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Why Antibiotics Can Be Deadly and What To Do


Experts have warned us that antibiotics can be dangerous, even though they are prescribed to kill harmful bacteria. Now Stanford University School of Medicine researchers have made a discovery about why antibiotics can be deadly, a finding that potentially could save lives.

What happens when you take antibiotics?

Let’s say your doctor has diagnosed you as having a bacterial infection, such as strep throat, cellulitis, or food poisoning, and prescribes a 10- to 14-day course of oral antibiotics. What happens once you take the medication?

The positive news is that the antibiotics should begin work on eliminating the pathogens that are causing your illness. However, the negative news is that within 24 hours of beginning treatment, two unhealthful activities take place: an excessive amount of carbohydrates populate your gut, and the number of beneficial or good bacteria in your gut declines.

The presence of beneficial bacteria (also referred to as probiotics) in the gut is critical, as they perform a variety of tasks, including maintaining and balancing the immune system, assisting in regulating blood pressure, and synthesizing vitamins. When the microbial population in the gut—consisting of both beneficial and “bad” bacteria—is in balance, it can usually protect the body against bacterial infections.

The combination of events that occurs within one day of antibiotic treatment, however, can open a door of opportunity for two potentially deadly bacteria—namely Clostridium difficile and Salmonella typhimurium—to quickly reproduce in treated individuals. Once these bad bacteria reach a certain level, they cause inflammation, a situation that further supports their growth.

Good bacteria and antibiotics
A research team under direction of senior author Justin Sonnenburg, PhD, explored how and why dangerous pathogens set up residence in the gut after antibiotic use. They used a mouse model to look at this relationship.

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Sonnenburg noted that their research “specifically supports the suggestion that our resident microbes hold pathogens at bay by competing for nutrients.” Among those nutrients are fucose and sialic acid, two types of sugar found in all cells in the body and thus necessary for existence.

Through a series of experiments with mice, the researchers found that both B. theta and S. typhimurium reproduced faster when sialic acid and fucose were present and without the presence of other competing microorganisms. In particular, B. theta created a surplus of sialic acid, which provided a super source of nutrition for these bad bacteria.

The researchers also discovered that when mice with a normal intestinal environment were given antibiotics, sialic acid levels increased dramatically along with a significant increase in the number of bad bacteria. However, if the mice were treated with antibiotics and not exposed to the two bad strains of bacteria, sialic acid levels began to decline within several days and the levels of beneficial bacteria began to recover.

Therefore, according to Sonnenburg, use of antibiotics causes beneficial bacteria in the gut to assist the bad bacteria. How can this be prevented?

In the future, a medication may be developed that stops the process by which the beneficial bacteria help nourish the pathogens, and this drug could be given along with antibiotics. Until then, use of probiotics that rapidly digest sialic acid may be effective, which may be why taking beneficial bacteria during and after antibiotic therapy is frequently helpful.

In addition, do not take antibiotics unless absolutely necessary (they only kill bacteria, not viruses such as those that cause the common cold and flu). If your doctor prescribes antibiotics, ask if there is an alternative treatment approach. If you must use antibiotics, be sure to complete the course, because stopping too soon may cause the infection to return.

Ng KM et al. Microbiota-liberated host sugars facilitate post-antibiotic expansion of enteric pathogens. Nature 2013 Sep. DOI:10.1038/nature12503

Updated 1/12/2016