Antibiotic-resistant bacteria are difficult enough to deal with on their own, but when “ganged up” with other bacteria, they can become deadly.

Eric Skaar, Ph.D., MPH, Ernest W. Goodpasture Professor of Pathology, Microbiology and Immunology, and colleagues from Vanderbilt University shed some light on questions regarding infectious diseases and possible new treatment strategies to combat them.

Staphylococcus aureus and other pathogens can become antibiotic-resistant by modifying the manner in which they generate energy, thereby becoming small colony variants.

To identify how bacteria that are less fit can cause persistent infections in humans, Skaar and his colleagues proposed a hypothesis that there may be many organisms that became resistant in various ways, and can exchange the molecules they’re each missing individually.

This hypothesis was tested by combining two different small colony variant strains of staphylococcus — one that could not generate heme and the other that could not generate menaquinone. They discovered that these strains exchanged the two metabolites, and developed as if they were wild-type staph.

Researchers then tested this idea in a mouse model of bone infection, and discovered that either staph strain alone caused only minimal bone infection, but when combined, they caused a lethal bone-destroying infection.

“Our findings show that these antibiotic-resistant infections are not what we thought they were — they’re not a single strain of bacteria with a single lesion leading to the small colony variant phenotype. Instead, they’re a mixed population of organisms that are sharing nutrients,” said Skaar in a statement.

The findings of the study are published in Cell Host & Microbe.