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Mechanisms of microbial disease

Mechanisms of microbial disease. Schaechter et al, Chapter 9 Burton & Engelkirk Chapter 7. Not all microbes are pathogens. “Normal” flora (endogenous, indigenous), resident or transient: commensal, symbiotic. Harmless, may be beneficial. Outcompete pathogens Provide necessary nutrients

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Mechanisms of microbial disease

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  1. Mechanisms of microbial disease Schaechter et al, Chapter 9 Burton & Engelkirk Chapter 7

  2. Not all microbes are pathogens • “Normal” flora (endogenous, indigenous), resident or transient: commensal, symbiotic. Harmless, may be beneficial. • Outcompete pathogens • Provide necessary nutrients • Skin: yeasts, mites, bacteria • Corynebacteria, propionibacteria • Staphylococcus spps, S. epidermis, S. aureus • Intestine (enteric flora): 1012 or more bacteria per gram feces

  3. Bacteria of the GI Tract Stomach pH 3 0 to 103 per g Duodenum, jejunum pH 6-7 0 to 104 per g • Enterobacteria • Bacteroides • Escherichia coli • Bifidobacteria • Steptococci • Clostridia Small intestine pH 7-7.5 105 to 108 per g Large intestine pH 7-8 1010 to1012 per g

  4. Opportunistic Pathogens • Pathogenic only under special circumstances: • Susceptible host: Immune system weakened/compromised/suppressed • Indigenous flora decreased (eg antibiotic treatment) • “Indigenous” flora in the “wrong” location • Frank Pathogens • Pathogenic at all times

  5. Pathogenicity – ability to cause disease • Virulence – extent or severity of disease • Both depend on ability to infect the host and to cause damage • Infection: • Colonization (usually at site of entry) • Attachment and/or invasion (Adhesins or pili specific to receptors on target cell) • Multiplication of pathogen • Persistence of pathogen

  6. Spread within initial host • “Local” : pathogen confined to single area, usually point of entry • “Systemic” or “generalized”: pathogen invades or is carried to other tissues, organs • Latent infection • Chronic infection Liver Duodenum

  7. Target organs • Location, environment • Consider route of exposure • Specific attachment (by piliated pathogens) • Hepatitis: HAV, HBV, HCV etc

  8. Some Enteric Diseases • Cholera Vibrio cholerae • Typhoid fever Salmonella typhi • Amebic dysentery Entamoeba histolytica • Hepatitis Hepatitis A virus • Norwalk disease Noroviruses • Polio Polioviruses

  9. Bacterial food poisoning • Staphylococcus aureus • Salmonella • Clostridium

  10. Airborne pathogens • Respiratory viruses • Flu, parainfluenza, respiratory syncytial virus, common cold (rhinovirus) • Bacteria • Legionnaire’s Disease (Legionella pneumophila) • Molds • Allergy, pneumonitis, mycosis, mycotoxicosis

  11. Microbe is Extracellular • Microbe secretes exotoxin • Botulinus, tetanus toxin (neurotoxins) • Enterotoxins (Cholera toxin, toxigenic E, coli, stimulate adenylate cyclase; Shigella toxin, cytotoxic; E. coli O157:H7, both) • Hemolysin, leukocidin, lecithinase • Microbe secretes enzymes • Coagulase, kinases (fibrinolysin), hyaluronidase, collagenase • Microbial membrane elicits reaction • Endotoxin, the lipopolysaccharide of the outer membrane of Gram-negative bacteria

  12. Functional Damage • Biochemical changes in host cell • Ion leakage, fluid leakage • Cholera toxin, targets intestinal epithelia • Lytic pores, S. aureusα-toxin • Disruption/destruction of membrane • Inhibition of protein synthesis • Diphtheria, Pseudomonas aeruginosa • Inhibition of nerve function • Clostridium toxins, tetanus, botulinum

  13. Microbe invades cell • Cell membrane weakened by enzymes • Fimbriae/pili allow attachment to cell wall – confers specificity for cell types

  14. Intracellular • Host cell killed: • Lysis during replication • Necrosis • Apoptosis • Immune system attacks infected cells

  15. The cell cycle Apoptosis, programmed cell death A G1 G0 S M G2 Mitosis (Cell division)

  16. APOPTOSIS In response to defined signals Follows defined sequence of events “Orderly shut-down” of cell functions Cell macromolecules recovered, recycled NECROSIS In response to non-specific damage Often starts with membrane destruction, events thereafter unpredictable Disorderly No recovery of contents Apoptosis vs necrosis

  17. Course of infectious disease • Exposure • Entry • Spread • Multiplication • Damage • Immune response • Outcome Infection Disease

  18. Spread to new host • Person-to-person spread • Communicable – no intermediate host • Contagious – easily transmitted (aerosol droplets, saliva) • Spread by contact – direct or via inanimate object (vehicle, fomite) • Environmental spread: intermediate host, reservoir and/or vector may be involved

  19. Animal Reservoirs • Cryptosporidium parvum • Single host, eg Beef, calves • Oocyst excysts, releases 4 sporozoites • Sporozoites invade intestinal epithlial cells • Sporozoites replicate asexually, differentiate into microgametes and macrogametes • Sexual replication • More oocysts Oocyst ?

  20. Comparison – viruses and bacteria • Ability to infect • Ability to spread • Ability to invade • Ability to cause damage • Ability to survive outside host

  21. Some viruses are carcinogens • Epstein-Barr virus • Herpesviruses • Nasopharyngeal carcinoma, Burkitt’s lymphoma

  22. Prions • “Infectious proteins” • Creutzfeld-Jacob disease • Bovine spongiform encephalopathy (BSE) • Template for protein misfolding • Transmission ?

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