Penicillin had contaminated his petri dishes from an

Penicillin

Jerrine Lukose 160045231

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Lay summary

Penicillin
was accidently discovered by bacteriologist Alexander Fleming in 1928. The drug
had the ability to kill certain bacteria, which was capable of causing
infection and death. We now know that penicillin works by inhibiting bacteria
from creating new cell walls, eventually causing the bacteria to die. However,
due to excessive use, antibiotic resistance began to develop, and doctors
sometimes had to prescribe various antibiotics to just treat one bacterial
infection. To fight resistance, antibiotics is only given in exceptional
circumstances. Despite this, penicillin is still the
most widely used antibiotic and is still effective in treating fatal diseases.

 

 

Prior to 1928,
bacterial infection was known to be the leading cause of death, killing
thousands of individuals every year. Roughly 90% of children diagnosed with
bacterial meningitis died. From those who survived, the majority had permanent
or long-lasting disabilities, ranging from epilepsy to mental retardation (Kaplan, 2017). Infections spread quickly; diseases
like syphilis, gonorrhoea, and pneumonia in addition to simple injuries and
childbirth infections were major killers (Sealey,
2015). Infections were difficult to control, even in places like hospitals
where surgical infections were a major killer and individuals had limited
protection (Sydnor, 2011). However, the discovery of penicillin ushered in a
new era of antibiotics, with treatment now available for a wide range of
previously life-threatening infections.

Penicillin was
discovered in London on September 1928 by Sir Alexander Fleming. When Fleming
returned from a vacation to his messy lab, he noticed that a petri dish
containing Staphylococcus had been mistakenly left open (Lax, 2004).
While inspecting the colonies of staphylococcus aureus, bacteria that cause sore throats and abscesses, he noticed that
the mould penicillium aureus had contaminated his petri dishes from an open
window, forming a visible growth. There was a clear halo of inhibited bacterium
growth neighbouring the mould (Bud, 2009). Fleming closely examined these
dishes using a microscope and was astonished as this mould disturbed the normal
growth of staphylococci, it was as though the mould produced and secreted
something which inhibited the bacterial growth (Aldridge,
1999). Fleming continued to carry out tests and after a few weeks he grew
enough persnickety mould to test out his findings. Fleming noticed there was an
ingredient, ”mould juice”, in the Penicillium mould which didn’t just inhibit
the growth of a variety of bacteria but was fundamentally capable of fighting
and killing infectious diseases (Markel, 2013), such as meningococcus,
streptococcus and diphtheria bacillus (Aldridge, 1999). Although the penicillium
mould could kill bacteria, for use in humans it was required pure penicillin be
isolated from the penicillium mould juice. However, it proved to be extremely
unstable and was only possible to make crude material for which to work with (Lax,
2004). Dr Fleming published his research in the Journal of Experimental
Pathology in June 1932 (Aldridge, 1999). It was Howard Florey, Ernst and their colleagues
at Oxford University who were able to isolate the penicillin from penicillium
mould and carried out the first ever clinical trials in 1941 (Woodward, 2009). A
year later, Anne Miller was the first patient to be successfully treated with
Penicillin (Markel, 2013).

The antibacterial mechanism of penicillin,
like other ?-lactam antibiotics, works by disturbing the synthesis of peptidoglycan
in bacterial cell wall (Garcia, 2016). The peptidoglycan complex is made of
polypeptides and sugars, together forming a durable and resilient lattice that
surrounds bacterial cells (Metzler, 2016). The peptidoglycan is a significant
component of the bacterial cell walls, helping the bacteria stay intact when
under osmotic pressure, preventing osmotic rupture (Byrne, 2011).

Penicillin is a ”Cell wall
inhibitor” which functions by stopping bacteria constructing its protective
cell wall. Without this cell wall, bacteria are more susceptible to the harsh
conditions within the human body and death due the body’s immune defences (Garcia,
2016). Penicillin, in particular, works by obstructing enzymes which catalyses
the last steps of bacterial cell wall assembly, which is the development of
cross-links that join the external peptidoglycan layer and gives the bacteria
its rugged cell structure (Chow, 2015). This causes extreme weakening of the
cell wall and eventually causes the bacterium to undergo lysis due to osmotic
pressure and directly killing the bacteria. Therefore, penicillin is known as
bactericidal, as it can kill bacteria rather than just reducing its action (Metzler,
2016). This is beneficial to humans as peptidoglycan is not present in human
cells. Penicillin is selectively toxic, therefore only affecting the bacterium
(Tronu, 2016).

Although penicillin was a huge
success, problems had arisen due to a phenomenon called antibiotic resistance (Fenton,
2016). Over time, genetic mutations occurred in bacterium that provided a survival
advantage in the population. This allowed bacteria to survive and reproduce
even in the presence of antibiotics. This caused the creation of resistant
strains, which can only be killed by using stronger, alternative antibiotics;
meaning many antibiotics are required to kill one type of bacteria (Chow,
2016). Growing antibiotic resistance meant many doctors became more cautious
when prescribing antibiotics, giving antibiotics only when absolutely necessary
(Majd, 2016).

Despite
this ”penicillin is still the most widely used antibiotic worldwide” and is
still effective in treating many fatal diseases (Kalvaitis, 2008). Millions of lives have
been enhanced and saved in result of the ”mistake” Fleming made, without it
countless would still be suffering from lethal diseases. Essentially the
finding of penicillin is responsible for the invention of all antibiotics and
truly forged the modern world of medicine.

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