Pathogenic Mechanisms of Infectious Diseases
Core concepts
Understand virulence factors: adhesins, invasins, capsules (antiphagocytic), toxins (endotoxin LPS, exotoxins such as diphtheria, tetanus, botulinum, cholera), and immune evasion (IgA protease, protein A, coagulase). Know Koch's postulates and their modern limitations (unculturable agents, asymptomatic carriage). Distinguish exotoxin (protein, heat-labile, specific action, toxoid-amenable) from endotoxin (LPS, heat-stable, causes fever and shock via TLR4).
Know host defense mechanisms: innate (phagocytes, complement, barriers) and adaptive (T and B cells). Understand hypersensitivity types and their role in infection-related pathology (e.g., type IV in TB). Recognize carrier states, latency (herpesviruses, TB), and biofilms (catheter infections, Pseudomonas).
Traps to expect
- Confusing endotoxin (Gram-negative LPS) with exotoxin - endotoxin is not neutralized by antitoxin.
- Assuming a positive culture equals disease - colonization vs infection requires clinical context.
- Forgetting that capsules are antiphagocytic and often vaccine targets (pneumococcus, meningococcus, H. influenzae type b).
- Overlooking superantigens (TSST-1, streptococcal pyrogenic exotoxin) causing nonspecific T-cell activation.
Worked example / rule of thumb
A patient has fever, hypotension, and a Gram-negative rod in blood. Rule of thumb: endotoxin-mediated septic shock is the mechanism - LPS triggers cytokine release via TLR4. Treatment is supportive plus appropriate antibiotics; antitoxin is not effective against endotoxin. This contrasts with C. diphtheriae or C. tetani, where antitoxin is central.