A DEAD zebra in the open savannah of Namibia’s Etosha National Park would be an off-putting encounter for most people. But for Holly Ganz of the University of California, Davis and an international team of researchers, the striped ungulate’s carcass reeked of opportunity. The zebra met its demise at the hands of Bacillus anthracis, the bacterium that causes anthrax. Grazing animals that ingest spores produced by this ubiquitous soil-dwelling microbe can develop a fatal gastrointestinal infection. Samples retrieved from the zebra carcass contained, as expected, cells of B. anthracis. But they also revealed a pleasant surprise: a novel virus infecting the anthrax bacterium. The researchers reported their findings in the journal PLOS ONE.

Viruses that prey on bacteria, known as bacteriophages (or phages for short), are interesting to microbiologists for two major reasons. First, while bacteria are considered to be the most abundant organisms on Earth, phages—pseudo-living entities that must hijack bacterial cells in order to reproduce—may outnumber them by ten-to-one. Second, phages may serve as a useful weapon in the battle against antibiotic resistance. Experiments with phage therapy began more than 80 years ago in Russia, but did not attract attention in the West until more recently.

The unfortunate zebra’s phage, named Tsamsa, is a member of the Siphovirus family. Bearing a slight resemblance to human sperm, its bulbous head contains about 170,000 base pairs (“letters”) of DNA encoding nearly 300 genes—quite large by phage standards. The long tail serves as its means of attachment to the bacterial cell and as an injection needle for the DNA. As is typical of phage, Tsamsa only infected a small group of closely related bacteria, showing a slight preference for B. anthracis.

Like all temperate viruses, Tsamsa exhibits a Jekyll-or-Hyde life cycle. Upon infecting a host cell, the virus faces an existential choice: it could either peacefully integrate into the bacterium’s genome, living in a sort of domestic partnership; or, it could become a self-serving homewrecker by churning out thousands of copies of itself before blowing the bacterium to smithereens. This latter option, called the lytic cycle, was of particular interest to the researchers.

To burst a bacterium like a balloon, many phages produce a protein, called an endolysin, that chews holes in the bacterium’s cell wall. Tsamsa virus contained its own version of the toxin, which Dr Ganz’s team cloned and expressed. When they applied the endolysin directly to bacterial cells, it also destroyed them.

This is a potentially useful find. In an era of increasing antibiotic resistance, innovative ways of treating bacterial infections are greatly needed. Phage therapy – the use of phage or their toxins to kill bacteria – is an area of great interest to scientists. Unlike antibiotics, the potential for bacteria to develop resistance to phage endolysins is thought to be much lower. It may also be possible to genetically engineer these toxins to avoid friendly bacteria and to target only unfriendly ones.

With an estimated ten million trillion trillion (that is, 1 followed by 31 zeroes) phages in existence, the possibilities for phage therapy are nearly limitless. The next cure for an antibiotic resistant bacterium could quite literally come from anywhere. A dead zebra carcass is just as good a place as any to begin looking.