How bacteria cause pain and what that reveals about the role of the nervous system

Abstract

Flesh-eating bacteria employ a devious strategy. When the bacteria, known as Streptococcus pyogenes , slip under the skin via a small cut or bug bite, they eat away at the tissue underneath, causing a condition called necrotizing fasciitis. One of the early, defining symptoms is that a minor wound or abrasion becomes intensely painful, far more painful than it ought to feel. When flesh-eating bacteria called S. pyogenes , pictured here, slip under the skin via a small cut or bug bite, they eat away at the tissue underneath. It turns out these infections are incredibly painful because the bacteria hijack the body's pain-sensing neurons. Image credit: Science Source/Eye of Science. No one knew why this type of infection hurt so much until neuroimmunologist Isaac Chiu and colleagues at Harvard Medical School in Boston showed that S. pyogenes hijacks the body’s pain-sensing neurons, dialing up the misery. These neurons, in turn, communicate with the immune system, greatly reducing its response to the infection, according to research published last May in Cell (1). This communication creates a double whammy for the host: intense pain and a tough battle to fight off the bug. Approximately 700 to 1,200 people in the United States get necrotizing fasciitis from Streptococcus every year; one-third of them die, and many others suffer scarring and even amputations. Over the past several years, Chiu and other researchers have started to build a picture of how certain bacteria, fungi, and viruses can ramp up pain—or in other cases numb their hosts. These interactions are complex: Sometimes they benefit the microbes, sometimes the host. But this work has already made one thing clear: There are three, not two, major players in infection. There’s the pathogen itself, the immune system, and the nervous system. And it’s the cross-talk among members of …