way which stops the antibiotic reaching its target , or which stops it from functioning normally at its target . The antibiotic can be stopped from reaching its target by , for example , modifying the cell wall of the bacterium to make it impermeable to the antibiotic , and therefore stop it from being able to get inside the bacterium , as seen in figure 2 .
Modification of the drug target is an example of a way to stop the normal function of an antibiotic ; if the antibiotic carries out its function by binding to a specific shaped region in the bacterium , then changing the shape of this region will stop the normal function of the antibiotic . This can be better understood with a lock and key model , where the antibiotic is a key and the binding region is the lock ; if the lock is changed then the key will no longer work as it is the wrong shape to open the lock .
Figure 2 shows one method of inactivating an antibiotic , which is to change its structure by adding a phosphate group . This impairs the normal function of the antibiotic , which would be to bind to the ribosomes of the bacterium , and affect the bacterium ’ s ability to produce proteins , which it needs in order to survive .
The mechanisms described above are all possible due to alterations in the DNA of the bacterium , known as mutations ( Benveniste and Davies , 1973 ). The DNA is the code to make proteins . For example , to modify the cell wall as in figure 2 , the DNA mutates so that it codes for the new , modified cell wall protein , which causes its impermeability , instead of the normal cell wall protein , which is permeable .
There are different types of mutation , but figure 3 shows an insertion mutation , where extra DNA is inserted into the bacterium ’ s existing DNA ( U . S . National Library of Medicine , 2020 ). In figure 3 the DNA is shown to code for a sequence of amino acids , which are the the building blocks of a protein .
In the lower DNA strand the insertion of the nucleotide has clearly changed the amino acid sequence , where the alterations are shown in orange . From this it can be seen how changes in the bacterial DNA can indirectly lead to the development of antibiotic resistance in bacteria .
What makes ‘ Superbugs ’ ‘ super ’?
Penicillins are a group of antibiotics that impair the ability of bacteria to repair their cell wall , the outer covering that protects all the internal structures of the bacteria . Penicillins , which include methicillin , are part of a wider group of antibiotics known as β-lactams . The example of MRSA is better adapted for resistance to β-lactams than non-superbug types of SA .
In SA and MRSA , transpeptidases , also known as penicillin-binding proteins ( PBPs ), are either partly or fully responsible for cell wall formation . For β-lactams , PBPs are good targets as they are essential for cell wall repair , and for bacterial survival . SA has four PBPs ; MRSA has the same four PBPs , but it also has a fifth , PBP2a . Figure 4 shows the difference between PBPs in SA , and PBP2a ; in A , PBP2 is seen to have a binding region for the β-lactam , which PBP2a does not , preventing the antibiotic from functioning normally . MRSA can then proceed to inactivate the β-lactam , as in B .
PBP2a is still able to continue functioning close to normally in the presence of β-lactams , where the functions of the other four PBPs would be severely impaired . This means that MRSA can sustain cell wall repair when β-lactams are used , while SA cannot . The capability to produce PBP2a is unique to MRSA , and the production gene was acquired from another , non-SA organism ( Chang et al ., 2014 ).
Superbugs have a particularly high ability to infect a patient and to spread rapidly . Of hospital based SA infections , many are caused by MRSA , which is antibiotic resistant , meaning it has resistance to more than one antibiotic ; a number of MRSA kinds are resistant to most commonly used antibiotics ( Foster , 2004 ). Several other bacteria have also been classified as being resistant to multiple antibiotics ( Bajpai et al ., 2017 ).
Until recently , MRSA had remained sensitive to the antibiotic vancomycin , but subsequently the bacteria developed low levels of resistance to the drug ; MRSA now has , however , developed high levels of vancomycin resistance due to the transfer of resistance genes to SA from another kind of bacteria known as Enterococcus ( Foster , 2004 ).
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