Concept and Fundamental Differences
In the early 20th century, the prominent researcher Paul Ehrlich introduced a new term into medical practice. Today, this term refers to a specialized method for treating infectious diseases, parasitic infestations, and malignant neoplasms. Special chemical substances, known as chemotherapeutic agents, are used for this purpose.
The fundamental principle underlying this entire branch of pharmacology is called selective toxicity. This principle involves using substances that act strictly selectively: they exert a powerful, lethal effect on the parasite or tumor cell while causing no significant harm to the host's (patient's) body.
It is crucial for medical students and physicians to understand the key difference between this approach and classic pharmacotherapy. In standard pharmacotherapy, the drug's target is always located within the human tissues themselves — drugs are used to correct impaired functions of organs and systems. In contrast, in chemotherapy, the target (or specific receptor) is located outside of human tissues. The site of drug action is directly within the foreign microbial cell or the structure of the malignant tumor.
Rule No. 1: Identification of the Pathogen
When prescribing treatment, a physician must follow a strict sequence of actions to ensure maximum therapeutic efficacy and safety. The first critical step is the identification of the pathogen.
The main challenge at this stage is that many severe and life-threatening conditions (such as pneumonia, meningitis, or sepsis) are polyetiological. This means they can be caused by entirely different microbes. At the same time, a strict time factor comes into play: complete microbiological identification requires significant time, yet delaying treatment in critically ill patients is strictly unacceptable.
To resolve this dilemma, the following clinical tactics are applied:
- Before receiving the exact results of laboratory cultures, the patient is immediately prescribed empirical therapy. Broad-spectrum drugs are used to cover the most likely pathogens.
- As soon as the laboratory completes the identification of the microorganism, transitioning to narrow-spectrum, targeted therapy becomes both possible and necessary.
Rule No. 2: Determination of Susceptibility
Once the enemy is identified, its vulnerabilities must be determined. For this, susceptibility testing is performed (an antibiogram is generated). The primary goal of this stage is to select the most effective and safest agent not just for the bacterial species, but for the specific strain isolated from the given patient.
The selection of the optimal drug is a complex analytical process in which the physician relies on several basic criteria:
- Proven maximal activity of the drug against the identified pathogen.
- Safety of the chosen agent for the patient.
- Mandatory consideration of individual host (patient) characteristics and the specifics of the disease course.
- Clinical pharmacology parameters of the drug in question.
Rules No. 3 and No. 4: Time of Initiation and Routes of Administration
Treatment success largely depends on the speed of response. Therapy must be initiated at the earliest stages. The biological rationale for early initiation lies in the life cycle of pathogens: microbial cells are most sensitive to drug exposure precisely during their phase of active growth and replication. Furthermore, there is a direct correlation with load: the smaller the initial microbial mass, the easier it is to suppress the infectious process. Early treatment also has tremendous epidemiological significance, as it effectively limits the spread of infection both within the patient's body and into the external environment.
The final principle is the judicious choice of the route of administration and dosage form. The physician's main task here is to achieve an adequate therapeutic concentration of the drug directly at the site of infection. The localization of the pathological process determines the optimal route of administration. The primary mechanism and goal of this rule are to ensure maximal, dense contact between the chemotherapeutic agent and the disease-causing pathogen.