A patient is admitted in ICU. He develops resp infection. Intratracheal aspirate is sent for culture. In the meantime he is started empirically on intravenous amikacin and ceftriaxone. The culture report says it is Klebsiella which is ESBL. What is the next treatment
|A||Ceftazidime is given in place of Ceftriaxone|
|B||Imipenem is given in place of ceftriaxone|
|C||Amikacin is replaced by fluoroquinolone|
|D||Don’t change the regime, just increase the dose of both drug.|
a. Members of the family Enterobacteriaceae commonly express plasmid-encoded β-lactamases (e.g., TEM-1, TEM-2, and SHV-1). Which confer resistance to penicillins but not to expanded-spectrum cephalosporins.
b. ESBLs are beta-lactamases that hydrolyze extended-spectrum cephalosporins with an oxyimino side chain.
d. Thus ESBLs confer resistance to these antibiotics and related oxyimino-beta lactams. In typical circumstances, they derive from genes for TEM-1, TEM-2, or SHV-1 by mutations that alter the amino acid configuration around the active site of these β-lactamases.
e. This extends the spectrum of β-lactam antibiotics susceptible to hydrolysis by these enzymes. An increasing number of ESBLs not of TEM or SHV lineage have recently been described.
f. The ESBLs are frequently plasmid encoded. Plasmids responsible for ESBL production frequently carry genes encoding resistance to other drug classes (for example, aminoglycosides).
g. Yet carbapenem-resistant isolates have recently been reported.