, but some have been found in both venom and venom glands, including, in one snake species, a common bacterium found in the human digestive tract, Enterococcus faecalis.

This was great because the team could compare them to E. faecalis specimens found in hospitals.

“When we sequenced their DNA, we clearly identified the bacteria and found that they had mutated to resist the poison.

This is unusual because the poison is like a cocktail of antibiotics, and it is so thick that you would think that the bacteria had no chance. But not only did they have a chance, they did it twice, using the same mechanisms,” says Moshos.

“We also directly tested the resistance of E. faecalis … to the poison itself and compared them to the classic hospital isolate: the hospital isolate did not tolerate the poison at all, and our two isolates thrived in the highest concentrations of poison we could give them.”

Considering how quickly a colony of bacteria can develop resistance to antibiotics, and how long it has been for microbes to do so, perhaps this shouldn’t come as a surprise.

Surprisingly or not, the results suggest that treating infected bites from venomous animals may not be as easy as treating a secondary infection due to microbial adaptations.

However, these adaptations may also give us a new tool for understanding antibiotic resistance and how to get around it in other circumstances.

“By investigating the resistance mechanisms that help these bacteria survive,” says molecular biologist Steve Trim of Venomtech, “we can find entirely new ways to combat multidrug resistance, perhaps through the development of antimicrobial venom peptides.”

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