Genetic Antibiotic Resistance

Antibiotic resistance began shortly after Penicillin was discovered and has become a bigger issue over time. The following have contributed to the growing resistance. Antibiotics have low specificity resulting in over prescription and over usage, sometimes for the wrong infection as no bacterial identification is done before prescribing. Inappropriate use of antibiotics is often seen in developing countries as there is less regulation and a lack of cost-effective alternative treatments. Farm animals are also given antibiotics to prevent bacterial infection outbreaks and to increase their weight, but this results in animals carrying resistant bacteria which is then ingested by humans.

Some species of bacteria are naturally or intrinsically resistant to a certain family or families of antibiotics without mutation. However, acquired resistance is caused by one of the following mechanisms: chromosomal, plasmid or transposon mediated resistance. Bacteria are then no longer inhibited or killed by concentrations of antibiotics administered at doses they were once susceptible to.

Chromosomal mediated resistance occurs when a gene mutates in one bacterial cell with replication leading to an increased number of resistant bacterial cells. All non-mutated bacterial cells are destroyed by antibiotics leaving mutated, resistant bacteria to survive. An example of this is a mutation in the rpoB gene of Mycobacterium tuberculosis resulting in resistance to Rifampicin, a first line drug used to treat Tuberculosis (TB). Alternative treatments such as chemotherapy are more expensive and extend the treatment time from 6 months to 2 years making treatment less accessible to those in developing countries where TB is endemic. Plasmid mediated resistance occurs when resistance genes are present on the plasmid making transmission to other cells quick and easy, leading to resistance to multiple antibiotics. This can result in conformational change in the active site of the bacterial enzyme so that the drug cannot bind which occurs with MRSA. An alternative target enzyme can also be synthesised by the bacterial cell in which the antibiotic drug cannot bind to, or enzymes specifically designed to break down and inactivate the antibiotic can be synthesised by the bacterial cell. Transposons can carry resistance genes and integrate into the chromosome in a plasmid leading again to quick and easy transmission between bacterial cells. This leads to transposon mediated resistance which can be seen as Tetracycline resistant genes on transposons are transferred from cell to cell enabling drug efflux as the genes code for the synthesis of bacterial membrane proteins.