Host-Microbe Interaction
The infectious process represents a specialized form of symbiosis. Contact with a microbe does not always lead to disease. Normal microflora is vital for humans: it maintains an optimal pH, helps organs perform their functions, and participates in metabolism. The eradication of beneficial bacteria (e.g., by antibiotics) leads to severe dysbiosis.
Pathology develops when this balance is disrupted and parasitism occurs—an antagonistic interaction that harms the host. Key properties of pathogens include:
- Pathogenicity — the fundamental ability to cause disease.
- Virulence — the degree of pathogenicity of a specific strain.
- Invasiveness — the ability to multiply and spread through tissues.
- Toxicity — the production of damaging substances.
Natural Body Barriers
From a general biological perspective, microbes are part of our environment. To protect against their aggression, the body has built three lines of defense:
- Anatomical barriers: Skin and mucous membranes. They physically block pathogens and are covered with secretions possessing antimicrobial properties (containing organic acids and the enzyme lysozyme).
- Physiological barriers: The acidic environment of gastric juice, intestinal peristalsis, continuous urine flow, coughing, and mucociliary clearance.
- Immune barriers: Resident cells (macrophages and lymphocytes) patrolling the dermis, alveoli, and sub-mucosal tissues, as well as the secretion of protective antibodies (IgA) on the epithelial surface.
Mechanisms of Damage and Immune Evasion
Upon penetrating tissues, pathogens cause inflammation and cell damage. Viruses integrate their genome into the host DNA, forcing the cell to synthesize new viral particles. Bacteria act differently: they attach to membranes using specific proteins (adhesins) and release toxins.
- Endotoxins — components of the gram-negative bacterial cell wall (lipopolysaccharides). They trigger fever and a massive release of cytokines.
- Exotoxins — enzymes secreted externally by microbes (hemolysins, fibrinolysins, hyaluronidases).
To survive, microorganisms have developed defense mechanisms. They can hide inside cells, suppress the immune response, or form dense capsules. For example, the carbohydrate capsule of meningococci and pneumococci reliably protects their antigens from recognition and hinders phagocytosis.
Morphology: The Primary Infectious Complex
The site of pathogen entry is called the portal of entry. It is here that the initial reaction unfolds, forming the primary infectious complex. This is an obligatory triad of changes for most infectious diseases:
- Primary affect — a focus of inflammation (often with necrosis) directly in the tissue to which the microbe is adapted.
- Lymphangitis — inflammation of the draining lymphatic vessels.
- Regional lymphadenitis — inflammation of the nearest lymph nodes, where the infection and toxins are carried via lymph flow.
It is important to understand that this complex is not merely a local issue, but a local manifestation of an already generalized infection. Simple surgical excision of the primary affect (such as the hard chancre in syphilis) does not cure the patient.
The Role of Host Reactivity
The outcome of an encounter with an infection depends on reactivity—the ability of the macroorganism to respond to a stimulus. Several response variants are distinguished:
- Normergy — a standard reaction upon primary contact with a pathogen.
- Hyperergy — a violent allergic reaction (hypersensitivity). This helps localize the infection at the portal of entry and determines the general manifestations of the disease.
- Hypoergy — a reduced response intensity, where local specific changes come to the forefront.
- Anergy — a lack of response. It can be protective (after successful vaccination) or pathological (upon profound exhaustion of compensatory reserves).