Antibiotics substances kill bacteria and fungi

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   Antibiotics are natural substances secreted by bacteria and fungi to kill other bacteria that are competing for limited nutrients. Antibiotics were first discovered through a providential experiment by Alexander Fleming in 1928. His work eventually led to the large-scale production of penicillin from the mold Penicillium notatum in the 1940s. As early as the late 1940s resistant strains of bacteria began to appear. Antimicrobial resistance occurs when bacteria change or adapt in a way that allows them to survive in the presence of antibiotics designed to kill them by mutation or by using a built-in design feature to swap DNA (called horizontal gene transfer) bacteria share resistance genes Currently, it is estimated that more than 70% of the bacteria that cause hospital-acquired infections are resistant to at least one of the antibiotics used to treat them.

The phenomenon of bacterial drug resistance was first documented around 1952. Interest in the phenomenon has increased as fewer antibiotics are effective against pathogens, and as deaths from bacterial infections increase. Scientific interest in this problem because live are at stake. In an academic sense, this issue is importance to evolutionists because they believe the mutations in bacteria responsible for drug resistance are, from the standpoint of the bacterial population, “good,” and thus offer significant proof of evolution.

   In the next pages, the origin of MRSA will be discussed. In addition, the attempts to answer of this question will be included: are these resistance mechanisms sufficient to explain evolution or helps the evolutionists' case?

The resistance to oxacillin or methicillin is associated with acquisition of a mobile genetic element called SCCmec, which contains the mecA resistance gene. The mecA determinant encodes PBP2a, a new penicillin binding protein with decreased affinity for oxacillin and most other beta-lactam drugs.

   The antibiotics resistance can be detected by phynotypic methods such as disc diffusion test or by genotypic methods such as detection antibiotic resistance genes or cloning the suspected gene.

The origins of the major MRSA clones are still poorly understood, two very different hypotheses have been put forth to explain the origin of MRSA strains (5, 16). The association of the mec gene with genetically diverse lineages of S. aureus, together with data indicating that the mec gene was horizontally transferable in the laboratory, led to the hypothesis that MRSA strains had evolved many independent times by lateral gene transfer of the mec element into phylogenetically distinct methicillinsusceptible precursor cell lines (5). In contrast, data obtained from study of MRSA by restriction fragment length polymorphism analysis with probes for mecA and Tn554 were interpreted to mean that MRSA organisms evolved from a susceptible clone that acquired the mec element and subsequently generated substantial chromosomal diversity (16). Another study discovered that MRSA strains were assigned to at least five distinct chromosomal genotypic groups that, relative to one another, are highly divergent, in some cases differing by greater than several hundred genes. Hence, the only reasonable interpretation of the data is that the MRSA strains have arisen multiple independent times by lateral transfer of the mec element into methicillin-susceptible precursors.

   The origins of antibiotic resistance genes are obscure because at the time that antibiotics were introduced the biochemical and molecular basis of resistance was yet to be discovered. As the evolutionary time frame has to be less than 60 years it is not possible to derive a model in which evolution could have occurred by mutation alone from common ancestral genes. They must have been derived from a large and diverse gene pool presumably already occurring in the bacteria.

   The issue here is not how the bacteria can develop resistance to antibiotics and how we can demonstrate and identify it. The issues is, are these resistance the result of bacteria evolving new genes in response to the presence of antibiotics, or are antibiotic-resistant bacteria selected for in the environment by possessing antibiotic resistance genes beforehand? And whether or not such resistance helps the evolutionists' case and sufficient to meet the evolution case criteria? We suggest that it does not, for the following reasons.

   First, the mutations responsible for antibiotic resistance in bacteria do not arise as a result of the “need” of the organisms, because the bacteria did not “mutate” after being exposed to antibiotics; the mutations conferring the resistance were present in the bacterial population even prior to the discovery or use of the antibiotics. The Lederbergs' experiments in 1952 on streptomycin-resistant bacteria showed that bacteria which had never been exposed to the antibiotic already possessed the mutations responsible for the resistance. Malcolm Bowden has observed: “What is interesting is that bacterial cultures from bodies frozen 140 years ago were found to be resistant to antibiotics that were developed 100 years later. Thus the specific chemical needed for resistance was inherent in the bacteria” . These bacteria did not mutate to become resistant to antibiotics. Furthermore, the non-resistant varieties did not become resistant due to mutations.

Second, while pre-existing mutations may confer antibiotic resistance, such mutations may also decrease an organism's viability. For example, the surviving strains are usually less virulent, and have a reduced metabolism and so grow more slowly. Just because a mutation provides an organism with a certain trait does not mean that the organism as a whole has been helped. Bacteria may be resistant to a certain antibiotic, but that resistance comes at a price. Thus, in the grand scheme of things, acquiring resistance does not lead necessarily to new species or types of organisms.





The mechanisms of mutation and natural selection aid bacteria populations in becoming resistant to antibiotics. However, mutation and natural selection also result in bacteria with defective proteins that have lost their normal functions. For example, rifampin resistance in Staphylococcus aureus (Wichelhaus et al., 2002) resulted from mutations to the RNA polymerase that also reduced the relative fitness of most of the mutant strains. Although the biological cost reported by these researchers was generally not severe, it was measurable.


The accumulation of mutations doesn't lead to a new kind of bacterium-it leads to extinction.


Apologetics Press :: Reason & Revelation August 1994 - 14[8]:61-63

Bacterial Antibiotic Resistance-Proof of Evolution? by Bert Thompson