Antibiotics-cell wall synthesis inhibitors

What is the primary function of bacterial cell walls?

To protect the cell from osmotic pressure and maintain structural integrity

Why are bacterial cell walls ideal targets for antibiotics?

Human cells lack cell walls, allowing selective toxicity

What is peptidoglycan?

A polymer consisting of sugars and amino acids forming the bacterial cell wall.

What is the role of penicillin-binding proteins (PBPs)?

They catalyze the final steps of peptidoglycan synthesis, facilitating cross-linking

How do beta-lactam antibiotics function?

They inhibit PBPs, preventing peptidoglycan cross-linking and weakening the cell wall.

What is the result of inhibiting cell wall synthesis in bacteria?

The bacteria become susceptible to osmotic lysis and death

Name two classes of beta-lactam antibiotics.

Penicillins and cephalosporins

What is the mechanism of action of glycopeptide antibiotics like vancomycin?

They bind to the D-Ala-D-Ala terminus of peptidoglycan precursors, inhibiting cell wall synthesis.

How do bacteria develop resistance to beta-lactam antibiotics?

By producing beta-lactamases that hydrolyze the beta-lactam ring, rendering the antibiotic ineffective

What is the significance of the D-Ala-D-Ala sequence in peptidoglycan?

It is the target site for glycopeptide antibiotics, crucial for cell wall synthesis.

What is D-Ala (D-Alanine)?

D-Alanine is an amino acid that is a key component of bacterial cell walls. It is incorporated into peptidoglycan, contributing to the structural integrity of the cell wall

How is D-Ala involved in peptidoglycan synthesis?

D-Ala is part of the peptide side chains in peptidoglycan, specifically at the terminal ends of the chains, where it forms cross-links between glycan strands to strengthen the cell wall

What is the D-Ala-D-Ala motif?

The D-Ala-D-Ala motif refers to the two D-Alanine residues found at the terminal ends of peptidoglycan precursors. This motif is a critical target for certain antibiotics like vancomycin

How do glycopeptide antibiotics like vancomycin target D-Ala?

Vancomycin binds to the D-Ala-D-Ala terminus in peptidoglycan precursors, preventing the formation of cross-links and disrupting cell wall synthesis. This weakens the bacterial cell wall.

What happens when the D-Ala-D-Ala motif is altered in bacteria?

Alteration of the D-Ala-D-Ala motif, such as replacing D-Ala with D-lactate, can lead to resistance against glycopeptide antibiotics, as vancomycin can no longer bind effectively to the cell wall precursors

What is the role of D-Ala in bacterial cell wall integrity?

D-Ala contributes to the stability of the peptidoglycan layer by forming cross-links between the sugar strands, ensuring the rigidity and strength of the bacterial cell wall.

How does bacterial resistance to vancomycin occur?

Resistance occurs when bacteria modify the D-Ala-D-Ala motif to D-Ala-D-Lactate, which prevents vancomycin from binding, thus allowing the bacteria to continue synthesizing their cell wall. This is seen in vancomycin-resistant enterococci (VRE)

What is the clinical significance of the D-Ala modification in antibiotic resistance?

The modification of the D-Ala-D-Ala motif is a major mechanism of resistance to glycopeptide antibiotics, making infections caused by resistant bacteria more difficult to treat. This has led to the development of alternative therapies and new antibiotics

How is the D-Ala-D-Ala motif involved in the final steps of peptidoglycan synthesis?

The D-Ala-D-Ala motif is one of the last components added during peptidoglycan biosynthesis and plays a crucial role in the cross-linking process that forms the rigid structure of the bacterial cell wall.