Antimicrobial chemotherapy applies chemical agents to treat infectious diseases within a host. It encompasses drugs that combat bacteria, viruses, fungi, and parasites. The overall purpose of this therapy is to control or eliminate harmful microorganisms that cause illness inside the body.
Defining the Primary Goal
The overarching aim of antimicrobial chemotherapy is to eliminate or inhibit the growth of disease-causing microorganisms within an infected individual, without causing significant harm to the host’s own cells. This principle is known as selective toxicity. Paul Ehrlich first articulated this concept, envisioning agents that would specifically act on pathogens while remaining harmless to the body’s normal components. Achieving selective toxicity relies on exploiting biological differences between microbial cells and human cells. For instance, the rigid cell walls of bacteria provide a distinct target absent in human cells.
Antimicrobial agents accomplish this goal through two main strategies. Some agents are microbicidal, directly killing microorganisms. Others are microbistatic; they inhibit the growth and reproduction of microorganisms, allowing the host’s immune system to clear the infection. While these categories provide a general distinction, some microbistatic agents can become microbicidal at higher concentrations.
How Antimicrobial Agents Achieve Their Purpose
Antimicrobial agents achieve their purpose by selectively interfering with structures or processes essential to the microorganism but different from or absent in human cells. Many antibacterial agents, for example, target the bacterial cell wall, a unique and rigid outer layer critical for bacterial survival. Disrupting its formation can lead to bacterial cell breakdown. Penicillins, a well-known class of antibiotics, interfere with the synthesis of peptidoglycan, a vital component of bacterial cell walls.
Other agents inhibit the microorganism’s ability to produce essential proteins. These drugs often target ribosomes, the cellular machinery for protein synthesis, which differ between microbes and human cells. Another mechanism involves disrupting the replication or function of nucleic acids, such as DNA or RNA, preventing pathogen multiplication. Additionally, some antimicrobials target metabolic pathways unique to the pathogen. For instance, sulfonamides block bacterial folic acid synthesis, a process not found in human cells.
Targeting Different Microbial Threats
Antimicrobial chemotherapy employs various types of agents, each designed to target specific microbial threats. Antibacterial agents, commonly known as antibiotics, are used to treat bacterial infections. These drugs often leverage fundamental differences, such as the presence of bacterial cell walls or unique bacterial enzymes, to achieve their effect.
Antiviral agents combat viruses, which present a unique challenge because they utilize the host cell’s machinery for replication. Antivirals target viral enzymes or proteins essential for the virus’s replication cycle but distinct from human cellular components.
Antifungal agents address fungal infections. While fungi are eukaryotes, sharing more cellular similarities with humans than bacteria, antifungals target specific fungal components like ergosterol in their cell membranes, not found in human cell membranes.
Antiparasitic agents are used against infections caused by protozoa and helminths. These agents disrupt life cycles or metabolic processes specific to the parasite, preventing their survival and proliferation within the host.
Maintaining the Effectiveness of Antimicrobial Chemotherapy
A significant challenge to the ongoing effectiveness of antimicrobial chemotherapy is the emergence and spread of antimicrobial resistance (AMR). This occurs when microorganisms develop the ability to withstand drug effects, rendering treatments less effective or entirely ineffective. This resistance threatens the ability to treat infectious diseases.
Resistance can arise through natural selection, where microbes with advantageous mutations survive and multiply in the presence of drugs, or it can be accelerated by the misuse and overuse of antimicrobial agents. Microorganisms acquire resistance by altering the drug’s target site, producing enzymes that inactivate the drug, or actively pumping the drug out of their cells. The transfer of resistant genes among different microbes further compounds this issue. Ensuring long-term effectiveness necessitates responsible use of existing treatments and continuous efforts to develop new drugs. This collective endeavor helps preserve treatment options for future generations.