Mice made more infectious by a dose of antibiotics may explain the transmission of a common cause of gastroenteritis.
Superspreaders represent one of the great challenges to public health programs. These are individuals who infect at rates far above the norm. In some cases, such as sexually transmitted infections, the reasons may have to do with behavior. In other cases, however, the form the infection takes or the presence of a secondary infection may be the issue.
Even more puzzling is how some people, such as the famous Typhoid Mary, can be such prodigious disease spreaders while not getting sick themselves.
Stanford researchers gave two antibiotics to mice carrying the bacteria Salmonella typhimurium, responsible for a million cases of food poisoning a year in the U.S. alone. Normally, typhimurium's infection pattern can be simplified as the following: 70 to 90% of those infected get sick but don't easily transmit the bacteria to others, while 10 to 30% suffer no ill effects themselves, but release large amounts of the bacteria through their feces, potentially infecting others in the process.
When antibiotics were given to the infected mice, however, their symptoms got worse and they started releasing bacteria like a superspreader. "They lost weight, had ruffled fur and hunched up the in corners of their cages," says Dr. Denise Monack.
In Proceedings of the National Academy of Sciences, Monack attributes the differences to a dampened immune response in superspreaders. Superspreaders have lower than average levels of proteins that produce regular inflammation responses to the bacterial infection. "Instead of jousting with the germ, they tolerate it,” says Monack.
From the bacteria's perspective, in some ways this puts them in jeopardy; some bacteria would kill their hosts if not suppressed by immune responses, which are suppressed in these mice. If a normal individual were to get infected with a regular case of typhimurium, it may be the immune system's reaction that makes that individual sick. Eliminate this response and an infected individual is fine, but becomes a superspreader.
The team's previous work suggests the antibiotics killed the beneficial bacteria in the rodents' digestive systems, leaving the field clear for typhimurium to make the sick mice more sick.
"We humans shouldn't take antibiotics lightly," says Monack
The first question the Stanford team want to study is whether the mice are actually a good model for humans in this case. If so, they hope to find a blood test to identify the superspreaders. They also wonder whether the widespread use of antibiotics in livestock is having perverse effects beyond those already recognized.
Further research may also reveal how relevant this discovery is to other diseases, as well as whether we can put the superspreader response to use. "If we can figure out what leads to this immune dampening in superspreaders, it could potentially be helpful in suppressing symptoms of people with chronic inflammatory intestinal disorders, such as Crohn's syndrome or inflammatory bowel disease." says Monach.
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