Pathogenic microbes cause different viral or bacterial infections and illnesses by getting into the body, start reproducing, and crowding out healthy microbes or growing into normally sterile tissues. Scientists discovered antimicrobial agents to cure these diseases and infections. New agents are developed since this discovery due to the resistance phenomenon that develops against existing antimicrobial agents.
The current paper discusses the different categories of antimicrobial agents, how viral and bacterial infections differ, and the importance of adequately identifying viral and bacterial infections to select the correct antimicrobial agent.
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The different categories of antimicrobial agents include antibacterial agents, antifungal agents, antiviral agents, and anti-parasitic agents (Toy et al., 2014).
Antibacterial agents are a group of drugs that selectively kill bacteria by disrupting bacterial growth or survival, and thus minimize their pathogenic effect in the body (Toy et al., 2014). Bacteriostatic agents act by inhibiting or slowing bacterial growth while bactericidal agents act by targeting the cell membrane or cell wall of the bacteria. Bacteriostatic agents inhibit protein synthesis or specific bacterial metabolic pathways. Antibacterial agents can also be categorized based on how they specify their targets. For example, narrow-spectrum agents focus on a narrow range of bacteria by targeting Gram-negative only or Gram-positive only pathogens (Toy et al., 2014). Broad-spectrum agents, nevertheless, target different pathogenic bacteria such as both Gram-negative and Gram-positive pathogens (Arcangelo et al., 2017). Antibacterial agents function by interfering with nucleic acid synthesis, protein synthesis, cell membrane function, and cell wall synthesis, which are the primary processes responsible for bacterial growth.
Antifungal agents act by interfering with the cell membrane. These agents capitalize on the small variations between humans and fungi in the biochemical pathways that produce sterols (Toy et al., 2014). Sterols ensure that the cell membrane functions appropriately by maintaining the correct fluidity within the membrane (Arcangelo et al., 2017). The primary membrane sterol for most fungi is ergosterol while humans use cholesterol. Antifungal agents act by targeting ergosterol synthesis in which agents such as imidazoles and triazole act by interfering with ergosterol biosynthesis. Allylamines, however, work by inhibiting an earlier stage of ergosterol biosynthesis. Polyenes, which are structurally associated with macrolides, act by binding to ergosterol in fungal cytoplasmic membranes to create pores. Other antifungal agents such as echinocandins work by blocking the synthesis of glucan in fungal cell walls but not in humans (Lumen, 2017).
Antiviral agents are mostly nucleoside analogs that inhibit nucleic acid biosynthesis (Toy et al., 2014). Acyclovir based agents cause chain termination after being activated by the enzyme thymidine kinase and being added to a growing DNA strand during replication. The specificity of this agent for viral infections originates from viral enzyme activation and the high affinity of the active agent from viral DNA polymerase (Lumen, 2017). Ribavirin agent function by interfering with both the RNA and DNA synthesis by decreasing intracellular guanosine triphosphate pools. The agent also acts by inhibiting the RNA polymerase of viruses. Other antiviral agents such as amantadine, work by binding to a transmembrane protein that aid viruses in escaping from endosomes, which in turn hinders the release of viral RNA into host cells, and viral replication.
Neuraminidase inhibitors act on viruses by blocking the activity of viruses, which prevents the virus from being released to other cells (Toy et al., 2014). Other antiviral agents such as reverse transcriptase inhibitors act by blocking the initial step that involves the conversion of the viral RNA genome into DNA. These inhibitors, such as non-nucleoside noncompetitive inhibitors and nucleoside analog inhibitors, bind reverse transcriptase to cause inactivating conformational changes (Lumen, 2017). Protease inhibitors such as ritonavir act by blocking the production of viral proteins, which hinders viral maturation. Integrase inhibitors such as raltegravir act by blocking the action of the HIV integrase that causes a DNA copy of the viral genome to be recombined into the chromosome of the host cell.
Anti-parasitic agents are used in the treatment of infections caused by the unicellular protozoa and the helminths (Toy et al., 2014). Anti-protozoa agents target infectious protozoans. Atovaquone agents act against fungal infections and block electron movement in protozoans. Antimetabolites such as proguanil inhibit the synthesis of protozoan folic acid. Artemisinins act by being metabolized by target cells to form reactive oxygen species that destroy the target cells. Quinolones and nitroimidazoles act by interfering with the synthesis of nucleic acid while pentamidine act by interfering with DNA replication. Quinolones work by interfering with heme detoxification that parasites require to effectively breakdown hemoglobin into amino acids within red blood cells (Lumen, 2017). Anti-helminths act against helminths. Benzimidazoles act by hindering the formation of microtubule in the intestinal walls of pathogens, which reduces the uptake of glucose. Avermectins act by binding to glutamate-gated chloride pathways specific to helminths to block neuronal transmission and starve, paralyze the pathogens and cause death (Lumen, 2017). Niclosamide acts by inhibiting ATP formation and inhibit oxidative phosphorylation within mitochondria of pathogens while Praziquantel act by causing the influx of calcium into the pathogen, leading to spasms and paralysis of the pathogen. Thioxanthenonones works by inhibiting the synthesis of RNA (Toy et al., 2014).
The main difference between viral infections and bacterial infections is that viral infections entail either the virus entering the cell or directly injecting its DNA into the cell. Inside the cell, the virus enslaves the functioning of the host cell to replicate and produce more viruses, which move out of the host cell to attack other body tissues (Eisenreich et al., 2019). Bacterial infections, however, do not invade the host cells to replicate but target specific tissues where they thrive and either acquire nutrients from the host cell, replicate inside the host cell and kill the cell when breaking out, or secrete toxins that kill the host cell (Eisenreich et al., 2019). Unlike viruses, bacteria replicate individually without the need for the host cell to replicate.
It is vital to accurately identify bacterial and viral infections during the selection of the correct antimicrobial agent to ensure that the targeted pathogens do not develop drug resistance (CDC, 2018). Many viruses and bacteria have evolved over the years to resist specific antimicrobial agents. Improperly identifying these pathogens can, thus, cause the applied treatment to fail (Arcangelo et al., 2017). Correctly identifying pathogens also ensures that the correct vaccine is used to help the body protect against pathogens before they cause illnesses.
Antimicrobial agents are used to hinder the pathogenicity of microorganisms. Different types of antimicrobial agents target different kinds of microorganisms. The categories of antimicrobial agents are antibacterial agents, antifungal agents, antiviral agents, and anti-parasitic agents. Inside the body, viruses must use the host cell to replicate while bacteria replicate individually without using the host cell. It is vital to correctly identify viral and bacterial infections when selecting the correct antimicrobial agent to prevent drug resistance and to ensure the selection of the correct vaccine.
References
Arcangelo, V. P., Peterson, A. M., Wilbur, V., & Reinhold, J. A. (2017). Pharmacotherapeutics for Advanced Practice: A Practical Approach . Lippincott Williams & Wilkins.
CDC. (2018, September 10). Antibiotic / Antimicrobial Resistance | CDC. Retrieved July 15, 2019, from https://www.cdc.gov/drugresistance/index.html
Eisenreich, W., Rudel, T., Heesemann, J., & Goebel, W. (2019). How Viral and Intracellular Bacterial Pathogens Reprogram the Metabolism of Host Cells to Allow Their Intracellular Replication. Frontiers in cellular and infection microbiology , 9 .
Lumen. (2017). Mechanisms of Other Antimicrobial Drugs. Retrieved July 15, 2019, from https://courses.lumenlearning.com/microbiology/chapter/mechanisms-of-other- antimicrobial-drugs/
Toy, E. C., DeBord, C. R. S., Wanger, A., Kettering, J. D., Pillai, A. S., & Mackenzie, R. C. (2014). Case Files Microbiology . McGraw Hill Professional.
