MRSA - page 2
Keywords: MRSA, infection hospital superdrug infection methicillin resistant staphylococcus aureus
By Einstein10 on 30/12/2009
Level: Foundation Degree
Page Number: 2 of 6 pages: 1 2 3 4 5 6
is ‘naked’, i.e. it is not incorporated in chromosomes but in a single, circular strand lying free in the cytoplasm. Some bacteria have additional small circular pieces of DNA called plasmids
Cell Division Usually by binary fission but sometimes by conjugate
Ribosome’s 70 s ribosome’s that only occur free in cytoplasm
Organelles’ Few organelles; no organelles are bound by a double membrane
Hair-like structures (Flagella) Flagella and Pili are simple: they are extracellular and they lack an internal system of microtubules
Cell Wall Rigid cell wall made of protein and polysaccharide Peptidoglycans. Murein is the protein
Respiratory Membranes Mesosomes act as respiratory surface in some bacteria: no mitochondria
Photosynthetic Membrane Intracellular membranes not organised into stacks
Table 1. Summary of bacterial structures and their function 10
Peptidoglycans are a molecular lattice formed by the repeating disaccharide units interconnect by polypeptides and make up the bacterial cell wall. They are present in both gram-positive and gram-negative bacteria and overall provide the cell with mechanical protection. Peptidoglycans are only found in prokaryotes and are made up of a glycan backbone of muraic acid and glucosamine.11 These peptide links are highly cross linked with bridges in gram-positive bacteria like SA. These cross linked bridges are target sites for B-Lactam antibiotics.12
Mechanism of antibiotic action against SA
Antibiotics are a large group of synthetic and naturally occurring drugs that combat bacterial infection. Antibiotics work by interfering with the prokaryote metabolism, leaving the eukaryotic cells of the host working normally.13 Bacterial antibiotics work in one of three ways: prevent the formation of bacterial cell walls; interfere with DNA replication and prevent protein synthesis.13 Table 2
Table 2. How different Antibiotics affect bacteria 14
Mode of action
Antibiotic type Bacterial resistance mechanism
Blocks protein synthesis Aminoglycosides; gentamycin
Inactivation
Blocks cell wall formation β-lactam; penicillin’s, cephalosporin’s
Inactivation, Mutation
Blocks cell wall formation Glycopeptides: Vancomycin
Mutation of binding molecules’
Blocks Protein Synthesis Macrolides
Ribosome protection
Inhibits DNA replication Quinolones
Mutation of binding molecules’
Inhibits bacterial TNA
Polymerase
Rifamin
Mutation of binding molecules’
Blocks protein synthesis
Tetracycline’s Inactivation
Blocks formation of nucleic acids and f-met Trimethoprim sulphonamides Mutation of binding molecules’
SA was the first organism to show resistance to any antimicrobial as hypothesized by Fleming. 27 Penicillin was first used against SA but after a few years MRSA showed resistance to the best antibiotic of that time so new antibiotics were synthesized. 28
The main antibiotics used nowadays are Vancomycin and rifampicin as they are most effective when used in combination. 12 As represented in table 2, B-lactam penicillin’s and cephalosporin’s block cell wall formation and result in the destruction of the SA cell wall, causing the contents of the cell to leak
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