A new strain of Clostridium difficile — known as C. diff transferase — has become increasingly common and deadly in recent years, killing up to 15 percent of those it infects, including patients who take antibiotics. Researchers have now discovered why the new strain is so deadly and subsequently identified a potential method for stopping the infection, according to a new study published in Nature Microbiology.
PhD student Carrie A. Cowardin was working in the lab of Bill Petri, MD, PhD, chief of the University of Virginia's Division of Infectious Diseases and International Health in Charlottesville, when she discovered the mechanism by which the troublesome C. diff strain subverts the immune system. The mechanism discovered was a toxin produced by C. diff that destroys protective cells in the gut. By destroying this barrier, the infection can spread inflammation throughout the body.
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"We think that this toxin makes disease more severe by killing beneficial eosinophils [protective gut bacteria], which seem to play an important role in promoting a healthy immune response during C. diff infection," said Dr. Cowardin, now a postdoctoral fellow at Washington University in St. Louis. "When the eosinophils were depleted with an antibody or by the toxin, we saw dramatically increased inflammation."
Further investigation revealed the toxin's mechanics. The toxin requires the presence of a particular human protein that recognizes bacteria in order to successfully subvert the human immune system. Introducing similar proteins from mice that cannot recognize the bacteria may help to restore eosinophils.
"Nearly every day that I care for patients I am faced with this potentially deadly infection," Dr. Petri said. "Carrie Cowardin's discovery of why this strain of C. diff is so dangerous, and most importantly how to combat it, is a huge and most needed advance."
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