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Chloramphenicol may cause bone marrow suppression during treatment; this is a direct toxic effect of the drug on human mitochondria. [23] This effect manifests first as a fall in hemoglobin levels, which occurs quite predictably once a cumulative dose of 20 g has been given. The anaemia is fully reversible once the drug is stopped and does not ...
Chloramphenicol acetyltransferase (or CAT) is a bacterial enzyme (EC 2.3.1.28) [1] that detoxifies the antibiotic chloramphenicol and is responsible for chloramphenicol resistance in bacteria. [2] This enzyme covalently attaches an acetyl group from acetyl-CoA to chloramphenicol, which prevents chloramphenicol from binding to ribosomes .
Chloramphenicol blocks the peptidyl transfer step of elongation on the 50S ribosomal subunit in both bacteria and mitochondria.; Macrolides (as well as inhibiting ribosomal translocation [8] and other potential mechanisms) bind to the 50s ribosomal subunits, inhibiting peptidyl transfer.
CTX-M-15-positive E. coli are a cause of community-acquired urinary infections in the UK, [27] and tend to be resistant to all oral β-lactam antibiotics, as well as quinolones and sulfonamides. Treatment options may include nitrofurantoin, fosfomycin, mecillinam and chloramphenicol.
Possible side effects [4] Mechanism of action Aminoglycosides; Amikacin: Amikin: Infections caused by Gram-negative bacteria, such as Escherichia coli and Klebsiella particularly Pseudomonas aeruginosa. Effective against aerobic bacteria (not obligate/facultative anaerobes) and tularemia. All aminoglycosides are ineffective when taken orally as ...
E. coli is a gram-negative, facultative anaerobe, nonsporulating coliform bacterium. [18] Cells are typically rod-shaped, and are about 2.0 μm long and 0.25–1.0 μm in diameter, with a cell volume of 0.6–0.7 μm 3. [19] [20] [21] E. coli stains gram-negative because its cell wall is composed of a thin peptidoglycan layer and an outer membrane.
Bacterial morphological plasticity refers to changes in the shape and size that bacterial cells undergo when they encounter stressful environments. Although bacteria have evolved complex molecular strategies to maintain their shape, many are able to alter their shape as a survival strategy in response to protist predators, antibiotics, the immune response, and other threats.
Antibiotics used in combination may also be antagonistic and the combined effects of the two antibiotics may be less than if one of the antibiotics was given as a monotherapy. [71] For example, chloramphenicol and tetracyclines are antagonists to penicillins. However, this can vary depending on the species of bacteria. [74]