Antiseptics (from Greek αντί - anti, '"against" + σηπτικός - septikos, "putrefactive") are antimicrobial substances that are applied to living tissue/skin to reduce the possibility of infection, sepsis, or putrefaction. Antiseptics are generally distinguished from antibiotics by the latter's ability to be transported through the lymphatic system to destroy bacteria within the body, and from disinfectants, which destroy microorganisms found on non-living objects. Some antiseptics are true germicides, capable of destroying microbes (bacteriocidal), whilst others are bacteriostatic and only prevent or inhibit their growth. Antibacterials are antiseptics that have the proven ability to act against bacteria. Microbicides which kill virus particles are called viricides or antivirals.


Usage in surgery

The widespread introduction of antiseptic surgical methods followed the publishing of the paper Antiseptic Principle of the Practice of Surgery in 1867 by Joseph Lister, inspired by Louis Pasteur's germ theory of putrefaction. In this paper he advocated the use of carbolic acid (phenol) as a method of ensuring that any germs present were killed. Some of this work was anticipated by:

and even the ancient Greek physicians Galen (ca. 130–200 AD) and Hippocrates (ca. 400 BC). There is even a Sumerian clay tablet dating from 2150 BC advocating the use of similar techniques.[2]

But every antiseptic, however good, is more or less toxic and irritating to a wounded surface. Hence it is that the antiseptic method has been replaced in the surgery of today by the aseptic method, which relies on keeping free from the invasion of bacteria rather than destroying them when present.

How it works

For the growth of bacteria there must be a food supply, moisture, in most cases oxygen, and a certain minimum temperature (see bacteriology). These conditions have been studied and applied in food preservation and the ancient practice of embalming the dead, which is the earliest known systematic use of antiseptics.

In early inquiries, there was much emphasis on the prevention of putrefaction, and procedures were carried out to find how much of an agent must be added to a given solution in order to prevent development of undesirable bacteria. However, for various reasons, this method was inaccurate, and today an antiseptic is judged by its effect on pure cultures of defined pathogenic celicular single helix microbes and their vegetative and spore forms. The standardization of antiseptics has been implemented in many instances, and a water solution of phenol of a certain fixed strength is now used as the standard to which other antiseptics are compared.

Some common antiseptics

Evolved resistance

Stuart B. Levy, in a presentation to the 2000 Emerging Infectious Diseases Conference, expressed concern that the over use of antiseptic and antibacterial agents might lead to an increase in dangerous, resistant strains of bacteria.[5] The theory states that this could cause bacteria to evolve to the point where they are no longer harmed by antiseptics.

Different antiseptics differ in how they cause bacteria to evolve, which leads to genetic defenses against particular compounds. It can also be dose dependent; resistance can occur at low doses but not at high; and resistance to one compound can sometimes increase resistance to others.


The body produces its own antiseptics, which are a part of the chemical barriers of the immune system. The skin and respiratory tract secrete antimicrobial peptides such as the β-defensins.[6] Enzymes such as lysozyme and phospholipase A2 in saliva, tears, and breast milk are also antiseptic.[7][8] Vaginal secretions serve as a chemical barrier following menarche, when they become slightly acidic, while semen contains defensins and zinc to kill pathogens.[9][10] In the stomach, gastric acid and proteases serve as powerful chemical defenses against ingested pathogens.


  1. Best M, Neuhauser D (2004). "Ignaz Semmelweis and the birth of infection control". Qual Saf Health Care 13 (3): 233–4. doi:10.1136/qhc.13.3.233. PMID 15175497. 
  2. Eming SA, Krieg T, Davidson JM (2007). "Inflammation in wound repair: molecular and cellular mechanisms". J. Invest. Dermatol. 127 (3): 514–25. doi:10.1038/sj.jid.5700701. PMID 17299434. 
  5. CDC - Antibacterial Household Products: Cause for Concern (Stuart B. Levy)Tufts University School of Medicine, Boston, Massachusetts, USA (Presentation from the 2000 Emerging Infectious Diseases Conference in Atlanta, Georgia)
  6. Agerberth B, Gudmundsson GH (2006). "Host antimicrobial defence peptides in human disease". Curr. Top. Microbiol. Immunol. 306: 67–90. doi:10.1007/3-540-29916-5_3. PMID 16909918. 
  7. Moreau J, Girgis D, Hume E, Dajcs J, Austin M, O'Callaghan R (1 September 2001). "Phospholipase A(2) in rabbit tears: a host defense against Staphylococcus aureus.". Invest Ophthalmol Vis Sci 42 (10): 2347–54. PMID 11527949. 
  8. Hankiewicz J, Swierczek E (1974). "Lysozyme in human body fluids.". Clin Chim Acta 57 (3): 205–9. doi:10.1016/0009-8981(74)90398-2. PMID 4434640. 
  9. Fair W, Couch J, Wehner N (1976). "Prostatic antibacterial factor. Identity and significance.". Urology 7 (2): 169–77. doi:10.1016/0090-4295(76)90305-8. PMID 54972. 
  10. Yenugu S, Hamil K, Birse C, Ruben S, French F, Hall S (2003). "Antibacterial properties of the sperm-binding proteins and peptides of human epididymis 2 (HE2) family; salt sensitivity, structural dependence and their interaction with outer and cytoplasmic membranes of Escherichia coli.". Biochem J 372 (Pt 2): 473–83. doi:10.1042/BJ20030225. PMID 12628001. 

See also