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Pathogenicity and Virulence Factors Mechanisms of Microbial Disease Pathogenicity: Ability of a microbe to cause disease Virulence: Measure of the degree/intensity of disease caused Focus: How pathogens invade, evade, and damage the host What it means: This sets the stage. Pathogenicity answers "Can this microbe make me sick?" It's yes or no. Salmonella = yes. Lactobacillus in yogurt = no. Virulence answers "If it can make me sick, how bad will it be?" Ebola virus = high virulence. Rhinovirus that causes common cold = low virulence. Why it matters: Not all microbes are bad. Understanding these terms helps explain why some infections are deadly and others are mild. --- Pathogenicity vs Virulence Pathogen: Any microorganism capable of causing disease Pathogenicity: Qualitative trait. A microbe is either pathogenic or non-pathogenic - Determined by presence of virulence genes Virulence: Quantitative trait. Describes severity of disease - Measured by LD₅₀ = dose that kills 50% of hosts - High virulence = fewer organisms needed to cause disease Opportunistic pathogens: Cause disease only in weakened hosts - Ex: Pseudomonas aeruginosa in cystic fibrosis patients This is the vocab slide. LD₅₀ ( lethal dose)is how scientists measure virulence. If it only takes 10 bacteria to kill 50% of test animals, that's more virulent than one that needs 1 million bacteria. Pathogenicity is qualitative: A microbe has the genes to cause disease, or it doesn’t. Like having a driver’s license vs not having one. Virulence is quantitative: How good of a driver are you? Aggressive or cautious? Opportunistic pathogens are the key nuance. Pseudomonas aeruginosa lives on your skin harmlessly, but if you’re on a ventilator, it can cause deadly pneumonia. The host matters too. --- Adhesion - Binding to host cells via pili, fimbriae, adhesins - Ex: E. coli type-1 fimbriae bind urinary tract Invasion & Colonization - Penetrate tissues using invasins, collagenase, hyaluronidase - Multiply to establish infection Evasion of Host Defenses - Capsules prevent phagocytosis: Streptococcus pneumoniae - Antigenic variation: Neisseria gonorrhoeae pili - Secretion systems inject effectors: Type III in Salmonella Damage to Host - Direct: toxins and enzymes - Indirect: inflammation and immune overreaction Disease isn’t random. Pathogens follow a 4-step playbook. First is adhesion. Bacteria use pili or adhesins like grappling hooks to stick to your cells. UTI E. coli sticks to your bladder so urine can’t wash it away. No sticking, no infection. Second is invasion. Once attached, they use enzymes like hyaluronidase to break down tissue barriers and spread. Third is evasion. Your immune system is the security guard, and pathogens have disguises. Capsules act like invisibility cloaks against white blood cells. Neisseria constantly changes its surface proteins so antibodies can’t track it. Fourth is damage. Sometimes toxins directly poison cells. Other times, like with COVID, your immune system overreacts and damages your own tissues. That’s when you feel sick." --- Adherence factors: Pili, fimbriae, M protein of S. pyogenes Invasion factors: Hyaluronidase, collagenase, lecithinase Antiphagocytic factors: Capsules, Protein A of S. aureus Exotoxins: Secreted proteins, highly toxic - A-B toxins: Cholera toxin, Diphtheria toxin - Membrane-disrupting: Streptolysin O - Superantigens: Toxic shock syndrome toxin-1 Endotoxin: LPS from Gram-negative outer membrane - Causes fever, inflammation, septic shock Iron acquisition: Siderophores like enterobactin steal iron from host Biofilms: P. aeruginosa, S. aureus. Resist antibiotics + immune cells Virulence factors are the actual weapons. Adhesins are velcro. Strep’s M protein lets it cling to your throat to cause strep throat. Invasion factors are battering rams. Flesh-eating bacteria use enzymes to melt tissue and spread fast. Antiphagocytic factors fight your immune system. Staph aureus Protein A grabs antibodies and holds them backwards so immune cells are useless. Exotoxins are secreted poisons. Botulinum toxin is lethal in tiny amounts. Cholera toxin causes deadly watery diarrhea. Endotoxin is LPS from dead Gram-negative bacteria. It triggers fever and septic shock. Siderophores are iron pirates that steal iron from your body. Biofilms are bacterial cities. They build slime fortresses on catheters that antibiotics can’t penetrate. That’s why those infections are so hard to treat." --- Environmental signals activate virulence genes - Temperature: Listeria virulence genes on at 37°C - pH: Vibrio cholerae toxin in alkaline gut - Iron limitation: Triggers siderophore production Quorum sensing: Bacteria coordinate via autoinducers - Virulence expressed only at high cell density - Ex: Staphylococcus aureus toxin production Pathogenicity islands: Clusters of virul
