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Historically, infections have been a major cause of death. However, until the discovery of bacteria in the 17th Century, understanding of how infections happened was poor. By the 19th century, it had been established that bacteria were involved. During the First World War, infection control became a priority – for example, 93% of soldiers who initially survived an abdominal wound would later die from the effects of an infection. This led governments and scientists worldwide to focus on the need to combat bacteria.

Antibiotics are drugs which kill bacteria (and certain other micro-organisms). They do NOT kill viruses. Most people use the term to refer specifically to drugs which target bacteria – technically, the correct term for such drugs is “antibacterials”. Antiseptics on the other hand are chemicals we can put onto our skin to kill bacteria; but they frequently are poisonous to us if taken internally (e.g. eaten or injected).

While some forms of antibiotics were discovered in the first decade of the 20th Century, antibacterial drugs as we now know them were discovered in 1928. Famously, Alexander Fleming accidentally stumbled on a chemical made by the Penicillium family of funguses which could kill the bacteria he was studying in his laboratory at the time.

This chemical was named Penicillin, after the fungus which made it. Fleming’s discovery revolutionised medicine – up until that point, many infections were fatal, many were treated by surgery, and many limb infections led to amputation.

Penicillin was analysed closely. Scientists refined and altered the chemical to make it more effective; meanwhile, a race started to find other antibiotics. This resulted in a large number of new types of antibiotics being discovered that worked in different ways to either kill bacteria directly (bacteriocidal) or to stop bacteria being able to grow and reproduce (bacteriostatic).

Over time, the different types of antibiotics were arranged into ‘families’. Members of a family share similar chemical structures (like houses with similar floorplans), or similar biological functions (e.g. how they attack bacteria), or commonly both.

Family names include Penicillins, Cephalosporins, Sulphonamides, Tetracyclines, Macrolides, Lincosamides, Aminoglycosides and Fluoroquinolones. Each family has several members.

Making it more confusing, medications containing each drug may be made by a host of different companies. For example, in the same way as Dairy Milk® and Galaxy® are made by different companies but contain cocoa alongside other ingredients, Rilexine® and Ceporex® both contain Cephalexin (the “active” ingredient) alongside other ingredients.

Unfortunately, after the initial discoveries, it became harder to find newer antibiotics, and particularly newer families – i.e. drugs that work in totally new ways. Additionally, as pharmaceutical companies now generally find most profit in drugs for long-term conditions (like arthritis), they are spending less on researching antibiotics. Only four totally new classes of antibiotic have been discovered in the last 30 years.

The small number of new drugs appearing becomes important in antibiotic resistance. When a bacterium becomes resistant to one member of a family, it often becomes resistant to several other ‘relatives’ in the family too, or even to members of similar families – for example, bacteria that become resistant to certain penicillins may simultaneously become resistant to certain cephalosporins. With fewer new types of drugs appearing, we have fewer options in these cases.

Author – The late Tony Sarma

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