Resisting Antibiotics: Some Bacteria Get By With a Little Help From Their Friends


Antibiotic resistance is often in the news, as it threatens the effectiveness of one of the foundations of modern medicine. Usually, the concern is about resistance that is inherent to the bacteria, or else develops in bacteria through genetic changes. A paper published today in PLOS ONE suggests another possibility.

In “Chemical communication of antibiotic resistance by a highly resistant subpopulation of bacterial cells,” authors Omar El-Halfawy and Miguel Valvano reveal that some species of bacteria may help others in surviving an antibiotic attack. In addition, they were able to provide insight into the mechanics of how the bacteria perform this action.

The study began with an observation of the bacterial species Burkholderia cenocepacia, which typically grows in the soil but can infect people who have cystic fibrosis and those with compromised immune systems. The authors noted that a subpopulation of the species was more resistant to the antibiotic polymyxin B than other bacteria of the species. In other words, these resistant bacteria were more likely to survive after treatment with polymyxin B, and levels of antibiotics that killed the less resistant bacteria did not harm this (more resistant) subpopulation.

When the authors grew the more-resistant B. cenocepacia with another strain of bacteria called Pseudomonas aeruginosa (a disease-causing bacterium that can co-exist with B. cenocepacia), the P. aeruginosa were much more resistant to the antibiotic than when they grew in isolation.

Why might the P. aeruginosa be more resistant when they were in the presence of B. cenocepacia?

The authors suspected that the B. cenocepacia were releasing something into their environment that interfered with the action of the antibiotic, making it less potent. Experiments revealed that the bacteria were indeed secreting two proteins molecules associated with increased antibiotic resistance: putrescine (named for its putrid odor!) and Ycel, a protein whose function was previously unknown.

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The large amounts of secreted putrescine blocked the antibiotics’ binding to the surface of the bacteria, and could make both B. cenocepacia and P.aeruginosa more resistant to polymyxin B when grown together.

Ycel, on the other hand, was able to bind to the antibiotic directly, presumably decreasing its potency. Ycel is predicted to bind amphiphilic molecules (such as detergents, which  are attracted to both water and oil). Consistent with this prediction, the authors showed that Ycel had a protective effect against amphiphilic antibiotics and less of an effect against others.

These results have implications for combating the growing problem of antibiotic resistance. If we could prevent bacteria from making putrescine or Ycel, antibiotic treatments might be more effective, helping us eventually outflank resistance.

Citations: El-Halfawy OM, Valvano MA (2013) Chemical Communication of Antibiotic Resistance by a Highly Resistant Subpopulation of Bacterial Cells. PLoSONE 8(7): e68874. doi:10.1371/journal.pone.0068874

Bragonzi A, Farulla I, Paroni M, Twomey KB, Pirone L, et al. (2012) Modelling Co-Infection of the Cystic Fibrosis Lung by Pseudomonas aeruginosa and Burkholderia cenocepacia Reveals Influences on Biofilm Formation and Host Response. PLoS ONE 7(12): e52330. doi:10.1371/journal.pone.0052330

Images: Pseudomonas aeruginosa doi:10.1371/journal.pone.0066257

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8 Responses to Resisting Antibiotics: Some Bacteria Get By With a Little Help From Their Friends

  1. Magnus Kjaergaard says:

    Cool story, but you write that putrescine is a protein, which is not the case. It is a small molecule:

  2. Miguel A. Valvano says:

    Dear Meg
    Thank you very much for your nice comment. Could you please correct the spelling of the microorganism. It should be listed as Burkholderia cenocepacia, not Burkholderia cenopecia. It is consistently misspelled throughout the article.
    Thank you

    • Meg Byrne says:

      Thank you so much for pointing this out. I apologize for the error and have corrected it throughout.

  3. Miguel A. Valvano says:

    Dear Meg
    To add more clarity to the link you have chosen to refer to Burkholderia cenocepacia, it would be worth indicating that the B. cenocepacia is one of the several bacterial species from the Burkholderia cepacia complex. The CDC site is considerably misinformed. B. cenocepacia, and in particular the strain we have used in our research has epidemic characteristics, as it can be transmitted across cystic fibrosis patients, hence its significance as an opportunistic bacterium.

  4. charu kothari says:

    We have recently investigated antibiotics load in new born baby (without antibiotics selection). Results indicate that antibiotic resistance is the community.
    Strict antibiotics policy need to be implemented in developing world especially.
    Results of our findings are published recently in BMC microbiology

  5. Miguel A. Valvano says:

    Dear Meg
    Magnus is right. The sentence that reads: “…secreting two proteins associated with increased antibiotic resistance: putrescine (named for its putrid odor!) and Ycel, a protein whose function was previous…” Should read as follows:

    “…secreting TWO MOLECULES associated with increased antibiotic resistance: putrescine (named for its putrid odor!) and Ycel, a protein whose function was previous…”

    This will clarify the confusion. Putrescine is a small molecule that derives from the metabolism of certain amino acids, the building blocks for proteins.


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