How Do Antibiotics Actually Work?
Antibiotics are substances that kill prokaryotic cells, such as bacteria, while leaving eukaryotic cells (in humans and others) untouched. Antibiotics work in two ways: either by killing microorganisms (being ‘bactericidal), and immediately removing the threat, or by inhibiting the growth of the microorganisms (being ‘bacteriostatic’), allowing the host’s defence system to fight the threat.
Antibiotics that affect a wide range of bacteria are called broad spectrum antibiotics, e.g. amoxicillin, and antibiotics that affect only a few types of specific bacteria are called narrow spectrum antibiotics, e.g. penicillin.
Each type of antibiotic targets different parts in bacteria. For example bacteria have cell walls, whilst human cells don’t, so some antibiotics prevent the formation of cell walls. This renders the bacteria vulnerable to water flooding inside and bursting, which means that these bacteria cannot replicate and spread the infection. This is known as osmotic lysis. (lysis meaning breaking, whilst osmotic refers to the movement of water molecules from an area of higher concentration to an area of lower concentration).
Another method with which antibiotics target and kill bacteria is through interference with their DNA Replication, so that bacteria are unable to replicate further, and through interfering with their protein synthesis, which fundamentally blocks the normal running of their metabolic functions, rendering them dead or unable to replicate.
In the latter method, antibiotics make use of the fact that cell structures in bacterial cells are different to cell structures in human cells, so whilst humans (and all other eukaryotes) have 80S ribosomes (organelles in the cell that are responsible for protein synthesis), bacterial cells have 70S ribosomes, with a smaller molecular weight and different shape. These ribosomes are different enough for antibiotics to be able to recognise bacterial ribosomes as separate to eukaryotic ribosomes, and able to target them specifically without damaging the host’s own cells. The antibiotics interfere with the ribosomes to render them incapable of carrying out their function, leaving the bacteria to die.
Treating a patient with antibiotics causes the microbes to either adapt by mutating their genes, or die, (providing a ‘selective pressure’). If a strain of a bacterial species acquires resistance to an antibiotic, it will survive the treatment. As the bacterial cell with acquired resistance multiplies, this resistance is passed on to its offspring. The gene for antibiotic resistance is passed rapidly, not only through vertical transmission (i.e. replication through binary fission), but also through horizontal transmission (where a conjugation tube can be set up between bacteria, even those of different species, and the plasmids (circular loops of DNA) are transferred from bacteria to bacteria). In ideal conditions some bacterial cells can divide every 20 minutes; therefore after only 8 hours in excess of 16 million bacterial cells carrying resistance to that antibiotic could exist.
This resistance to many of our drugs means that it is increasingly difficult to treat infections of the antibiotic resistant bacterial strains, and so health officials warn that antibiotics should not be used to treat common colds, most sore throats, or the flu because these infections are caused by viruses, against which antibiotics are useless anyway. When used unnecessarily, antibiotics can lead to the spread of resistant bacteria.
A strain of bacteria is often referred to as a superbug if it is resistant to several different antibiotics. Antibiotic resistance has been observed in bacteria such as E.coli and MRSA (methicillin resistant staphylococcus aureus). These “super bugs” represent a threat to public health since they are resistant to the most commonly used antibiotics, and therefore scientists are pushed to discover new antibiotics, to remain one step ahead of the bacteria in the fight for survival.
Staphylococcus aureus (also known as staph) is a common type of bacteria, often carried on the skin and inside the nostrils and throat, and can cause mild infections of the skin, however, MRSA can be more aggressive in its effects, and can be fatal, causing life-threatening infections such as blood-poisoning, and also harder to treat, as it is resistant to many of the commonly used antibiotics, leaving attempts futile.
If someone was to be infected with MRSA, there still remain certain drugs that are effective against MRSA, one of them being vancomycin. However, the more it is used, the more vancomycin resistance will be observed. If this drug were to become ineffective, then other stronger drugs would have to be resorted to, such as daptomycin, harbouring the risk of more antibiotic resistance. Currently, cases of VRSA, although low, are still present.
Looking To The Future
Whilst scientists are rapidly trying to understand how bacteria gain resistance to antibiotics, and are also looking into how to prevent the bacteria from causing infections or spreading their own genetic information, the main focus for now should be reducing the spread of MRSA, with the most effective way being labelled as hand washing, especially in hospitals, as this is the place where MRSA is most likely to be contracted and spread.
Due to overuse and misuse, antibiotics are no longer as effective as they ere before, and if we continue frivolity when it comes to their prescription, then we are looking at an era akin to one centuries ago, where operational, invasive procedures are not possible, and simple infections are not only difficult to cure, but also more aggressive.
The World Health Organisation has rightly called antibiotic resistance as one of the biggest threats to human health today, requiring action from all global communities and societies.