Antibiotic Resistance

 

 

Basic Mechanisms of Antibiotic Action against Bacterial Cells

One of the mechanisms of antibiotic action is the inhibition of cell wall synthesis in the bacteria (Kawai et al. 1716). Drugs used in this mechanism are the beta-lactams and bacitracin. Another mechanism is the inhibition of protein synthesis. This is achieved through interference in either the 30s or 50s ribosome sites (Connell et al. 3676). Examples of drugs used in this process include chloramphenicol and aminoglycosides. Other antibiotics alter the cell membrane which results in interference with cell membrane permeability. Examples include polymyxins and bacitracin. Antimetabolite antibiotics such as trimethoprim and sulfonamides work by inhibiting the synthesis of nucleotides which are required for DNA synthesis. The final mechanism is the inhibition of nucleic acid synthesis hence preventing DNA and RNA synthesis. Examples include metronidazole and rifampin.

 

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Ways of Building Resistance

Resistance to antibiotics develops with time. One of the ways bacteria manage this feat is by restricting access to the antibiotic. Another way is by altering or destroying the antibiotic. This is done by secreting enzymes that break down the drugs. Getting rid of the antibiotic is yet another means of resistance. Some bacteria change the target of the antibiotic while others develop new cell processes different from those targeted by antibiotics. Such processes utilize enzymes that are insensitive to the drugs (Peters et al. 10787). Bacteria can also alter the structure of molecules that antibiotics are meant to bind with. Finally, some bacteria can offer protection to antibiotic target sites. An example is the protection of 30s ribosomes, whereby molecules within the cell can dislodge the antibiotic from the ribosomes hence preventing its inhibitory effects (Connell et al. 3677). These are the different ways bacteria develop resistance against antibiotics.

Works Cited

Connell, Sean R., et al. “Ribosomal Protection Proteins and Their Mechanism of Tetracycline Resistance.” Antimicrobial Agents and Chemotherapy, vol. 47, no.12, 2003, pp. 3675-3681.

Kawai, Yoshikazu, et al. “Cell Wall Inhibition in L-Forms or Via Β-Lactam Antibiotics Induces Reactive Oxygen-Mediated Bacterial Killing through Increased Glycolytic Flux.” Nature Microbiology, vol. 4, no. 10, 2019, pp. 1716-1726.

Peters, Katharina, et al. “Copper Inhibits Peptidoglycan LD-Transpeptidases Suppressing Β-Lactam Resistance Due to Bypass of Penicillin-Binding Proteins.” Proceedings of the National Academy of Sciences, vol. 115, no. 42, 2018, pp. 10786-10791.

 

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