Week 3 Flashcards
(21 cards)
How does penicillin work?
inhibits the formation of peptidoglycan in the bacterial cell wall by binding to transpeptidases, which prevents the cross-linking of peptide chains, leading to cell lysis due to osmotic shock.
Why do penicillins have little toxicity to human cells?
target peptidoglycan, a structure not found in human cells, making them highly selective for bacterial cells, with minimal harm to human cells.
What is the structure of peptidoglycan in bacterial cell walls?
consists of N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) sugars, cross-linked by tetrapeptides to form a mesh-like structure that provides structural integrity.
What is the periplasmic space in Gram-negative bacteria?
area between the outer membrane and the cell membrane, containing enzymes and transport proteins.
Why do penicillins work only on Gram-positive bacteria?
Targets the peptidoglycan layer, which is thicker in Gram-positive bacteria, while Gram-negative bacteria have an outer membrane that prevents the drug from reaching the peptidoglycan layer.
What modification led to the development of ampicillin?
was developed as a semisynthetic derivative of penicillin G, allowing it to cross the outer membrane of Gram-negative bacteria, making it broad-spectrum.
What are penicillinases or β-lactamases?
are enzymes produced by some bacteria that break open the β-lactam ring of penicillins, rendering them ineffective.
What is the mechanism of action of vancomycin?
Vancomycin binds to the peptide side chains of peptidoglycan precursors, preventing the transpeptidase enzymes from forming peptide bridges, thus inhibiting cell wall synthesis
Why is vancomycin ineffective against Gram-negative bacteria?
Vancomycin is too large to cross the outer membrane of Gram-negative bacteria
How does bacitracin inhibit cell wall synthesis?
Bacitracin blocks the dephosphorylation of bactoprenol, preventing it from flipping and carrying peptidoglycan subunits across the cell membrane, thus inhibiting peptidoglycan synthesis.
How does polymyxin work as an antimicrobial agent?
binds to the phospholipids in the cell membrane of Gram-negative bacteria, disrupting both the inner and outer membranes, leading to cell death.
What is the unique feature of the Mycoplasma bacteria?
bacteria lack a cell wall, making them resistant to antibiotics like penicillin that target cell wall synthesis.
What is primary atypical pneumonia caused by Mycoplasma pneumoniae?
causes a milder form of pneumonia known as walking pneumonia, often transmitted through respiratory secretions
How does the lipid bilayer of cell membranes contribute to antimicrobial resistance?
in Gram-negative bacteria acts as a barrier to many antimicrobial agents, including polymyxin, preventing them from reaching their target sites.
What makes Neisseria meningitidis dangerous in terms of its structure?
outer membrane containing lipopolysaccharide (LPS), which acts as an endotoxin that can cause septic shock, fever, and low blood pressure.
How does lipopolysaccharide (LPS) affect the immune system?
triggers an overactive immune response, leading to the production of cytokines, fever, vasodilation, and septic shock.
What are the treatment options for Mycobacterium tuberculosis?
Isoniazid: Targets mycolic acid synthesis.
Rifampin: Inhibits RNA transcription.
Bedaquiline: Inhibits ATP synthase to block energy production in Mycobacterium tuberculosis.
What is multidrug-resistant tuberculosis (MDR-TB)?
Mycobacterium tuberculosis strains resistant to the first-line drugs isoniazid and rifampin, often requiring second-line drugs for treatment.
What is extensively drug-resistant tuberculosis (XDR-TB)?
MDR-TB strains resistant to isoniazid, rifampin, and additional second-line drugs like fluoroquinolones and injectable antibiotics.
What are acid-fast bacteria?
have a waxy lipid layer (mycolic acid) that makes them resistant to staining with the Gram stain, requiring the acid-fast stain instead.
How does the acid-fast stain work?
carbol fuchsin as a primary stain, which is driven into the lipid layer by heat, then washed with acid-alcohol, and counterstained with methylene blue.
