Cell wall synthesis inhibitors: Cephalosporins
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Cell wall synthesis inhibitors: Cephalosporins
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Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Cell wall synthesis inhibitors: Penicillins
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Cell wall synthesis inhibitors: Cephalosporins
Cell wall synthesis inhibitors: Penicillins
DNA synthesis inhibitors: Fluoroquinolones
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Miscellaneous cell wall synthesis inhibitors
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Antimetabolites: Sulfonamides and trimethoprim
Cell wall synthesis inhibitors: Cephalosporins
Cell wall synthesis inhibitors: Penicillins
Miscellaneous protein synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Pharmacodynamics: Agonist, partial agonist and antagonist
Pharmacodynamics: Desensitization and tolerance
Pharmacodynamics: Drug-receptor interactions
Pharmacokinetics: Drug absorption and distribution
Pharmacokinetics: Drug elimination and clearance
Pharmacokinetics: Drug metabolism
Cell wall synthesis inhibitors: Cephalosporins
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Cell wall synthesis inhibitors: Cephalosporins
Cell wall synthesis inhibitors: Penicillins
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Cell wall synthesis inhibitors: Cephalosporins
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Cell wall synthesis inhibitors: Cephalosporins
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First Aid
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Ceftriaxone
Chlamydia spp. p. 146
Chlamydia trachomatis p. , 723
for gonococci p. 140
for Haemophilus influenzae p. , 140
mechanism and use p. 186
mechanism (diagram) p. 184
meningitis p. 177
meningococci p. 140
prophylaxis p. 195
typhoid fever p. 142
Gonorrhea
ceftriaxone p. 186
Lyme disease p. 144
ceftriaxone p. 186
Meningitis
ceftriaxone p. 186
Transcript
Content Reviewers
Contributors
Cephalosporins are antibiotics which got their name from a mold known as cephalosporium, from which they were originally extracted.
They belong to the pharmacological group of beta-lactam antibiotics.
What all beta-lactams have in common is a beta-lactam ring in their structure, which gives them their name, and also the mechanism of action - which is the inhibition of cell wall synthesis in bacteria.
So, our body is made out of eukaryotic cells.
Bacterias belong to a different type of cells, called the prokaryotes.
From the outside to inside, they have a slimy capsule made out of polysaccharides.
Then, there’s a cell wall in most prokaryotes.
A cell wall is a structural layer, which encapsulates bacteria, and offers structural support and protection, like a suit of armor. It also offers some filtering capabilities, as not everything can pass freely through it.
Finally, on the inside, there’s a pretty standard cell membrane.
Should something happen to this wall, say, if its synthesis mysteriously stopped, its owner’s life expectancy will turn to that of a snowflake in Sahara. And that’s exactly what we’re hoping to do.
Bacterial cell walls are made of a substance called peptidoglycan, or murein.
Peptidoglycan is a very strong, crystal lattice resembling three-dimensional structure, composed out of long using “strands” of amino polysaccharides, running in parallel.
These are made of made out segments of N-acetylglucosamine, or NAG, and N-acetylmuramic acid, or NAM, in an alternating pattern - so, NAG, NAM, NAG, NAM, and so on, like a pearl necklace.
These strands are also cross linked by short, four to five amino acids long, or tetrapeptide chains, protruding from NAM subunits.
Those pentapeptides reach out and link to pentapeptide chains from the neighboring strands, for structural stability, a sub-process known as transpeptidation.
All of this is made possible by enzymes called DD-transpeptidases, that are also better known as penicillin binding proteins, or PBPs.
These enzymes are highly specialized to grab and hold two pentapeptide ends and fuse them together, creating a stable link between the two polysaccharide strands, essentially creating peptidoglycan.
If you imagine the enzyme as a “lock”, then the pentapeptide chain would be a key, so it fits perfectly in, and allows the enzyme to do its work.
In essence, all beta lactam antibiotics, like the cephalosporins, somewhat resemble the tetrapeptide chains.
Inside the bacteria, PBP enzymes will mistakenly bind to the beta lactams antibiotic molecule instead of a tetrapeptide and stick inside the PBP forever, like chewing gum in a keyhole, permanently disabling it.
As more and more of PBPs get disabled, the crosslinking fails to occur, and the wall becomes weak and unstable.
Sources
- "Katzung & Trevor's Pharmacology Examination and Board Review,12th Edition" McGraw-Hill Education / Medical (2018)
- "Rang and Dale's Pharmacology" Elsevier (2019)
- "Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th Edition" McGraw-Hill Education / Medical (2017)
- "Penicillin-Binding Proteins of Gram-Negative Bacteria" Clinical Infectious Diseases (1988)
- "Methicillin-resistant Staphylococcus aureus: A consensus review of the microbiology, pathogenesis, and epidemiology with implications for prevention and management" The American Journal of Medicine (1993)
- "A Comparison of Ceftriaxone and Cefuroxime for the Treatment of Bacterial Meningitis in Children" New England Journal of Medicine (1990)
- "Third-generation cephalosporins" Medical Clinics of North America (1995)
- "Summary of Ceftaroline Fosamil Clinical Trial Studies and Clinical Safety" Clinical Infectious Diseases (2012)
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