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Penicillin resistance in Staphylococcus aureus [3] appeared very soon after penicillin entered general clinical use in 1943, and the mechanism of resistance was the production of β-lactamase. Modification of the penicillin molecule so that it was resistant to being broken down by β-lactamase was able to temporarily overcome this problem.
Penicillin molecules are small enough to pass through the spaces of glycoproteins in the cell wall. For this reason Gram-positive bacteria are very susceptible to penicillin (as first evidenced by the discovery of penicillin in 1928 [46]). [47] Penicillin, or any other molecule, enters Gram-negative bacteria in a different manner. The bacteria ...
Wide range of infections; penicillin used for streptococcal infections, syphilis, and Lyme disease: Gastrointestinal upset and diarrhea; Allergy with serious anaphylactic reactions; Brain and kidney damage (rare) Same mode of action as other beta-lactam antibiotics: disrupt the synthesis of the peptidoglycan layer of bacterial cell walls ...
The so-called delabeling of penicillin allergies, doctors say, would have major health impacts: faster and more effective treatments for people who have spent their lives avoiding penicillin and ...
β-Lactam antibiotics are indicated for the prevention and treatment of bacterial infections caused by susceptible organisms. At first, β-lactam antibiotics were mainly active only against gram-positive bacteria, yet the recent development of broad-spectrum β-lactam antibiotics active against various gram-negative organisms has increased their usefulness.
Nafcillin sodium is a narrow-spectrum, [1] second-generation beta-lactam antibiotic [2] of the penicillin class. As a beta-lactamase-resistant penicillin, it is used to treat infections caused by Gram-positive bacteria, in particular, species of staphylococci that are resistant to other penicillins.
A defining characteristic of MRSA is its ability to thrive in the presence of penicillin-like antibiotics, which normally prevent bacterial growth by inhibiting synthesis of cell wall material. This is due to a resistance gene, mecA , which stops β-lactam antibiotics from inactivating the enzymes (transpeptidases) critical for cell wall synthesis.
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