An estimated 80 percent of all antibiotics in the U.S. are given to livestock, which raises concerns among some scientists about the fostering of antibiotic-resistant pathogens. But a study on antibiotics just published by researchers from the Stanford University School of Medicine might introduce a whole new concern to the equation. Mice given antibiotics to treat Salmonella infections have been found to grow even sicker and start shedding more pathogens afterward. In fact, they begin to shed the same levels of bacteria as so-called “superspreaders,” the small minority of infected mice in the population who exhibit no signs of illness but spread large amounts of bacteria. “We’ve shown that the immune state of an infected mouse given antibiotics can dictate how sick that mouse gets and also carries implications for disease transmission,” said Denise Monack, Ph.D., associate professor of microbiology and immunology at Stanford and the study’s senior author. “If this holds true for livestock as well — and I think it will — it would have obvious public health implications. We need to think about the possibility that we’re not only selecting for antibiotic-resistant microbes, but also impairing the health of our livestock and increasing the spread of contagious pathogens among them and us.” It’s not entirely clear why some animals — and humans — are superspreaders while others are not. Approximately 10-30 percent of mice are superspreaders who will shed large amounts of Salmonella while exhibiting no signs of illness, while the remaining 70-90 percent shed only small amounts and sometimes develop symptoms. In the Stanford study, mice given antibiotics went from shedding small amounts to much higher levels of Salmonella. Within days, they also became very ill and several died. But, when given the same antibiotics, the superspreaders continued shedding large amounts of bacteria without any ill effects. The researchers found that, compared to the normal mice, the superspreaders had dampened immune responses, which explained why they didn’t get sick. Instead of fighting off the infection, their immune systems tolerated it. “Their immune cells have been rewired and aren’t responding to the inflammatory signals in the intestines the same way,” said Smita Gopinath, Ph.D., the study’s lead author. And with the mice who do experience symptoms of illness, the antibiotics do exactly the opposite of what they’re intended to do. These same conditions have not been observed in humans, but it’s an area worth studying, the researchers said.