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Lecture notes of 5 pages for the course Mechanisms of pathology at Aston (immunology notes)
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Voorbeeld 2 van de 5 pagina's
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Antibiotics.What are antibiotics?
Antibiotics are chemical compounds which are used to treat infections caused
primarily by bacteria and they should be sufficiently non-toxic to be given to the
infected host.
You target the bacteria that is causing the infection without targeting the host.
They are used to supplement the body’s natural defences to a bacterial infection by
either killing bacteria or by inhibiting the bacterial growth so that the immune
system can get the upper hand.
They are selective poisons for treating bacterial infections not viral infections.
Classification of antibiotics:
Antibiotics are traditionally classified on their biosynthetic origin.
Natural antibiotics (true antibiotics): they are produced naturally by fungi or bacteria
to selectively inhibit the growth of others. For example, penicillium chrysogenum
produces penicillin.
Semi-synthetic antibiotics: these are antibiotics that were natural products that have
been chemically modified to add various different characteristics that may make
them more amenable to us taking them as medicine.
Totally synthetic antibiotics: these have been made in a laboratory, they are
chemicals that have been synthesised by chemists that have antibacterial properties,
so they are manufactured.
Antibiotics are clustered within a large group of drugs called antimicrobials or
chemotherapeutic agents.
How do antibiotics work.
This is the major mechanism of action of lots of different types of antibiotics.
They can broadly be summarised into several classes:
They are either cell wall inhibitors or they are nucleic acid inhibitors, or they are
protein inhibitors, or they are metabolism inhibitors.
These are the main areas of bacteria physiology that we try and target with
antibiotics.
Cell wall synthesis inhibitors: beta lactam antibiotics: the penicillins.
These are the most used antibiotics globally.
The first one that was identified was penicillin G and this is acid labile which means
that the acid in the stomach will break open the penicillin nucleus and render the
antibiotic infective. It is spontaneously hydrolysed in the presence of acid. This
means that it is not orally viable, you have to inject it into people if you want
penicillin G to be active.
However, by manipulation of the organism that produces penicillin we can get it to
produce penicillin V which is acid stable, this means that you can take it orally and it
will not be spontaneously hydrolysed as a consequence of the acid in your stomach.
So, the beta lactam ring remains intact. This is oral intravenous penicillin.
Amoxicillin has also been developed and this is a semi-synthetic penicillin.
And also, methicillin, which is semi-synthetic.
, Inhibition of transpeptidase by beta lactam antibiotics.
Beta lactam antibiotics work as they are structurally analogous to the terminal D-ala
D-ala of the pentopeptide cross bridge that we get that appears between the sheets
of N-acetyl glucose and N-acetyl veronic acid that make up the peptidoglycan layer
of the bacterial cell wall.
The enzyme that connects these two, that recognises the terminal D-ala D-ala is the
transpeptidase enzyme and this forms the cross-link between the sheets.
But if penicillin is present, the transpeptidase will be inhibited by the penicillin, so as
a consequence it does not bind the D-ala D-ala.
It is a competitive irreversible inhibition by penicillin.
Beta lactam antibiotics: clinical usage.
We use the beta lactam antibiotics for upper respiratory tract infections, such as
tonsilitis.
We also use them for lower respiratory tract infections such as pneumonia.
We can also use them for sexually transmitted infections such as gonorrhoea,
syphilis.
Also, can be used for skin and soft tissue infections like diabetic foot ulcers.
Inhibitors of DNA gyrase: the quinolones.
Quinolones were first used for urinary tract infections.
There are now 10,000 analogues of the quinolones and they all started with the first
quinolone antibiotic which is nalidixic acid.
There are 6 FDA approved quinolones that are used in chemotherapy for different
bacterial infections, and they represent 24% of the worlds manufactured antibiotics.
Quinolones are synthetic antibacterial compounds; this means that they are made in
a laboratory.
They are inhibitors of DNA gyrase, and DNA gyrase is found in all bacteria.
Because DNA gyrase is found in all bacteria this means that they are broad spectrum
antibiotics. They inhibit gram + and gram negative bacteria -.
All the quinolones are derivatives of nalidixic acid.
And they are fluorinated, so there is a fluorine that is present on the double ring
structure.
They are called the quinolones because they have a quinoline backbone. Which is
where two aromatic rings are joined together with two nitrogen’s at the bottom.
They all have a different functional R group, this creates different characteristics and
different properties and different specificities. So it enables us to produce a wide
range of quinolone antibiotics.
Quinolones: mechanism of action.
Quinolone antibiotics interfere with changes in DNA super coiling. By binding directly
to DNA gyrase.
The 1st- and 2nd-generation quinolones will bind to topoisomerase 2. Or the 3 rd and
4th generation bind to topoisomerase 4.
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