Bacteria interchange a lot of genes, a process known as horizontal gene transfer. That's a big part of the reason antibiotic resistance is such a threat to society. We've now discovered a new way these transfers occur, with bacteria killing their rivals and acquiring their victim's resistance to antibiotics in the process.

Similar to other lifeforms, bacteria frequently have to fight for access to food and other resources, so being armed against competitors provides an advantage. One potent weapon is the capacity to inject a toxic mix of proteins, known as effectors, into rivals.

"Some of these toxic proteins kill the bacterial competition very effectively, but do not destroy the cells," Professor Marek Basler of the University of Basel explained in a statement. "Others severely damage the cell envelope, which leads to lysis [cell disintegration] of the attacked bacterium and hence the release of its genetic material."

The released DNA is then free to be acquired by other bacteria, particularly the one that killed the unfortunate bacterium in the first place. In a move worthy of a supervillain, the killer sometimes takes on attributes encoded in this DNA. If the prey was resistant to certain antibiotics, this resistance can pass to the predator cell.

In Cell Reports, Basler identifies five effectors used by Acinetobacter baylyi to kill its competitors. As venomous animals have found, chemical warfare works best when mixing toxins, making it possible to target a wider range of victims and harder for prey to develop immunity. Each effector uses a different method to kill the target, and the chance of A. baylyi getting to inherit useful genes from its prey depends heavily on the mechanism of killing.

A. baylyi was chosen as a model organism, one that has already been well studied, but it is also a close relative of A. baumannii, which is becoming a problem in hospitals since acquiring antibiotic resistance. A. baumannii is also known as the “Iraq bug” because multi-drug resistant versions plagued hospitals treating US soldiers in Iraq.

Mutations that make a bacterium resistant don't come along all that often. Once they do, however, they spread rapidly, to the point where some strains are resistant to all existing antibiotics, having acquired multiple resistance genes. Initially, this speed was attributed to the standard evolutionary feature that the mutant has a better chance of surviving and multiplying in an antibiotic-rich environment.

Although this is certainly important, microbiologists have come to realize this is not the whole story, with horizontal transfer of resistance genes turbocharging the process. Balser's work extends our understanding of how this transfer occurs, and particularly why certain bacteria so quickly accumulate multiple drug resistances. Fighting it will be another story.