Chapter 20, Problem 1R

DRAW IT Show where the following antibiotics work: ciprofloxacin, tetracvcline, streptomycin, vancomycin, polymyxin B, sulfanilamide, rifampin, erythromycin.

Summary Introduction

To review:

Themode of action of given antibiotics in a bacterial cell.

Concept introduction:

The antibiotics can either act as a bacteriostatic (prevent growth of bacteria) or bactericidal (kill bacteria) agents. These drugs with a specific mode of action inhibits the essential biological processes of the target pathogen, including disruption of plasma membrane permeability, inhibition of cell wall, protein and nucleic acid synthesis, and inhibition of essential metabolites synthesis.

Answer to Problem 1R

Correct answer:

ANTIBIOTICS	MODE OF ACTION
Ciprofloxacin	Inhibition of the nucleic acid replication
Tetracycline	Inhibition of the protein synthesis
Streptomycin	Inhibition of the protein synthesis
Vancomycin	Inhibition of the cell wall synthesis
Polymyxin B	Injury to the plasma membrane
Sulfanilamide	Inhibition of the essential metabolite synthesis
Rifampin	Inhibition of the nucleic acid transcription
Erythromycin	Inhibition of the protein synthesis

Explanation of Solution

Diagram:

Explanation:

The mechanism of action of the given antibacterial drugs:

Ciprofloxacin – A broad spectrum of the bactericidal agent inhibits the bacterial enzyme DNA gyrase and blocks DNA synthesis. The DNA gyrase is an essential enzyme which is specifically involved in the introduction of negative supercoiling.

Tetracycline – A broad spectrum of the bacteriostatic agent prevents the attachment of aminoacyl tRNA from binding to bacterial 30S ribosome. By binding to the 30S subunit of bacterial ribosome, the tetracycline blocks the association of aminoacyl tRNA with the acceptor site.

Streptomycin – A broad spectrum of the bactericidal agent by acting on 70S ribosome inhibits the protein synthesis. It binds to the 30S subunit of bacterial ribosome and disrupts the protein synthesis (initiation and elongation step).

Vancomycin – A broad spectrum of the antibacterial agent inhibits the assembly of cell wall of bacteria. The N-acetylmuramic acid (NAG) and N-acetylglucosamine (NAM) monomers are the the building blocks of peptidoglycan cell wall. By binding to NAG and NAM, the vancomycin prevents the action of transpeptidase enzyme which is involved in the cross-linking of peptidoglycan.

Polymyxin B – A broad spectrum of the bactericidal agent with a cationic detergent action disrupts the permeability of the plasma membrane.

Sulfanilamide – A broad spectrum of the bacteriostatic agent acts as a competitive inhibitor of p-aminobenzoic acid (PABA). The sulfanilamide with a similar chemical structure competitively prevents the action of PABA and inhibits the folic acid biosynthesis. This arrests the bacterial growth and ultimately results in the elimination of the bacteria.

Rifampin – A broad spectrum of the bactericidal agent specifically inhibits the function of RNA polymerase in the bacteria. Rifampin forms a stable complex with the enzyme, thereby inhibits its activity in the nucleic acid transcription.

Erythromycin – A broad spectrum of the antibacterial agent inhibits the protein synthesis by binding to the bacterial 50S ribosome. It inhibits the activity of peptidyl transferase and intervenes with the amino acid translocation and protein assembly.

Conclusion

The specific site of action of the given antibacterial agents, namely cell wall synthesis (vancomycin), protein synthesis (tetracycline, streptomycin, erythromycin), essential metabolite synthesis (sulfanilamide), nucleic acid synthesis (ciprofloxacin), nucleic acid transcription (rifampin), and plasma membrane integrity (polymyxin B) is shown.