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One of the most common forms of resistance is produced through the actions of beta-lactamases, enzymes which hydrolyze the beta-lactam ring of beta-lactam antibiotics. Generally, extended spectrum cephalosporins, such as the third generation cephalosporins, were thought to be resistant to hydrolysis by beta-lactamases (especially those produced by enteric bacilli such as E coli and Klebsiella). However, in the mid 1980's it became evident that a new type of beta-lactamase was being produced by Klebsiella spp and in some cases by E coli that could hydrolyze the extended spectrum cephalosporins. These new beta-lactamases have been collectively termed the 'extended spectrum beta-lactamases' (ESBL's). Beta-lactamse inhibitors such as clavulanic acid, tazobactam and sulbactam do not inhibit these extended spectrum beta-lactamases sufficiently.

Monobactams such as aztreonam are
also inactivated. Recently, it has been discovered that the cephamycins (cefoxitin, cefotetan, moxalactam) have diminished activity against the ESBL-producing bacteria. More troubling is the observation that resistance to non beta-lactams is associated with ESBL's. Equally disturbing is the fact that ESBL's are carried on plasmids which can be transferred to other bacteria. Below is a table on treatment recommendations for ESBL-producing bacteria from a recent review of antibiotic resistance.

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