Pathogenesis Fundamentals Flashcards
(39 cards)
In what ways can infectious disease be transmitted?
Respiratory, contact, faecal-oral, sexual, injection
What types of infectious agents are there?
Prions, viruses, bacteria, fungi, parasites
How do gram positive and gram negative cell walls differ?
Gram Positive
- Thick peptidoglycan
- Cell wall has teichoic acids o Lipid and protein inner membrane
- Resistant to drying
Gram Negative
- Thin peptidoglycan
- Outer membrane with lipopolysaccharide
- Porin proteins for transport (OM)
- Periplasmic space
What are characteristics of viruses?
Replicate in host, ss or ds RNA or DNA, protein coat protects nucleic acid
What are the steps in viral replication?
• 1. Attachment
- Penetration
- Uncoating
- Early mRNA transcription
- Early protein translation
- Viral DNA replication
- Late mRNA transcription
How are opportunistic pathogens different to other pathogens?
They cause disease when defence mechanisms are compromised
How are virulent and avirulent organisms different?
• Virulent is most likely cause of disease, avirulent doesn’t cause disease in host with normal immune system
What are some features of normal microbiota?
- Colonise host without causing disease
- Specific and sustainable association with host
- May become pathogenic if moved
- Protect host against disease
- Transient or permanent
What processes occur during infectious disease?
• Colonisation, penetration, replication, damage and disease, dissemination(maybe), immunity (maybe)
What processes are involved in the asymptomatic phase?The symptomatic phase?
- Colonisation, penetration, replication
- Symptomatic = Damage and disease, dissemination(maybe), immunity (maybe)
What are the two types of ligands used by bacteria to colonise/adhere hosts?
Fimbrial and non-fimbrial
What are the functions of pilli?
• Conjugation and adhesion
How does Uropathogenic E.coli colonise a host?
- Attaches to receptors on bladder epithelia cells using type 1 pilli or P fimbriae
- Bacteria internalise, allowed to replicate to high levels
- Avoid being flushed out with urine
What do bacteria use to colonise a host using non-fimbrial adhesion?
- Use molecules in call wall
- Can use glycocalyx (polysaccharide capsule or slime layer)
- Can adhere in a biofilm
What are differences between capsules and slime layers?
- Capsules have strong adherence to cell envelope, help aid evasion of innate immune system (cover PAMPs)
- Slime layers are loose, unorganised and easily removed
How can a pathogen penetrate epithelial cells?
- Penetrate into cells
- Penetrate between cells and into tissue
What processes are used for penetration directly into cells?
- Take advantage of Receptor Mediated endocytosis (RME)
- Use invasion ligands
- Bind receptor for cytoskeleton, directly induce penetration
- Molecular interaction are adhesion causes penetration
How do pathogens penetrate tissue and between cells?
• Penetration causes morphological change, change tight junctions, allow entry
How can microorganism replicate within epithelial cells?
• Grow in endosome (RME) • Grow in cytoplasm
What are the pros/cons of each method?
- Endosome, less nutrients but better protection
- Cytoplasm, more nutrient, but less protection
Why is quorum sensing important?
• Signals can control expression of genes for replication, biofilm production, virulence factors
What features of the host immune system must microorganisms avoid and how?
- Physical barriers (surgery, trauma)
- Complement (enzymes destroy C’)
- Phagocytes (capsules, inhibit phagosome-lysosome function, escape phagolysosome, resist contents of lysosome, kill phagocyte)
- Antibodies (enzyme destruction, coat in self-antigen) • APCs (down regulate MHC)
- T cells (cytokines, CTL, impair T cells)
In what ways can microorganisms damage cells?
• Exotoxins, endotoxins, immunopathology
What are some features of exotoxins and endotoxins and how do they differ?
Exotoxins
- G+ and G-
- Secreted
- Action depends on target molecule
- Cytotoxic = cell death
- Cytotonic = change cell function
Endotoxins
- G-
- Not secreted, part of cell wall
- Lipopolysaccharides
- Predominantly produced when G- cells die
- Trigger alternate complement cascade
- Trigger clotting cascade
- Bind/activate macrophages and neutrophils
- Activated macrophages release cytokines, enzymes etc.
