Chapter 16 - Host microbe interactions

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Host Microbe Interactions Chapter 16
1. Compare and contrast the terms normal microbiota, opportunistic pathogen, and primary pathogen. 2. Distinguish between infection and disease, and describe how they combine to produce an infectious disease. 3. Define virulence and explain how virulence factors and infectious dose can impact virulence. 4. Compare and contrast the three types of infection: acute, chronic, and latent. 5. Define the terms “ID50” and “LD50”, describe how they are determined, and relate strain differences in them to virulence. 6. Outline Koch’s Postulates, state their significance and limitations, and apply them to the study of an infectious disease. 7. Outline processes of microbial adherence and entry into the host (penetration), and the role of antiphagocytic factors during infection. 8. Compare and contrast endotoxins and exotoxins 9. Briefly describe the mechanism of AB Toxins
Normal Human Microbiota • Fetus is sterile • Colonization by normal flora due to • Delivery • Handling • Environment • Food • Normal flora changes over lifetime • Body region specific
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Figure 16.1
Normal Human Microbiota 2 • Usually live symbiotically • Commensalism and mutualism • Protection against pathogens by normal flora • Prevent attachment • Competition for nutrients • Production of antimicrobial substances • Stimulation of immune system (cross-reaction) • Some are opportunistic pathogens • immune system compromised • introduced in an unusual location
Group Question: A baby delivered via C-section has a different normal gut microbiome than those born vaginally. What are the possible repercussions? https://medicalxpress.com/news/2018-11-microbiome-caesarean-section-impacts-baby.html
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Microbes from Mom • What process introduces a baby to its microbiome? • How does this microbiome affect the early months of a baby’s life? • How does a C section differ from a vaginal birth? • How does this affect the health of the baby?
Infection and Disease • Infection: Establishment and proliferation of a microbe on or within a host • Usually must pass through skin or mucous membranes • Disease: Harmful alteration of host tissues or metabolic activities • Infectious Disease: A combination of the two • Signs & symptoms
Pathogenicity vs. Virulence • Pathogenicity: Ability to produce a disease • Virulence: Degree of pathogenicity • Based on • Infectivity: Ability to enter host and reproduce • Invasiveness: Ability to spread • Pathogenic potential: Ability to do damage • Some pathogens are highly virulent – a few bacteria can cause disease
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Virulence • Virulence can be determined by • ID 50 • Number of organisms needed to establish an infection • LD 50 • Amount of toxin needed to be lethal
Infectious Dose vs Lethal Dose • ID 50 • # of organisms needed is inversely proportional to virulence • Isn’t a measure of lethality • Infectious doesn’t necessarily mean severe • Depends on portal of entry • LD 50 • Lethal dose is an amount (g) • Dependent of weight of patient ID 50 Foodborne Infections EHEC O157 10 1 -10 2 ETEC 10 6 -10 9 S. enterica 1 S. dysenteriae 10-200
Can Virulence Change? • How can the same bacterial species become • more virulent? • less virulent?
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Entry into the Host •Microbial Adherence • Attachment to surface tissues–usually specific (bacterial adhesins on pili or viral spikes) • Host Protection • Competition with normal flora • Antibody in mucus (sIgA) Figure 16.4
Entry into the Host • Penetration of Epithelial Layers • Passive Penetration • e.g., wounds, burns, arthropods • Endocytosis • Invasins of Salmonella cause alteration of host’s cytoskeleton and induce phagocytosis • Type III secretion system (Gr–) • “Nanosyringe” • Effectors alter host cell
Pathogen entry by endocytosis
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Other Microbial Virulence Factors • Immune System Evasion • Anti-phagocytic Factors • Capsule • Complement peptidases • Fc receptors
Other Microbial Virulence Factors • Damage to the Host • Toxins • Exotoxins • AB toxins • Superantigens • Pore formers • Endotoxins • LPS
Exotoxins • Protein secreted by living cells • Heat labile–inactivated by boiling • Strong antigens • Can be converted to toxoids and are easily neutralized by antitoxin (Ab) • Each has a characteristic effect • e.g., neurotoxin, enterotoxin, leukocidin, hemolysin... • Small lethal dose • C. botulinum: MLD mouse is 2.5 X10 -5 µg • C. tetani: MLD mouse is 4 X10 -5 µg
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Exotoxins • Superantigens • Cause Th cells to become activated regardless of specificity • AB Toxins • uptake into cells by B unit • toxic effect by A unit • can exploit the B unit to make • vaccines • directed medications
Endotoxins • Released from walls of lysed Gram (-) cells • Lipopolysaccharide (LPS) • Lipid A (toxic portion) • O polysaccharide (variable antigen) • Poor antigens (therefore cannot form toxoids) • Heat stable–withstand autoclaving • All have similar effects • Pyrogenicity–endogenous pyrogen (IL-1) from WBC • Body aches • Shock (if severe infection) • Usually have a larger lethal dose
Make a Venn-Diagram: • Compare and contrast exotoxins and endotoxins produced by bacteria. Exotoxins Endotoxins
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Determining the Causative Agent • Koch’s Postulates ( 1890) • See Figure 16.3 • Limitations • Some diseases have more than one causative agent ( e.g., meningitis, pneumonia) • Suitable animal hosts are not available • Ethical issues
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Dose (pg/kg)
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