Antibiotics affect the mouth and gut differently

When we discuss antibiotic resistance, it’s not always clear where the resistance is developing or how exactly the resistance develops. A study out of the UK and Sweden looked at two niches, the gut and the mouth, to understand the difference between how the different parts of the body react to antibiotics.

The scientists discovered that these two parts of the body reacted and recovered very differently after a one-week course of antibiotics. They took fecal and saliva samples prior to the antibiotic regime and then gave the study participants a weeklong course of clindamycin, ciprofloxacin, minocycline, amoxicillin, or a placebo and continued taking fecal and saliva samples for a year.

They found that the oral microbiome recovered much faster than the gut microbiome back to its normal state. It took much longer for the gut microbiome to recover and for participants taking ciprofloxacin, diversity was changed even after 12 months. They also found that while participants largely had genes associated with antibiotic resistance in their gut prior to the trial, the amount of antibiotic resistant genes increased after taking the antibiotic. Antibiotic resistant genes in the mouth remained largely stable before and after treatment.  It was also observed that butyrate production, a health associated short-chain fatty acid, was severely affected by ciprofloxacin and clindamycin.

This raises a number of questions like why does the oral microbiome recover so much faster than the gut microbiome? And why isn’t there a similar increase in antibiotic resistant genes in the mouth like we see in the gut? While this study raises many questions, it provides an opportunity to look at the mouth and better understand what is unique about that environment in comparison to the gut. 

A new probiotic candidate to treat C. diff

Molecular structure of the antibiotic enroflaxcin.

A brief letter was recently published in Nature that identifies a bacteria that may confer resistance to C. difficile.  In addition, they discovered how three commonly prescribed antibiotics alter a patient's risk for C. diff.  

The researchers treated mice with 3 different antibiotics, enrofloxacin, ampicillin, and clindamycin. While the overall microbiome bacterial density was unchanged for each antibiotic, each one altered C. diff susceptibility differently: enrofloxacin did not increase likelihood of getting infected, ampicillin induced transient susceptibility, and clindamycin greatly increased long-term chances of getting infected.

The researchers then identified 11 bacteria that were associated with C. diff resistance.  They  tested one of these bacteria, Clostridium scindens, on humans taking antibiotics that either already had C. diff infections or were susceptible for infection.  They discovered that the probiotic conferred substantial resistance to infection.  Interestingly, this probiotic also led to weight loss.

The researchers then studied how this bacteria could be preventing C. diff infection.  They discovered that this particular bacteria had a rare ability to break down bile into secondary structures, called secondary bile acids.  They tested these secondary bile acids against C. diff and they inhibited C. diff growth.

These results, taken collectively, may be immensely important in treating d. Diff.  Specific types of antibiotics that are known to not increase infection risk, along with probiotics like C. scindens could be combined into new therapies.  This could be important in treating this disease without more rudimentary approaches like fecal microbiota transfers (FMTs).