Overview
Clinical Meaning
Host pathogen interactions determine the outcome of infectious encounters through the interplay between pathogen virulence factors and host immune defenses.
CNPLE
CNPLE
Host-pathogen interactions determine the outcome of infectious encounters through the interplay between pathogen virulence factors and host immune defenses. Adhesins (pili, fimbriae) allow bacterial attachment. Biofilm formation (Pseudomonas, S. epidermidis on devices) creates antibiotic-resistant polysaccharide matrix. Capsules (S. pneumoniae, N. meningitidis, Klebsiella) prevent phagocytosis. Toxins: exotoxins are secreted proteins with specific targets (botulinum = blocks ACh release; cholera = activates adenylyl cyclase; diphtheria = inhibits protein synthesis); endotoxin (LPS from gram-negative walls) triggers massive cytokine release causing septic shock. Host defense layers: physical barriers (skin, mucosal surfaces, ciliated epithelium, gastric acid), innate immunity (neutrophils, macrophages, NK cells, complement, toll-like receptors recognizing PAMPs), and adaptive immunity (T cells — cell-mediated against intracellular pathogens; B cells — humoral antibodies against extracellular pathogens). Immunodeficiency patterns: neutropenia → bacterial/fungal infections; T-cell deficiency (HIV) → opportunistic infections (PCP, toxo, CMV); B-cell deficiency → encapsulated organisms; complement deficiency → Neisseria; splenectomy → overwhelming infection from encapsulated organisms (OPSI).
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