Question

In: Biology

Clindamycin binds to the 50S ribosomal subunit of bacteria. Using this information, respond to the following:...

Clindamycin binds to the 50S ribosomal subunit of bacteria. Using this information, respond to the following:

a. Referring to the 5 modes or mechanisms of actions of antibiotics, which one applies to clindamycin?

b. Is this a broad or narrow spectrum antibacterial agent? Explain

c. Does clindamycin have selective toxicity for bacteria? Explain

Solutions

Expert Solution

a. Clindamycin works primarily by binding to the 50s ribosomal subunit of bacteria. This agent disrupts protein synthesis by interfering with the transpeptidation reaction, which thereby inhibits early chain elongation. Clindamycin may potentiate the opsonization and phagocytosis of bacteria even at subinhibitory concentrations. By disrupting bacterial protein synthesis, clindamycin causes changes in the cell wall surface, which decreases adherence of bacteria to host cells and increases intracellular killing of organisms. The drug also exerts an extended postantibiotic effect against some strains of bacteria, which may be attributed to persistence of the drug at the ribosomal binding site.

b.      Clindamycin is a broad spectrum antibiotic used orally, topically and parenterally for bacterial infections due to sensitive organisms. Clindamycin has been linked to rare instances of acute liver injury

c. Yes, The clindamycin have selective toxicity

The selective toxicity of antibiotics means that they must be highly effective against the microbe but have minimal or no toxicity to humans. In practice, this is expressed by a drug's therapeutic index (TI) - the ratio of the toxic dose (to the patient) to the therapeutic dose (to eliminate the infection). The larger the index, the safer is the drug (antibiotic) for human use. The selective toxicity of antibiotics is brought about by finding vulnerable targets for the drug in the microbe that do not exist in the animal (eucaryote) that is given the drug. Most antibiotics in clinical usage are directed against bacterial cell wall synthesis, bacterial protein synthesis, or bacterial nucleic acid synthesis, which are unique in some ways to bacteria. For example, the beta lactam antibiotics (penicillin and its relatives) inhibit peptidoglycan synthesis in the cell wall. Humans have neither a cell wall nor peptidoglycan and so are unaffected by the action of the drug. Other antibiotics, including streptomycin and the tetracyclines, target bacterial protein synthesis because bacterial ribosomes (termed 70S ribosomes) are different from the ribosomes (80S) of humans and other eucaryotic organisms. Antibiotics such as the flouroqinolones (e.g. ciprofloxacin) inhibit procaryotic (not eucaryotic) DNA replication, and rifamycins inhibit bacterial (not eucaryotic) DNA transcription.From a patient point of view, the most important property of an antimicrobial agent is its selective toxicity, i.e., that the agent acts in some way that inhibits or kills bacterial pathogens but has little or no toxic effect on the patient.


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