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10. Treatment
For treatment of neotropenia, the bacteriostatic
agents are not effective. Therefore the
bacteriosidals are used for the treatment of
neotropenia.The bacteriostatic antibiotics are used
to fight bacterial infection. In some cases the bone
marrow transplant is also an option. But here we
discuss about the bacteriocidal antibiotics with
their mode of action.
Beta lactum Antibiotics
β-lactam antibiotics (beta-lactam antibiotics) are
antibiotics that contain a beta-lactam ring in their
molecular structure. This includes
11. penicillin derivatives (penams), cephalosporins (cephems),
monobactams, carbapenems and carbacephems. Most β-lactam
antibiotics work by inhibiting cell wall biosynthesis in the bacterial
organism and are the most widely used group of antibiotics. The first β-
lactam antibiotic discovered, penicillin, was isolated from a rare variant
of Penicillium notatum.
Bacteria often develop resistance to β-lactam antibiotics by
synthesizing a β-lactamase, an enzyme that attacks the β-lactam
ring. To overcome this resistance, β-lactam antibiotics can be
given with β-lactamase inhibitors such as clavulanic acid.
Mechanism of Action
12. • Penicillin and most other
β-lactam antibiotics act by
inhibiting penicillin-binding
proteins, which normally
catalyze cross-linking of
bacterial cell walls
13.
14. In the absence of β-lactam antibiotics (left), the cell wall plays an
important role in bacterial reproduction. Bacteria attempting to grow
and divide in the presence of β-lactam antibiotics (right) fail to do so,
and instead shed their cell walls, forming osmotically fragile
spheroplasts.
β-lactam antibiotics are bactericidal, and act by inhibiting the
synthesis of the peptidoglycan layer of bacterial cell walls. The
peptidoglycan layer is important for cell wall structural
integrity,especially in Gram-positive organisms, being the outermost
and primary component of the wall. The final transpeptidation step in
the synthesis of the peptidoglycan is facilitated by DD-transpeptidases,
also known as penicillin binding proteins (PBPs). PBPs vary in their
affinity for penicillin and other β-lactam antibiotics. The number of
PBPs varies between bacterial species. β-lactam antibiotics are
analogues of d-alanyl-d-alanine—the terminal amino acid residues on
the precursor NAM/NAG-peptide subunits of the nascent
peptidoglycan layer.
15. The structural similarity between β-lactam antibiotics and d-alanyl-d-
alanine facilitates their binding to the active site of PBPs. The β-lactam
nucleus of the molecule irreversibly binds to (acylates) the Ser403
residue of the PBP active site. This irreversible inhibition of the PBPs
prevents the final crosslinking (transpeptidation) of the nascent
peptidoglycan layer, disrupting cell wall synthesis. β-lactam antibiotics
block the division of bacteria.
Under normal circumstances, peptidoglycan precursors signal a
reorganisation of the bacterial cell wall and, as a consequence, trigger
the activation of autolytic cell wall hydrolases. Inhibition of cross-
linkage by β-lactams causes a build-up of peptidoglycan precursors,
which triggers the digestion of existing peptidoglycan by autolytic
hydrolases without the production of new peptidoglycan. As a result,
the bactericidal action of β-lactam antibiotics is further enhanced.
