Rattlesnakes Two Hours Apart Pack Totally Different Venoms
If you’re walking through the flat desert of Phelan, California, and you’re bitten by a Southern Pacific rattlesnake, you will start to bleed badly. The snake’s venom is loaded with proteins that break down the walls of your blood vessels and that prevent the now-leaking blood from clotting.
Let’s say you survive. You bid goodbye to the desert and drive up some twisting mountain roads to the town of Idyllwild, swapping Joshua trees for pine trees. But the Southern Pacific rattlesnake lives here too, and you get bitten again. And this time, the venom doesn’t go for your blood. The toxins of these snakes include proteins that stop nerves from sending signals into muscles. They start to paralyse you.
It takes two hours to drive between these two sites. In one, you’ll find a rattler with purely haemotoxic (blood-destroying) venom. In the other, you’ll find snakes of the same subspecies with purely neurotoxic (nerve-destroying) venom.
Scientists who study snake venom know that it’s an incredibly variable weapon. Its composition can differ dramatically between different species, subspecies, individuals, or even sexes.
Still, the differences between the Phelan and Idyllwild snakes are extreme. “It’s the most complex variation that I’ve ever seen especially within such a geographically short distance,” says Bryan Fry from the University of Queensland, who led the study that team that analysed the different venoms. Even the haemotoxic venoms varied considerably in how potent they are, what toxins they contain, and what targets those toxins attack.
Fry suspects that the rattlesnakes use such diverse cocktails because they live in such different environments. The Idyllwild snakes, in particular, live on high mountain ridges that are 1,600 metres above sea level. They are extremely isolated from the other populations. “It’s like they’re on islands,” says Fry.
The mountains also contain different prey to the deserts, and the snakes there might need to kill their prey more quickly. “Your ability to track prey is very different if you’re in a rocky outcrop than if you’re in grassland. If an animal gets away, it might disappear down to a crack and you’ll never see it again,” says Fry. “We hypothesise that the neurotoxic venoms are needed to drop the prey faster.”
If that’s the case, why don’t all the rattlesnakes have the faster-acting venom? It may be that the desert-dwellers simply haven’t had the pressure to stray from their traditional haemotoxic blends, or that their venoms are adapted to killing their local prey. The short answer is: we don’t know. We barely know what these different populations eat, let alone how their venoms are adapted to killing those prey.
“It’s a perfect example of the importance of basic evolutionary studies,” says Juan Calvete, a venom researcher from the Biomedical Institute of Valencia. In 2012, he found a similar pattern in the Mojave rattlesnake from southern Arizona, whose venom also changes from haemotoxic to neurotoxic as you from east across the state. “Geographic variability in venom composition [within a species] seems to be the rule rather than the exception, particularly for wide-ranging species,” says Calvete. “However, the variability is unpredictable, and must thus be experimentally determined.”
Indeed, people who are bitten by rattlesnakes often experience very different symptoms and complications depending on where they are. For example, Calvete’s team found that if you’re bitten by a Mojave rattlesnake in Cochise County rather than in neighbouring Pima County, you’re 10 times more likely to die.
In California alone, around 800 people are bitten by rattlesnakes every year. Although just a handful die, the venom is painful, debilitating, and can lead to lengthy hospital stays. To make things worse, Fry says that the antivenom that Americans use for rattlesnake bites—CroFab—is ineffective against the Southern Pacific rattler.“It’s notoriously poor,” he says. “People have to be kept in the hospital for up to a week getting continuous infusions just to keep them alive.”
There are two problems. First, CroFab uses antibodies that are less allergenic than those in other antivenoms, but get cleared from the body very quickly. “You end up with very expensive urine,” says Fry. Second, it doesn’t contain antibodies that target the specific proteins used by the Southern Pacific rattlesnake. “They were relying on toxins to be similar to stuff from other rattlesnakes, but even within this one [subspecies], you get completely different venoms. It’s been a debacle.”
Fry thinks that both the effectiveness of antivenoms and our ability to care for patients will be greatly improved if we get a better understanding of the idiosyncracies of venom in local snakes.
The media should take note too. Several news reports have suggested that rattlesnakes in southwest USA are becoming deadlier, and rapidly evolving more toxic venom. Fry says that’s rubbish—the venoms are naturally very varied, and evolved that way a long time ago. It’s not the toxins that have recently changed, but our appreciation of just how diverse they are.
Reference: Sunagar, Undheim, Scheib, Gren, Cochran, Person, Koludarov, Kelln, Hayes, King, Antunes & Fry. 2014. Intraspecific venom variation in the medically significant Southern Pacific Rattlesnake (Crotalus oreganus helleri): Biodiscovery, clinical and evolutionary implications. Journal of Proteomics.
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