1 / 22

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

loe
Download Presentation

Mechanisms of microbial disease

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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 ?

More Related