Beta-lactam antibiotics share the structural feature of a beta-lactam ring. This feature is responsible for inhibition of bacterial cell wall synthesis. The target molecules are peptidoglycan cross-linking enzymes (e.g. transpeptidases and carboxypeptidases) which can bind beta-lactam antibiotics (penicillin binding proteins, PBP). Bacterial cell death is initiated by beta-lactam antibiotic-triggered release of autolytic enzymes. In contrast to gram-positive bacteria (absence of an outer membrane) the antibiotic has to penetrate through porins of the outer membrane of gram-negative bacteria before touching PBP's. Bacterial resistance to beta-lactam antibiotics includes modification of porins (permeability barrier) and of targets (low affinity of PBP's for the drug), production of inactivating enzymes (beta-lactamases) and inhibition of release of autolytic enzymes. Moreover, bacteria have developed sophisticated genetic mechanisms to adapt to treatments with novel beta-lactam antibiotics. To allow successful antibiotic treatment of bacterial infection in the future, knowledge about antibiotic resistance mechanisms is required.