A Brief History of Antibiotic Usage & Resistance


Chinese herbalists use antimicrobial-rich plants, such as Artemisia, before the Common Era.[1]

Ancient Greeks, Indians, and others, use mouldy bread, plants, soil, to treat infections.

This long association with medicinal plant use may be a factor in the accumulation of antibiotic resistance genes in human populations.[2]


Dietary tetracycline in human skeletal remains from ancient Sudanese Nubia.[3]


Girolamo Fracastoro proposes transferable tiny particles or "spores" that can transmit infectious disease. Coins the term "fomite" - used today to indicate an object or substance capable of carrying infectious disease.[4]


John Parkington, herbarian to King Charles 1, recommends the therapeutic use of mould in his book on pharmacology.


John Tyndall explains antibacterial action of the Penicillium fungus to England's Royal Society.


Louis Pasteur and Jules Francois Joubert observe that cultures of the anthrax bacilli become inhibited when contaminated with moulds.


Ehrlich, Bertheim and Hata introduce Salvarsan, the world's first chemotherapeutic drug.[4] Salvarsan's success in treating syphilis establishes Ehrlich's systematic screening approach as the cornerstone of pharmaceutical drug-search strategies.


Alexander Fleming discovers penicillin.


Gerhard Domagk discovers Prontosil, the first synthetic sulfonamide. Sulfa drugs credited with saving thousands of lives during WWII.


Penicillin purified and concentrated by Florey and Chain, widely used by Allies during World War II for surgical and wound infections.


Penicillinase, a penicillin-resistant enzyme, isolated by Abraham and Chain from Gram-negative E. coli several years before penicillin enters clinical use.[5]


First indications of bacterial resistance to sulfa drugs.


Streptomycin introduced, the first effective treatment for tuberculosis.


Penicillin begins mass production. Alexander Fleming tells the New York Times: "The greatest possibility of evil in self-medication is the use of too-small doses, so that instead of clearing up infection the microbes are educated to resist penicillin."


Resistance to streptomycin noted during clinical trials.[6]


Tetracyclines introduced.

Some 40% of hospital Staphylococcus aureus isolates now penicillin-resistant.[7]


Methicillin, a form of penicillin, introduced (UK) to counter the growing problem of penicillin-resistant Staphylococcus aureus infections.


Some 80% of hospital Staphylococcus aureus isolates penicillin-resistant.[7]


Trimethoprim first used, mainly for the treatment of bladder infections.

Quinolone introduced for the treatment of urinary tract infections.

British scientists identify the first strains of Staphylococcus aureus to resist methicillin.


Resistance to quinolone develops.


Bacterial resistance to tetracycline class develops.

Trimethoprim-sulfonamide combination introduced in an attempt to counter bacterial resistance. Nevertheless, resistance spreads, particularly in countries where the combination is used.[8]

Methicillin resistant Staphylococcus aureus, (MRSA), first reported in the United States. Over the next 30 years, MRSA becomes resistant to an entire class of antibiotics (beta-lactams), including penicillin, amoxicillin, oxacillin, methicillin, and others.


MRSA outbreaks become increasingly common. MRSA recognized as an endemic pathogen.


MRSA shows resistance to vancomycin, one of very few antibiotics of last resort for use against Staphylococcus aureus infections.

Fluoroquinolones the most commonly prescribed class of antibiotics for adults in 2002. Nearly half (42%) of these prescriptions are for conditions not approved by the FDA.[9]


World Health Organization (WHO) report states, "Antibiotic resistance—when bacteria change so antibiotics no longer work in people who need them to treat infections—is now a major threat to public health."


President Barack Obama issues Executive Order – Combating Antibiotic-Resistant Bacteria (CARB). “Combating antibiotic-resistant bacteria is a national security priority.”


  1. Cui, L., Su, X-z. 2009. The discovery, mechanisms of action, and combination therapy of artemisinin. Exp. Rev. Anti Infect. Ther.  7, 999-1013.
  2. Aminov RI. A Brief History of the Antibiotic Era: Lessons Learned and Challenges for the Future. Frontiers in Microbiology. 2010;1:134.
  3. Bassett E. J., Keith M. S., Armelagos G. J., Martin D. L., Villanueva A. R. (1980). Tetracycline-labeled human bone from ancient Sudanese Nubia (A.D.350). Science 209, 1532–153410.1126/science.7001623
  4. https://en.wikipedia.org/wiki/Girolamo_Fracastoro
  5. Lloyd, N.C., Morgan, H.W., Nicholson, B.K., Ronimus, R.S., Riethmiller, S. Salvarsan – The First Chemotherapeutic Compound. Retrieved from: http://researchcommons.waikato.ac.nz/bitstream/handle/10289/188/content.pdf?sequence=1
  6. Abraham EP, Chain E (1940). An enzyme from bacteria able to destroy penicillin. Nature 46 (3713): 837–837.
  7. D’Arcy Hart P (August 1999). “A change in scientific approach: from alternation to randomised allocation in clinical trials in the 1940s”. British Medical Journal 319 (7209): 572–3.
  8. Chambers HF (2001). “The changing epidemiology of Staphylococcus aureus?”. Emerg Infect Dis 7 (2): 178–82.
  9. Huovinen P. Trimethoprim resistance. Antimicrobial Agents and Chemotherapy. 1987;31(10):1451-1456.
  10. Neuhauser, MM; Weinstein, RA; Rydman, R; Danziger, LH; Karam, G; Quinn, JP (2003). “Antibiotic resistance among gram-negative bacilli in US intensive care units: implications for fluoroquinolone use”. JAMA: the Journal of the American Medical Association 289 (7): 885–8.