Virgin birth infections shift wasp targets.

Scientists have found a second bacterial infection that can cause an insect version of virgin births. And this one can do a new trick.

Not only does this bacterium cause unfertilized female wasps to produce daughters, but it can also affect which insects the female wasps inject with a fatal dose of eggs, says Molly S. Hunter of the University of Arizona in Tucson.

She and her colleagues report that this bacterium isn't a near relative of Wolbachia, the first infectious microbe found to cause virgin births in insects and other arthropods. This lack of genetic similarity suggests that the weird power of each bacterium over insects may have arisen independently, the researchers report in the Oct. 23 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES.

"There may be more such bacteria," says John H. Werren, a longtime Wolbachia researcher at the University of Rochester in New York.

Wolbachia infections spread via host eggs but not the stripped-down cells of sperm. The bacteria benefit when they increase the number of a host's female, offspring. Depending on the microbial and host species, Wolbachia can turn males into females, power procreation without fertilization, and prevent infected males from mating successfully with uninfected females (SN: 11/16/96, p. 318).

Hunter and her colleagues discovered the second bacterium to cause such mayhem. It infects a Brazilian parasitic wasp, Encarsia pergandiella. These wasps, less than a millimeter long, lay eggs that somehow double their chromosome number without fertilization and grow into normal daughters within the tissues of other insects. A search for Wolbachia carne up empty, but electron microscopy revealed the previously unknown bacterium in the wasp's ovarian tissue.

Genetic analysis of the find, referred to at the moment as "EB" for Encarsia bacterium, revealed that it's not closely related to Proteobacteria, which include Wolbachia. Instead, EB fits into the Cytophaga-flexibacter-bacteroid group of bacteria, whose members include the culprit for pelvic inflammatory disease in women.

As Hunter and her colleagues were unraveling EB's oddities, they heard that Andrew Weeks of Monash University in Melbourne, Australia, had discovered a bacterium that makes male mites reproduce without mating (SN: 6/30/01, p. 405). In comparing DNA sequences, the researchers found a 96 percent overlap, indicating that they had happened upon the same microbe, says Hunter.

Both groups caution that EB might have acquired its disruptive powers from a Wolbachia species, or vice versa. However, the teams rank independent evolution as a more probable explanation.

The discovery raises doubts about earlier work in the field, Hunter says. Researchers sometimes have given antibiotics to insects and then, if reproductive behavior changed when infections cleared, the researchers would infer that Wolbachia had been present. "I was as guilty as everybody else of thinking everything was Wolbachia," Hunter says.

When her team treated E. pergandiella with an antibiotic, the wasps laid fewer eggs. "We were puzzled," she says. The researchers then compared treated and untreated females' host selection and began to learn what EB infections do to the wasps.

Usually, Encarsia wasps inject unfertilized eggs, which become sons, into other wasps, but they lay fertilized eggs, which become daughters, in different species. In Hunter's test, antibiotic-treated E. pergandiella female wasps lay eggs as usual on other wasps but stopped laying eggs on whiteflies. That explains the wasps' reduced egg counts, says Hunter.

Unchecked by antibiotics, an EB infection makes the female act as if she had been fertilized by a male, which researchers suspect doesn't actually occur in this species. What's more, EB somehow causes the insect to double its genome as a step in the virgin production of daughters.