Power in numbers – collective antibiotic resistance


For over 70 years, antibiotics have been a critical component of the arsenal used by healthcare providers to combat bacterial infections worldwide (1). Antibiotic use has become so prevalent that over 70 billion doses were consumed globally in 2010 (1). Due to the widespread use of antibiotics, some bacteria have developed antibiotic resistance and become superbugs. This transformation can result in normally treatable conditions turning into potentially life-threatening events even in hospital settings, which is a major public health challenge. Last week, the CDC reported that a woman in Nevada who had recently returned from India died in September from superbug infection resistant to 26 antibiotics (2).

To overcome the growing challenge of antibiotic resistance, scientists are engaging in research to better understand it. Antibiotic resistance can be conferred by several mechanisms. Bacteria can be either intrinsically resistant to certain antibiotics and/or they can develop resistance through genetic mutations and gene transfer (2). Acquired resistance to antibiotics is due to three main mechanisms. First, intracellular concentrations of an antibiotic may be reduced due to poor penetration of the drug or antibiotic efflux (3). Second, antibiotic targets can be changed by genetic mutation or post-translational modification of the target (3). And third, antibiotics can be hydrolyzed or modified directly (3).

However, in addition to molecular mechanisms of antibiotic resistance, the ecological niche and the presence of bacterial communities also play important roles in antibiotic resistance. In a recent study by Sorg, R.A. et al. (2016), nonresistant Streptococcus pneumoniae bacteria grew in the presence of the antibiotic chloramphenicol (Cm) when they were mixed with resistant Staphylococcus aureus bacteria (4). Although gene transfer did not occur, sensitive S. pneumoniae bacteria survived and multiplied when they were grown in conjunction with resistant S. aureus bacteria (4). S. aureus bacteria expressed chloramphenicol acetyltransferase (CAT) and deactivated the antibiotic intracellularly resulting in reduced extracellular concentrations of Cm (4). This then allowed S. pneumoniae bacteria to be passively resistant and multiply in growth culture, semisolid surfaces of microscopy slides, and in a mouse infection model (4). Therefore, due to collective resistance in the bacterial community, the ability of the antibiotic therapy to be successful became more difficult. Collective resistance can also give rise to multidrug resistance in bacterial communities due to increased survival of sensitive cells that leads to opportunities for horizontal gene transfer (4).

The life sciences community is addressing the need to better understand antibiotic resistance mechanisms and how to overcome them. The development and use of technologies such as real-time PCR and next-generation sequencing platforms is contributing to the identification of antibiotic resistance genes and improving understanding of virulence (5). If you are a research scientist interested in investigating antibiotic resistance, QIAGEN provides several tools from sample preparation to data analysis to help you with your research. In order to detect the presence of antibiotic resistance genes in a reliable way from a variety of sample types, we recommend Microbial DNA qPCR Arrays. These arrays can help you profile microbial species, virulence genes or antibiotic resistance genes using real-time PCR for specific and sensitive results.

Do you want to learn more about antibiotic resistance genes and hospital-acquired infections? Download the following resources:

•   Webinar recording of “Antibiotic Resistance and Hospital-acquired Infections”
•   Antibiotic Resistance Gene Resource and Assay List



  1. 1. Blaser, M.J. (2016) Antibiotic use and its consequences for the normal microbiome. Science. 352, 544– 545. Link
  2. 2. Chen, L. (2017) Notes from the Field: Pan-Resistant New Delhi Metallo-Beta-Lactamase-Producing Klebsiella pneumoniae — Washoe County, Nevada, 2016. MMWR, 66, 33. Link
  3. 3. Blair, J.M., Webber, M.A., Baylay A.J., Ogbolu D.O., and Piddock, L.J. (2015) Molecular mechanisms of antibiotic resistance. Nat Rev Microbiol. 13, 42–51. Link
  4. 4. Sorg, R.A. et al. (2016) Collective Resistance in Microbial Communities by Intracellular Antibiotic Deactivation. PLoS Biol. doi: 10.1371/journal.pbio.2000631. Link
  5. 5. Frieri, M., Kumar, K., and Boutin, A. (2016) Antibiotic Resistance. J Infect Public Health. doi: 10.1016/j.jiph.2016.08.007. Link


Nesrin Soetkamp

Nesrin Soetkamp, PhD is a Content Marketing Manager at QIAGEN. She received her PhD in Physiology and Biophysics from Georgetown University, where she studied the molecular mechanisms of taxane resistance in breast cancer. Prior to entering the biotech industry, Dr. Soetkamp worked as a postdoctoral fellow at the National Institutes of Health. At the NIH, she developed new methods to distinguish malignant adrenocortical tumors from benign tumors and normal tissue in the adrenal glands/cortex using epigenetic methylation patterns.

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