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(Pediatrics in Review. 2008;29:264-273.)
© 2008 American Academy of Pediatrics

Cephalosporins

A Review

The first 300 words of the full text of this article appear below.

	Objectives

 
After completing this article, readers should be able to:

1. Describe the mechanism of action of cephalosporins.
   
2. Delineate the two most common mechanisms of resistance to penicillins.
   
3. Discuss the most common adverse effects of common cephalosporins.
   
4. List which cephalosporins have activity against Pseudomonas.
   

	Introduction

 
Cephalosporins are beta-lactam antimicrobials that share mechanisms of action and a similar structure with penicillins (Figure). Penicillins and cephalosporins have the same four-member "core" beta-lactam ring, but cephalosporins have an additional atom in the side ring. Modified side chains on either ring alter antimicrobial activity, resistance to beta-lactamases, or pharmacokinetics. Penicillin-susceptible pathogens usually are cephalosporin-susceptible. Exceptions are Listeria and Pasteurella sp. Cephalosporins have activity against common gram-negative organisms such as Escherichia coli, nontypeable Haemophilus influenzae (ntHi), and methicillin-susceptible Staphylococcus aureus (MSSA), but all methicillin-resistant S aureus (MRSA) and enterococci are cephalosporin-resistant. Because of minimal use or current unavailability, we will not discuss cephalothin, moxalactam, cefamandole, cefonicid, ceforanide, ceftizoxime, cefoperazone, cefpirome, cefmetazole, or cefotetan.

View larger version (11K):   Figure. Cephalosporin versus penicillin ring structures. The solid arrows indicate the core four-member beta-lactam ring within both penicillins and cephalosporins. Open arrows indicate the five- and six-member side rings for penicillins and cephalosporins, respectively. R indicates additional side chain sites where substitutions of various chemical groups produce different antimicrobial spectra, pharmacokinetics, or stability to beta-lactamases.

	Mechanism of Action

 
To help understand the mechanism of action of cephalosporins, rigid bacterial cell walls can be considered as a series of repeating interlocking units reminiscent of floor tiles. During replication, a bacterium removes "tiles" circumferentially to allow cell division via a pinching-like action, while quickly placing new "tiles" at the ends of what have become two bacteria. This process requires enzymes to interlock replacement tiles. Such enzymes are the targets of beta-lactam antibiotics and are called penicillin-binding proteins (PBPs). Antibiotic action requires binding to PBPs, preventing them from closing the . . . [Full Text of this Article]