Tuesday, 15 May 2012

the "EVOLUTION" of antibiotic resistance

Antibiotic are powerful medicine to treat bacterial infection by either killing the bacteria or interact with the protein of the bacteria to stop the replication of DNA. According to the articles written by Daniel Criswell, the number of antibiotic resistance in bacteria has increase since the year 1950.
In the year 1929, a British microbiologist, Alexander Fleming was exposed the penicillin.  The antibiotic penicillin is derived from the bread mold or fungi called penicillium. Alexander Fleming was multiply the antibiotic and successfully used as medicine to fight against bacterial infection in 1940. However, the penicillin is not always the strongest antibiotic against the bacteria, the bacteria will undergo several gene mutation which resistance to penicillin. In 1967, the first penicillin resistant Streptococcus pneumonia was discovered in Australia. According to the statistical research by Doern, 2011, he predicted that 3-5% of S. pneumonia were penicillin resistant in 1980. This number is continuously increase to 34% in 1998. This scenario not only occurs in penicillin but also other antibiotic such as tetracycline and kanamycin (Shoemaker, 2001)
The bacteria is not evolving new genes in resistance to the antibiotic, but it acquire resistance by either genetic mutation or receiving advantages gene from other bacteria. Mutation can lead to change in DNA and sometimes lead to change in the gene product which is resistance to antibiotic. For example, protein gyrase is an essential enzyme for DNA replication. The antibiotic such as novobiocin interfere with protein gyrase to block the replication of the DNA and lead to cell death (Contreras and Maxwell, 1992). However, when spontaneous mutation occurs, it changed the shape and conformation of the active size and so the antibiotic can no longer bind efficiently to the protein gyrase.

Some bacteria posses gene which produce the enzyme that chemically degrade, destroy or neutralize the antimicrobial before it reach the target cell and damage the bacteria. In addition, a mechanism knows as efflux pump which located in the cell membrane make certain bacteria become resistance to antibiotic. The antibiotic entered to the bacterium through a channel called porin and pumped back out of the bacterium by the efflux pump (Chopra and Robert, 2001). The efflux pump actively pumped out the antibiotic to prevent intracellular accumulation.
Bacterium has a special characteristic to transfer the advantages gene from one bacterium to another. This unique feature is not found in either animal cell or plant cell. When two bacteria come close to each other, a bridge-like structure form and allow the copy of plasmid transfer from one bacteria to another. This process is called conjugation. Conjugation is mediated by a particular kind of circular DNA called plasmid which contain antibiotic-resistant genes.
Genetic mutation may provide an advantage of antibiotic resistance to the bacteria, but this will come with some negative effect.  For example, genetic mutation of the ribosome may change the conformation of the active site, so the antibiotic is not able to bind with the ribosome. However, the changed of the shape of the ribosome will slow down the protein synthesis and growth rate (Gregory, ST, 2001).

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