March: Biodefense & food supply safetyToxic newts lose war against immune-enhanced garter snakes

Published 12 March 2008

A newt is armed with a poison so deadly that a single animal can kill a dozen people; garter snakes, the newt’s main predator, have developed resistance to the poison; researchers say this does not bode well for humans: Our bodies may develop resistance which would make medications ineffective

An ancient battle between snakes and their prey could be over — with the snake victorious. This is not only a story about the animal kingdom, as the outcome could have ominous implications for the battles playing out between humans and the microbes that infect us. The New Scientist’s Phil McKenna writes that garter snakes along the west coast of North America have evolved what may called “super-immunity” against a newt armed with a poison so deadly that a single animal can kill a dozen people. The poison has escalated in power as the snake — the newt’s main predator — has developed resistance to it. Charles Hanifin of Stanford University and colleagues measured the toxicity of 383 rough-skinned newts (newts of the genus Taricha) at twenty-eight sites from British Columbia to central California. The newts carry extremely high levels of tetrodotoxin (TTX) — the same deadly poison found in blowfish. “Ounce for ounce, some of these populations are the most toxic amphibians on the planet,” Hanifin says.

The researchers compared this toxin data to the resistance found in common garter snakes (Thamnophis sirtalis) throughout the region. In most locations, the snakes’ level of resistance closely matched newt toxicity. In such cases, the poison temporarily slows the snakes down but is not enough to kill them. This supports “arms race” theories explaining how toxicity and resistance co-evolve. In some areas where newt toxicity was relatively high, however, the poison had no measurable affect on snake mobility. The team found that resistant snakes had a single genetic mutation on TTX receptor sites on their neural and muscle cells, which prevented the toxin from binding. It made snakes with this mutation “untouchable.”: “It is pretty much biologically impossible for the newts to ever catch up,” Hanifin says.

The snakes achieved this super-immunity from a single mutation, but Hanifin says that increases in toxicity only occur in smaller incremental changes in a number of genes. Hanifin also thinks microbes infecting humans could also develop super-immunity. “The rapid evolution of resistance in snakes doesn’t bode all that well [for humans],” Hanifin says. “When you have relatively simple toxins or simple drugs you can get this rapid, extreme resistance — and it doesn’t take that long to happen.” Craig Benkman of the University of Wyoming cautions, however, against extrapolating from snakes and newts to antibiotics and microbes. “It might apply to these examples that they are alluding to, but it may not,” he says, noting that there is great variation in the molecular pathways and number of genes controlling chemical receptors on microbes. “If there are a lot of genes with small affect than this analogy won’t apply,” Benkman adds.

-read more in Charles T. Hanifin et al., “Phenotypic Mismatches Reveal Escape from Arms-Race Coevolution,” PLoS Biology 6, no. 3 (doi:10.1371/journal.pbio.0060060): e60