Fruit flies across North America are evolving at breakneck pace – and it has nothing to do with their genes.

Instead they've acquired a bacterial infection that protects against the sterilizing ravages of a common parasite. The infection's spread is much like the spread of a genetic mutation, only much faster.

"They're using endosymbionts" – organisms that live inside other organisms – "to adapt, rather than relying on mutations in their genes," said biologist John Jaenike of the University of Rochester.

Jaenike's findings, published July 8 in Science, originate in work he started decades ago on nightmarish infections of the Drosophila neotestacea fly species by Howardula aoronymphium, a roundworm parasite.

A mother Howardula worm would swell to massive size inside a host fly, laying thousands of eggs. After they hatched, larvae coursed through the host's body. The flies didn't die, but they no longer had the strength to reproduce. In the eastern United States, the worms infested nearly one in four D. neotestacea flies, and sterilization seemed absolute.

But, Jaenike found, in some flies, Howardula didn't lead to sterilization. Instead it was the worms who were sickly, and their offspring few. And the only difference between fertile and infertile Howardula-infected flies was the presence of a bacteria called Spiroplasma.

How Spiroplasma weakens isn't known, but it clearly does. And in their new findings, Jaenike's team shows that Spiroplasma is racing through fruit flies across North America. In the early 1980s, it was present in just 10 percent of eastern fruit flies. Now it's in 80 percent, and moving rapidly west.

The pattern fits with what's predicted by traditional evolutionary theory: A beneficial mutation arises, confers a reproductive advantage, and over time spreads through a population – except that the adaptation isn't genetic, but bacterial. Microbes can be passed from mother flies to offspring, but also carried by mites between flies, and even between species.

This kind of evolution "allows an adaptation in one species to be moved to another species," said Yale University evolutionary biologist Nancy Moran, who was not involved in the study.

According to Moran, the spread of beneficial bugs gives animals a version of the horizontal gene transfer present in ultra-adaptable bacteria, which can pick up new genetic material over the course of their lives. "This is a way that animals can steal adaptations from each other and from other branches of the tree of life," she said.

The resulting "instantaneous acquisition" of traits between unrelated hosts is quite different than "normal" Darwinian evolution, which occurs through the accumulation of small changes, said University of Georgia entomologist Kerry Oliver.

An important question is whether the findings are a rare example of a beneficial infection, or a snapshot of a common phenomenon. If the latter, "we will have to revise our view of insect defense mechanisms," said University of Liverpool parasite ecologist Greg Hurst.

Oliver noted that invertebrates are especially likely to benefit from protective bacteria, as they lack the sophisticated immune systems found in more complex creatures. "It's essentially an alternative immune system," he said. "This phenomenon is likely widespread in insects and other arthropods.

Other examples of insect endosymbioses include Moran's specialty, a microbe that protects aphids from parasitic wasps. Another bacteria called Wolbachia causes some male insects to turn female – a relationship that doesn't make obvious evolutionary sense. In one species of fruit fly, Wolbachia can also kill all male offspring, but only if their mother alone is infected. If both parents are infected, the offspring are fine.

"It's really bizarre," said Jaenike. "I have a graduate student trying to figure out what's up with that."

In the near future, Jaenike's attention will turn to what Spiroplasma might do in people. He received a Gates Foundation grant to explore whether the bug could control roundworm-borne diseases like river blindness and elephantiasis, which afflict millions of people in the developing world.

That research is preliminary, but "there's a possibility for using Spiroplasma as a novel mechanism for controlling control human diseases," said Jaenike.

Image: A dissected fruit fly infected by the Howardula parasite, but not by protective Spiroplasma. The mother parasite is at bottom right, and larvae around the fly./John Jaenike.

See Also:

*Citation: "Adaptation via Symbiosis: Recent Spread of a Drosophila Defensive Symbiont," by J. Jaenike, R. Unckless, L.M. Boelio, S.N. Cockburn, S.J. Perlman. Science, Vol. *

Brandon Keim's Twitter stream and reportorial outtakes; Wired Science on Twitter. Brandon is currently working on a book about ecological tipping points.