16  Resistance to antibiotics
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The fact that bacteria can become resistant to antibiotics is often seen as an observable example of evolution. However, mutations which lead to a resistance to antibiotics will result, as a rule, in a loss of information in the genome. In the vast majority of cases, only a single base in the genome is altered, making it impossible for a certain bacterium to establish itself in the body of the host. In the process, there is no increase of information in the genome.


In a sufficiently large population, antibiotic resistant mutations on culture media containing antibiotics can be established particularly easily. Antibiotic resistant cells are, however, present even before the antibiotic takes effect. The antibiotic itself only fulfils a selection function. Lederberg’s replica test (growth despite antibiotics) provides direct proof of this.


An extract from Evolution, a Critical Textbook (1):

“In order to understand the development of resistance on a molecular level, one should first of all observe antibiotics which inhibit protein synthesis by binding to ribosomal proteins. The resistance to antibiotic spectinomycin is associated with the structure of the S5 protein of the small ribosomal subunit. That is where the antibiotic binds. A mutation leads to an exchange of the amino acid serin with prolin at a particular place on the S5 protein. This exchange results in an alteration of the spatial structure of the protein, by which the binding site for spectinomycin is also affected. As a result, the antibiotic can no longer attack the S5 protein; the bacterium has become resistant.

A further possibility of the formation of resistance (e.g., to chloramphenicol) exists in detoxification by acetylation (binding of an acetic acid residue). This happens as a result of the enzyme chloramphenicol o-acetyltransferase (CAT) and is the result of gene duplication.
 
It is understandable that bacteria have mechanisms to degrade antibiotics, as fungi produce antibiotics naturally to use them for defence against bacteria.


Penicillin synthesis (2):

The discovery of penicillin synthesis by brush-mould penicillium is a famous example. Penicillin inhibits the cell wall synthesis of bacteria and is split by resistant strains by penicillinase (beta-lactamase) and thereby rendered harmless. The gene for this enzyme is often localised on plasmids. One important class of antibiotic resistances is based on the new acquisition of genes by plasmid absorption (horizontal gene transfer).
 
There can be no doubt that the acquisition of antibiotic resistance is a micro evolutionary process with selection positive effect, if bacteria are exposed to antibiotics as a selection factor.



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References:

(1) Junker und Scherer, Evolution, ein kritisches Lehrbuch, Weyel Verlag, 2006, page 142.
(2) Junker und Scherer, page 143.
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