Emerging Drug Resistance
Drug resistance is when bacteria adapt to the antibiotics designed to kill them, making our antibiotics less effective and limiting our treatment options. Infections from resistant organisms can be difficult to treat and often require costly and sometimes toxic alternatives that the bacteria have not developed resistance to yet. CDC works with public health partners worldwide to rapidly identify when new resistance mechanisms or resistance genes emerge, and uses this data to quickly inform outbreak support, when needed, and prevention activities to stop spread.
About Resistance Mechanisms
Bacteria will inevitably find ways to avoid the effects of the antibiotic drugs we develop. Some of these strategies, called “resistance mechanisms,” are listed below.
|Examples of Resistance
Mechanisms (or Strategies)
|Restrict access of the antibiotic||
By limiting the number or changing the size of the openings in the cell wall, resistant bacteria can keep antibiotic drugs from entering the cell altogether.
Example: Gram-negative bacteria have an outer layer that protects them from their environment. These bacteria can use this membrane to selectively keep antibiotic drugs from entering.
|Get rid of the antibiotic||
Resistant bacteria can use pumps in their cell walls to remove antibiotic drugs that enter the cell.
Example: Some Pseudomonas aeruginosa bacteria can produce pumps to get rid of several different important antibiotic drugs, including fluoroquinolones, beta-lactams, chloramphenicol, and trimethoprim.
|Destroy the antibiotic||
Some resistant bacteria use enzymes to break down the antibiotic drug and make it ineffective.
Example: Klebsiella pneumoniae bacteria produce enzymes called carbapenemases, which break down carbapenem drugs and most other beta-lactam drugs.
|Change the antibiotic||
Other resistant bacteria use enzymes to alter the antibiotic drug so that it loses its effectiveness.
Example: Staphylococcus aureus bacteria add compounds to aminoglycoside drugs to change its function.
|Bypass the effects of the antibiotic||
Some antibiotic drugs are designed to disrupt important processes critical to a bacteria’s survival, like the process of making nutrients. If successful, the antibiotic drug will keep the bacterium from performing all the steps needed in the process. Some resistant bacteria, however, have developed different and new processes to get around these drug disruptions. The new process may be slower but they can still bypass the effects of the drug.
Example: Some Staphylococcus aureus bacteria can bypass the drug effects of trimethoprim.
|Change the targets for the antibiotic||
Many antibiotic drugs are designed to single out and destroy specific parts (or targets) of a bacterium. Resistant bacteria can change the look of their targets so that the antibiotic does not recognize and destroy them, allowing the bacteria to survive.
Example: E. coli bacteria with the mcr-1 gene can add a compound to the outside of the cell wall so that the drug colistin cannot latch onto it.
About Resistance Genes
Bacteria develop the resistance mechanisms described above by using instructions provided by their DNA, or genes. Often, resistance genes are found within plasmids, pieces of DNA that can move between bacterial species in the same family (e.g., between two Enterobacteriaceae like E. coli) and sometimes even across bacterial families (e.g., from an E. coli to a non-Enterobacteriaceae like Pseudomonas aeruginosa). Because of this ability to easily move and share these genetic instructions, plasmids with resistance genes can help bacteria that cause treatable infections to develop new or different resistance mechanisms.
Tracking Emerging Resistance in the U.S.
CDC works to prevent the spread of drug resistance by tracking emerging resistance genes and infections caused by resistant bacteria. By knowing where and how changes in resistance are occurring, we can inform solutions—like outbreak response, drug development, and diagnostic development—to prevent spread and slow resistance.
CDC tracks reports of resistance mechanisms, including:
- Klebsiella pneumoniae carbapenemase (KPC) – KPC enzymes break down carbapenem drugs, making these drugs ineffective. See the KPC tracking map.
- New Delhi Metallo-beta-lactamase-1 (NDM-1) – NDM-1 also makes bacteria resistant to carbapenem drugs, which makes infections caused by bacteria with these resistance genes particularly difficult to treat. See the NDM-1 tracking map.
- Oxacillinase-48 (OXA-48) – OXA-48 makes bacteria resistant to carbapenem drugs and infections difficult to treat. See the OXA-48 tracking map.
- Plasmid-mediated Colistin Resistance (mcr -1) – mcr -1 make bacteria resistant to the antibiotic called colistin, a last-resort drug used to treat difficult-to-treat infections. See the mcr -1 tracking map.
- Verona Integron-Encoded Metallo-beta-lactamase (VIM) – VIM enzymes also makes bacteria resistant to carbapenem drugs. See the VIM tracking map.
- Page last reviewed: September 8, 2016
- Page last updated: February 23, 2017
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