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Antibiotics are drugs which are used to treat infections. When they were first discovered they were thought to be a wonder drug that would eliminate all worldwide infection. However, it was soon realised that the bacteria they were treating would develop resistance against them. This resistance can be either intrinsic or acquired resistance. Acquired resistance is when the antibiotics are effective at treating the infection but over time they develop resistance[1]. Intrinsic resistance is when the bacteria never respond to the antibiotics they have always had resistance. In response to the increase in antibiotic resistance new drugs keep being synthesized in an attempt to find new cures – however, the amount of new effective antibiotics being found is rapidly decreasing[2][3].

It was Alexander Fleming who discovered the first known antibiotics. This was in the 1920s when he saw Staphylococci being inhibited by Penicillin. However discovering how to extract the penicillin and use it effectively did not occur until the 1940s[4].

There are three different types of antibiotics; bacteriostatic, bactericidal and bacteriolytic. Bactericidal antibiotics, on the other hand, kill all of the bacteria present, ridding the body of any present infection[5][6]. If you were to plot this on a graph of log cell number vs time, the total number of cells would remain constant (dead cells count towards total cell number), but the number of viable cells would drop dramatically. Bacteriostatic antibiotics act by simply halting the growth and proliferation of bacterial cells, to give the body time to deal with the infection. On the same type of graph, both total cell count and viable cell count would remain the same. Bacteriolytic antibiotics act to lyse the bacteria, dramatically decreasing the total cell count and the viable cell count. Many common antibiotics such as Penicillin act in this way. Penicillin acts by irreversibly binding to and inhibiting the enzyme (Transpeptidase) that creates cross-links between the peptidoglycan in the cell wall. The cell wall is now not functional to protect the bacterial cell from Lysis via Osmotic action. Bacteriolytic antibiotics may not be favourable in bacteria that contain endotoxins which would release upon cell lysis as these can be very harmful to the body.

Antibiotics are used to treat bacteria that cause infection. The first antibiotic to be discovered was penicillin and was founded by Alexander Fleming.


How was Penicillin discovered?

Alexander Flemming discovered penicillin completely by accident. He was working with a strain of Staphylococcus bacteria and found that the Petri dishes became infected with fungi. However, there was a ring around each colony where the bacteria had died. Flemming did some research into the fungi and found it came from the Penicillium genus which is how penicillin got its name[7].

Why do antibiotics work?

Bacteria and eukaryotes form two different kingdoms meaning that there are many differences between them. These differences can be exploited when trying to beat an infection. Drugs can directly inhibit a process in bacteria without causing any disruption to a similar process in the host organism. Many antibiotics target the cell wall biosynthesis as eukaryotic cells don’t have cell walls making it an easy target[8].

Antibiotic resistance.

The one factor that limits the use of antibiotics is the antibiotic resistance. The AR exists because of bacterial adaption (survival of the fittest), which comes from a high reproduction rate and enormous genetic plasticity of bacterial pathogens. The are two genetic mechanisms responsible for AR: mutational resistance and horizontal gene transfer. During the mutational resistance, the small part of the population of bacteria, which is under the effect of a drug, will develop a resistance (that may be "costly" to the bacteria, so predominant only in the presence of antibiotics). In HGT the resistant DNA material is adjusted from the environment[9].


  1. H P Rang, M M Dale et al. (2007). Rang and Dale's Pharmacology. 7th ed. Spain: Elsevier. 609-37.
  2. Yassin, Dawson (2007). Pharmacology. 3rd ed. China: Mosby. p201-210.
  3. H P Rang, M M Dale et al. (2007). Rang and Dale's Pharmacology. 7th ed. Spain: Elsevier. 609-37.
  4. Yassin, Dawson (2007). Pharmacology. 3rd ed. China: Mosby. p201-210.
  5. Yassin, Dawson (2007). Pharmacology. 3rd ed. China: Mosby. p201-210.
  6. H P Rang, M M Dale et al. (2007). Rang and Dale's Pharmacology. 7th ed. Spain: Elsevier. 609-37.
  7. Sadava et al. (2012). Life, the Science of Biology. 10th ed. Sunderland: Sinauer Associates Inc. 608
  8. Alberts et al. (2008). Molecular Biology of the Cell. 5th ed. New York: Garland Science. 1521-1522.
  9. Munita J, Arias C. Mechanisms of Antibiotic Resistance. Virulence Mechanisms of Bacterial Pathogens, Fifth Edition. :481-511.
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