Cell Structure and Antibiotic Resistance

According to the World Health Organization (WHO), the rise of antibiotic resistance is one of the world’s most significant threats to public health, food security, and development. While antibiotic resistance can occur naturally, it is being exacerbated by the widespread misuse of antibiotics worldwide.

Antibiotic Resistance

Image Credit: Lightspring/Shutterstock.com

Antibiotic Resistance Explained

As a result of improper antibiotic use, infections that were once easily treatable are becoming harder to manage as antibiotics lose their effectiveness. Diseases such as gonorrhea, pneumonia, salmonellosis, and tuberculosis are becoming increasingly difficult to treat due to rising antibiotic resistance. This growing resistance is placing pressure on healthcare systems, leading to longer hospital stays and increased mortality rates from hard-to-treat infections.

To combat this, understanding how antibiotic resistance develops is crucial. Studies investigating the mechanisms of resistance at the cellular level are key to revealing how bacterial structures like the cell wall contribute to resistance. This article explores current knowledge in this field.

The Structure of Bacterial Cells

Infections are caused by either Gram-positive or Gram-negative bacteria. Gram-positive bacteria have a rigid cell wall surrounding a cytoplasmic membrane, while Gram-negative bacteria have an outer lipid membrane (OM) that encases a thinner cell wall. The space between the OM and the cytoplasmic membrane, known as the periplasm, provides additional protection to Gram-negative bacteria by shielding them from harmful substances.

For decades, scientists have developed antibiotics that compromise bacterial cell walls, causing bacterial lysis. These antibiotics were effective for many years, but due to the increasing misuse of these drugs, bacteria causing serious infections are now becoming resistant.

How Bacterial Cell Structures Contribute to Antibiotic Resistance

While the OM offers protection to bacteria, it also provides opportunities for therapeutic intervention. This membrane contains porins—channels that allow molecules, including antibiotics, to pass through. Scientists have developed therapeutic molecules that exploit these natural structures.

Drug molecules, like antibiotics, can enter bacteria either through diffusion or by utilizing these porins. Hydrophilic molecules pass through the OM via these channels, but a reduction in porin numbers can increase resistance to certain antibiotics, such as β-lactams.

Another mechanism bacteria use to resist antibiotics involves efflux pumps, which are proteins that actively remove antibiotic molecules from the cell, maintaining low intracellular concentrations. Efflux pumps are located in the cytoplasmic membrane and are often multidrug transporters capable of expelling a wide range of antibiotics. As a result, resistance can develop against various antibiotic classes through the action of these pumps.

Other Mechanisms of Antibiotic Resistance

Modification of antibiotic target sites is another common resistance mechanism. Natural variations or mutations in these target sites can prevent antibiotics from binding effectively, reducing their efficacy. Even minor alterations can significantly impact drug effectiveness due to the precision with which antibiotics are engineered to target specific sites.

Several common mutations can lead to antibiotic resistance:

  • Alterations in the 30S or 50S subunits of ribosomes result in resistance to antibiotics targeting protein synthesis, including aminoglycosides, chloramphenicol, macrolides, and tetracyclines.
  • In Gram-positive bacteria, resistance often arises from modifications to penicillin-binding proteins. For example, Enterococcus faecium becomes resistant to ampicillin through this mechanism. Streptococcus pneumoniae develops resistance to oxacillin and methicillin via a similar pathway. Studies show that the integration of the "staphylococcal cassette chromosome mec" (SCCmec) into the S. aureus chromosome confers resistance.
  • Some strains of Enterococcus faecium and Enterococcus faecalis have developed high levels of resistance to teicoplanin and vancomycin by altering their cell wall precursors.
  • Resistance to fluoroquinolones can occur due to modifications of the DNA gyrase and topoisomerase IV enzymes, preventing DNA replication and blocking the antibiotic's binding ability.
  • Mutations in RNA polymerase can lead to resistance to rifampicin.

Overall, a wide range of genetic mutations can alter bacterial cell structures, resulting in antibiotic resistance. Different antibiotics are threatened by various mutations. Understanding these cellular changes is essential to developing more effective antibiotics that can overcome resistance and continue to treat infectious diseases.

Sources:

Further Reading

Article Revisions

  • Oct 3 2024 - Clarification of Antibiotic Resistance: Simplified wording and structure for better flow. Original: "As a result of improper use of antibiotics, some infections that were once easily controlled..." Revised: "As a result of improper antibiotic use, infections that were once easily treatable..." Section Titles: Added clearer section headers for ease of navigation and readability (e.g., "The Structure of Bacterial Cells" and "How Bacterial Cell Structures Contribute to Antibiotic Resistance"). Simplified Technical Language: Reworded overly complex technical language to improve clarity without losing scientific accuracy. Example: Changed “hydrophilic molecules can cross the bacterium’s OM via the porins” to “Hydrophilic molecules pass through the OM via these channels.” Added Explanation of Mechanisms: Clarified explanations of resistance mechanisms, particularly efflux pumps and porins, for broader understanding. Expanded Explanation on Common Mutations: Grouped and summarized common antibiotic resistance mutations more clearly, separating examples into bullet points for better readability. Conclusion and Significance: Added a concluding paragraph summarizing the importance of understanding mutations for future antibiotic development.

Last Updated: Oct 3, 2024

Sarah Moore

Written by

Sarah Moore

After studying Psychology and then Neuroscience, Sarah quickly found her enjoyment for researching and writing research papers; turning to a passion to connect ideas with people through writing.

Citations

Please use one of the following formats to cite this article in your essay, paper or report:

  • APA

    Moore, Sarah. (2024, October 03). Cell Structure and Antibiotic Resistance. AZoLifeSciences. Retrieved on October 14, 2024 from https://www.azolifesciences.com/article/Cell-Structure-and-Antibiotic-Resistance.aspx.

  • MLA

    Moore, Sarah. "Cell Structure and Antibiotic Resistance". AZoLifeSciences. 14 October 2024. <https://www.azolifesciences.com/article/Cell-Structure-and-Antibiotic-Resistance.aspx>.

  • Chicago

    Moore, Sarah. "Cell Structure and Antibiotic Resistance". AZoLifeSciences. https://www.azolifesciences.com/article/Cell-Structure-and-Antibiotic-Resistance.aspx. (accessed October 14, 2024).

  • Harvard

    Moore, Sarah. 2024. Cell Structure and Antibiotic Resistance. AZoLifeSciences, viewed 14 October 2024, https://www.azolifesciences.com/article/Cell-Structure-and-Antibiotic-Resistance.aspx.

Comments

The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of AZoLifeSciences.
Post a new comment
Post

While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. We do not provide medical advice, if you search for medical information you must always consult a medical professional before acting on any information provided.

Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles.

Please do not ask questions that use sensitive or confidential information.

Read the full Terms & Conditions.

You might also like...
Insights into Host Defense Mechanisms Through Cell Death and Immune Pathways