Antibiotic resistance

Being able to treat infections quickly and efficiently with antibiotics such as penicillin is very important.  In the news this week it was reported that bacterial strain NDM-1 has shown resistance to our most effective antibiotics. How do these strains of bacteria gain resistance against antibiotics, and why is it important to be cautious about their indiscriminate use?

Antibiotics such as penicillin are known as beta-lactam antibiotics. They work by tricking bacteria to incorporate it into its cell wall. Once inserted, the cell wall weakens, eventually collapses and the bacterial cell dies. Best of all, these antibiotics are selective against bacterial cells and not normal cells, meaning that side-effects are minimised.

 

Unfortunately, bacterial strains gain resistance by introducing a ‘defensive’ enzyme. These enzymes, known as beta-lactamases, change the chemical structure of the antibiotics. This stops incorporation of the antibiotics into the cell wall and therefore, the bacteria stay alive. To combat this, we can develop new antibiotics that have a similar chemical structure to penicillin, but cannot be altered by the beta-lactamases. Some examples of these, such as Carbapenems have also recently appeared in the news here, and here, and also here.

Beta-lactamases are an evolutionary response to the use of antibiotics. The overuse of our new shiny antibiotics such as carbapenems will only lead to new defensive enzymes that can also neuter these antibiotics. Therefore, it is important to minimise the use of these antibiotics to when they are really needed.