How antibiotics work and their limitations
Antibiotics are substances that kill or inhibit the growth of bacteria. Different antibiotics target different bacterial processes: cell wall synthesis, protein synthesis or DNA replication. They are effective against bacterial infections such as cholera, TB and bacterial pneumonia.
Antibiotics have no effect on viruses because viruses do not have their own metabolic machinery. A virus reproduces inside a host cell, so killing the virus would require damaging the host cell. This is why antibiotics cannot treat influenza, the common cold or HIV/AIDS.
The development of resistance
Within any bacterial population, random mutations occasionally produce an individual with a gene that confers resistance to a particular antibiotic. When the antibiotic is applied, non-resistant bacteria are killed but the resistant individual survives. It reproduces rapidly, passing the resistance gene to its offspring.
Over time, the proportion of resistant bacteria in the population increases. This is natural selection: the antibiotic provides the selection pressure, and bacteria with the advantageous mutation are selected for. The antibiotic does not cause the mutation: the mutation arises randomly, and the antibiotic selects for those that already have it.
Reducing the spread of resistance
Key measures to slow resistance include: completing the full course of prescribed antibiotics so that all susceptible bacteria are killed, leaving none partially exposed; not using antibiotics for viral infections where they are ineffective; reducing antibiotic use in agriculture where they are used as growth promoters; and developing new antibiotics to replace those that have become ineffective.
MRSA (methicillin-resistant Staphylococcus aureus) is a well-known example of a resistant bacterium. It is difficult to treat because it has evolved resistance to several commonly used antibiotics, making infections in hospitals particularly dangerous.