How do antibiotics work?

A magnified shot of Penicillium notatum mold.
© Visuals Unlimited/Corbis

Before we had antibiotics, there were few choices when it came to treating infections: You could wait and see if the infection improved on its own, or you could cut the infection off of your body. It wasn't until 1928 that the very first antibiotic was discovered -- accidentally, at that -- when researcher Alexander Fleming came back to work after a weekend away from his lab and found a certain type of mold, Penicillium notatum, had halted the growth of Staphylococcus (staph -- a bacteria that can cause skin infections, pneumonia and some food-borne illness, among other infections) in his petri dishes. And not only did it kill Staphylococcus, it also worked when he tried it against other bacteria, including Streptococcus, Meningococcus and Diphtheria bacillus.

Antibiotics work against bacterial infections; many of us have used them to treat infections ranging from strep throat to bladder infections and many types of skin infections. But they won't do any good against a viral infection, including colds and most coughs, influenza or gastroenteritis (which is often referenced by the misnomer "stomach flu"). While all antibiotics will kill or stop the growth of bacteria, not all antibiotics are effective against the same bacteria, and not all antibiotics fight bacteria in the same way.


The type of antibiotic your doctor prescribes to treat your infection depends on the type of bacteria causing that infection. Most bacteria fall into two types: Gram-positive and Gram-negative. These classifications are based, basically, on the type of cell wall that the bacteria has. Gram-positive bacteria -- such as Streptococcus -- have thin, easily permeable, single-layered cell walls. Gram-negative bacteria -- such as E. coli -- have thicker, less penetrable, two-layer cell walls. For an antibiotic to successfully treat a bacterial infection, it needs to be able to penetrate either or both types of bacterial cell walls.

Let's get down and dirty with how antibiotics destroy bacteria.


Antibiotics vs. Bacteria

Antibiotics work in one of a few ways: by either interfering with the bacteria's ability to repair its damaged DNA, by stopping the bacteria's ability to make what it needs to grow new cells, or by weakening the bacteria's cell wall until it bursts.

Most antibiotics on the market are considered broad spectrum, which means they are effective against a lot of different types of bacteria, both Gram-positive and Gram-negative. Fluoroquinolones (used to treat infections ranging from urinary tract infections to pneumonia and anthrax) and tetracyclines (used to treat everything from acne to gonorrhea as well as stomach ulcers) are both examples of broad spectrum antibiotics -- these antibiotics can clear up many types of bacterial infections. Narrow spectrum antibiotics, on the other hand, are effective against specific, targeted groups of bacteria -- either Gram-negative or Gram-positive but not both.


Quinolones, for instance, are a type of broad-spectrum antibiotic that kills bacteria with hydroxyl radicals, which are molecules that destroy the lipids and proteins that make up a cell's membrane and damage cell DNA, halting replication.

Penicillins, an example of narrow-spectrum antibiotics, work by destroying the structure of a cell wall, the layer that holds the whole cell together; glycopeptide antibiotics also go to work on the structure of a cell wall, specifically preventing Gram-positive bacteria from being able to build new walls -- and a cell can't live without the wall that holds all of its innards, well, inside.

Instead of destroying a cell from the outside in, like penicillin, some antibiotics block a cell's ability to make what it needs to proliferate from the inside out. Macrolide antibiotics are protein synthesis inhibitors; for example, the common macrolide antibiotic erythromycin works by binding to specific molecules -- subunits -- in a cell's ribosome, destroying the cell's ability to form the proteins it needs for cell growth. Sulfa antibiotics (sulfonamides) have been used to battle bacterial infections since the 1930s. They target specific chemical reactions within a cell -- the metabolic pathways -- by binding to an enzyme called dihydropteroate synthase (DHPS), which then blocks bacteria's ability to synthesize dihydriofolic acid. When this type of bacterial cell stops being able to metabolize folate, it can no longer grow or multiply.


Antibiotic Resistance: When Antibiotics Stop Working

Vancomycin-resistant Enterococci, a bacteria that's adapted over time to the point that antibiotics are not as effective in fighting it.
© CDC/PHIL/Corbis

Antibiotics were once heralded as a miracle, and while they really are still a stroke of therapeutic good fortune, taking them does come with some risk.

Some antibiotics are associated with some nasty side effects; while they're designed to kill the infection-causing bacteria in your body, they can also cause problems when they kill the good bacteria living inside you. Antibiotics may cause vaginal infections (what we commonly call yeast infections), as well as upset stomach and diarrhea, among other problems.


When we overuse antibiotics we can run into trouble, too. For example, of the 68 percent of people with acute respiratory tract infections (such as sinus infections) who are prescribed antibiotics by their doctor, only 20 percent of them actually need those prescriptions [source: CDC]. Taking antibiotics when you don't need them not only can cause side effects, but may also contribute to a bigger problem: antibiotic-resistant bacteria.

When you don't use antibiotics as prescribed -- not taking the complete run of your medication or taking antibiotics when you don't need them -- you contribute to the problem of antibiotic-resistant bacteria. What this means is that the antibiotic designed to kill a specific type of bacteria is less effective against that organism because that organism has adapted -- it's evolved with exposure and time -- to be stronger against the treatment. Methicillin-resistant Staphylococcus aureus (MRSA) is well-known example of a so-called superbug, as is vancomycin-resistant Enterococci (VRE). Some strains of gonorrhea have developed resistance to multiple drugs, and some types of tuberculosis have also developed resistance to multiple drug therapies (isoniazid and rifampicin).

Antibiotic-resistant bacterial infections take longer to treat and cause more and longer hospitalizations. The CDC estimates that annually more than 2 million Americans develop antibiotic-resistant infections -- and more than 23,000 people die from these infections and their complications each year [source: CDC].


Lots More Information

Author's Note: How Antibiotics Work

Hot job of 1939? Penicillin girls, employed to extract mold juice for antibiotic production. Where do I sign up?

Related Articles

More Great Links

  • American Academy of Pediatrics - Healthy Children. "How Do Antibiotics Work." July 31, 2013. (March 15, 2014)
  • American Chemical Society (ACS). "Discovery and Development of Penicillin." (March 15, 2014)
  • Boggs, Will. "Narrow-spectrum antimicrobials favored for children hospitalized with pneumonia." Reuters Health. Oct. 28, 2013. (March 15, 2014)
  • Centers for Disease Control and Prevention (CDC). "Antibiotic / Antimicrobial Resistance." March 4, 2014. (March 15, 2014)
  • Centers for Disease Control and Prevention (CDC). "Get Smart: Know When Antibiotics Work - Fast Facts." Nov. 4, 2013. (March 15, 2014)
  • Centers for Disease Control and Prevention (CDC). "Get Smart: Know When Antibiotics Work -- What Everyone Should Know and Do - Snort. Sniffle. Sneeze. No Antibiotics Please!" Nov. 4, 2013. (March 15, 2014)
  • Centers for Disease Control and Prevention (CDC). "Threat Report 2013." March 10, 2014. (March 15, 2014)
  • Diffen. "Gram-negative Bacteria vs Gram-positive Bacteria." (March 15, 2014)
  • Earl, Lesley. "How Sulfa Drugs Work." National Institutes of Health (NIH) - NIH Research MattersMarch 12, 2012.(March 15, 2014)
  • Foti, James J.; Devadoss, Babho; Winkler, Jonathan A.; Collins, James J.; and Graham C. Walker. "Oxidation of the Guanine Nucleotide Pool Underlies Cell Death by Bactericidal Antibiotics." Science. Vol. 336. Pages 315-319. April 20, 2012. (March 14, 2014)
  • Kohanski, Michael A.; Dwyer, Daniel J.; and James J. Collins. "How antibiotics kill bacteria: from targets to networks." Nature Reviews Microbiology. Vol. 8. Pages 423-435. June 2010. (March 15, 2014)
  • Mayo Clinic. "Antibiotics: Misuse puts you and others at risk." Feb. 4, 2012. (March 15, 2014)
  • Michigan State University - Antimicrobial Resistance Learning Site. "Classification according to spectrum of activity." (March 15, 2014)
  • Mobley, Harry. "How do antibiotics kill bacterial cells but not human cells?" Scientific American. March 13, 2006. (March 15, 2014)
  • Neu, Harold C.; and Thomas D. Gootz. "Chapter 11: Antimicrobial Chemotherapy." Medical Microbiology. 4th edition. The University of Texas Medical branch at Galveston. 1996. (March 15, 2014)
  • NIH - National Institute of Allergy and Infectious Diseases. "Antimicrobial (Drug) Resistance." Feb. 4, 2014. (March 15, 2014)
  • NIH - National Institute of Allergy and Infectious Diseases. "Antimicrobial (Drug) Resistance -Gram-negative Bacteria." April 30, 2012. (March 15, 2014)
  • NPS MedicineWise. "What are antibiotics and how do they work?" (March 15, 2014)
  • Paddock, Catharine. "Antibiotics Kill Bacteria By Damaging Their DNA." Medical News Today. April 23, 2012. (March 15, 2014)
  • PBS. "People and Discoveries: Fleming discovers penicillin." 1998. (March 15, 2014)
  • Sigma-Aldrich. "Inhibition of Cell Wall Biosynthesis by Antibiotics." 2006. (March 15, 2014)
  • SRS Pharmaceuticals. "Narrow Spectrum Antibiotics." (March 15, 2014)
  • U.S. Library of Medicine - Genetics Home Reference. "Cells and DNA." March 10, 2014. (March 15, 2014)