How Antibiotic Resistance Happens
Antibiotic resistance is a naturally occurring process. However, increases in antibiotic resistance are driven by a combination of germs exposed to antibiotics, and the spread of those germs and their resistance mechanisms.
Antibiotic resistance does not mean our body is resistant to antibiotics. It means the bacteria or fungi causing the infection are resistant to the antibiotic or antifungal treatment.
- Germs are microbes—very small living organisms including bacteria, fungi, parasites, and viruses.
- Most germs are harmless and even helpful to people, but some can cause infections. Harmful germs are called pathogens.
- Antimicrobials is a term used to describe drugs that treat many types of infections by killing or slowing the growth of pathogens causing the infection.
- Bacteria cause infections such as strep throat, foodborne illnesses, and other serious infections. Antibiotics treat bacterial infections.
- Fungi cause infections like athlete’s foot, yeast infections, and other serious infections. Antifungals treat fungal infections.
- People sometimes use “antibiotic” and “antimicrobial” interchangeably.
Antibiotics save lives but their use can contribute to the development of resistant germs. Antibiotic resistance is accelerated when the presence of antibiotics pressure bacteria and fungi to adapt.
Antibiotics and antifungals kill some germs that cause infections, but they also kill helpful germs that protect our body from infection. The antibiotic-resistant germs survive and multiply. These surviving germs have resistance traits in their DNA that can spread to other germs.
To survive, germs develop defense strategies against antibiotics called resistance mechanisms. DNA tells the germ how to make specific proteins, which determine the germ’s resistance mechanisms. Bacteria and fungi can carry genes for many types of resistance.
When already hard-to-treat germs have the right combination of resistance mechanisms, it can make all antibiotics ineffective, resulting in untreatable infections. Alarmingly, antibiotic-resistant germs can share their resistance mechanisms with other germs that have not been exposed to antibiotics.
This table gives a few examples of defense strategies used to resist the effects of antibiotics.
|Restrict access of the antibiotic||Germs restrict access by changing the entryways or limiting the number of entryways.
Example: Gram-negative bacteria have an outer layer (membrane) that protects them from their environment. These bacteria can use this membrane to selectively keep antibiotic drugs from entering.
|Get rid of the antibiotic||Germs get rid of antibiotics using 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.
|Change or destroy the antibiotic||Germs change or destroy the antibiotics with enzymes, proteins that break down the drug.
Example: Klebsiella pneumoniae bacteria produce enzymes called carbapenemases, which break down carbapenem drugs and most other beta-lactam drugs.
|Change the targets for the antibiotic||Many antibiotic drugs are designed to single out and destroy specific parts (or targets) of a bacterium. Germs change the antibiotic’s target so the drug can no longer fit and do its job.
Example: Escherichia 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.
|Bypass the effects of the antibiotic||Germs develop new cell processes that avoid using the antibiotic’s target.
Example: Some Staphylococcus aureus bacteria can bypass the drug effects of trimethoprim.
How Antibiotic Resistance Spreads
Bacteria and Fungi Fight back Against Antibiotics
How Antibiotic Resistance Moves Directly Germ to Germ
Select Germs Showing Resistance Over Time