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How do antibiotics work at the cellular level?

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How do antibiotics work at the cellular level?

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  1. Antibiotics work a lot of different ways, depending on the class.  There are two main types of antibiotics--bacteriocidal and bacteriostatic.  The first actually penetrate the cell wall and kill the bacteria, where the latter simply prevent further multiplication of the bacteria.

    Then there are several classes of antibiotics.  Some, like the penicillins (penicillin, amoxicillin), are bacteriocidal, and weaken the cell wall, causing bacteria to take up excessive water and rupture.

    Cephalosporins (cefazolin, cefaclor, ceftriaxone) are beta-lactam antibiotics that are similar to the penicillins and are also bacteriocidal.  These disrupt cell wall synthesis by activating autolysins that damage the cell wall.

    Tetracyclines are bacteriostatic antibiotics.  These supress bacterial growth by inhibiting protein sythesis, making it very difficult for the bacteria to replicate.

    The macrolides (erythromycin, clindamycin) are bacteriostatic antibiotics that also inhibit protein synthesis.  These antibiotics are great for patients allergic to the penicillins.

    Aminoglycosides (gentamicin) are bactericidal antibiotics that work by inhibiting protein sythesis. This class is dose-dependent, and is not effective unless a steady serum concentration is obtained.

    Sulfonamides are bacterialstatic antibiotics that supress bacterial growth by inhibiting  the synthesis of folic acid 9a compound required by cells for synthesis of DNA/RNA.

    Floroquinolones (ciprofloxacin, levofloxacin) are bacterialstatic antibiotics that inhibit bacterial DNA gyrase, making DNA replication impossible.  Bacteria are becoming increasingly resistant to these antibiotics.

    This is a general overview; there are a lot more anti-fungal agents, antivials, and anti-protozoals, but that gets pretty specific.


  2. Wow that's a big question.

    Lets start at the beginning( I hope I'm not being patronising here,I don't mean to be !!!!).

    There are two types of Bacteria in general .

    Gram +ve and Gram -ve.

    This simply means they have different cell wall structures.

    Quite simply there are 5 major pathways of attack by antibiotics.

    On the Ribosomes,cell wall,cell membrane,chromosomes and on folate metabolism.

    Lets start with the last one.

    Folic acid metabolism is crucial in DNA synthesis.

    Drugs such as Trimethoprim,and the sulphonamides interfere with the folic acid synthesis and disrupt DNA synthesis.

    Chromosomal synthesis is affected by introducing drugs such as the fluororoquinolones which fragments DNA strands rendering them incapable of multiplying while drugs such as Rifampicin act on RNA polymerase which is resposible for gene transcription. No RNA polymerase= no cell multiplication.

    Polymyxins bind to the Lipopolysaccharide regions of Gram -ve bacteria.The outer component of the cell membrane is distorted and a damage to the permeability of the membrane is conferred.This results in leakage of the cytoplasmic contents and cell death.

    Cell wall antibiotics act by interfering with peptidoglycan production(beta lactams,penicillin,cephalosporin and monobactams). They disrupt amino acid configuration within the cell and ultimately prevent them from growing.

    Some antibiotics are more effective on -ve and+ve Bacteria.

    This is mainly due to permeability issues,for exampleVancomycin (a Glycopeptide) is too large a molecule to penetrate Gram negative Bacteria and so is only used to treat serious Gram +ve infections E.G. MRSA and other complicated skin diseases.

    The ribosomes are used in protein synthesis.

    Tetracylines,chhloramphenicol,and the macrolides which are used in targetting ribosomal activity.

    Their mode of action is to bind to the various ribosomal sub-units(30s /50s) within the cell and disrupt protein synthesis.

    This is a very simplistic explanation,BUT if you can get ahold of acopy of HUGO and RUSSEL'S pharmaceutical microbiology you would glean a lot more.

    It's not that complicated but very interesting.

    Hope my diatribe didn't make you fall asleep.!!!!!!!!!

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