Determinants of Infectious disease Flashcards
Virulence factors
Adhesion, invasion, evasion of host defence, obtaining nutrients from host and toxicity.
Types of transmission
Direct (host-to-host transmission).
Indirect (host-to-host transmission through living of inanimate objects).
Direct routes of transmission
Respiratory (M. tuberculosis), body contact (S. aureus), faecal-oral (S. enterica), body fluids and vertical.
Indirect transmission types
Vehicles and vectors. Vehicles include: Soil, contaminated water (V. cholerae), contaminated food, fomites (C. difficile).
Vectors include: Anopheles spp (mosquito), warm-blooded animals (rabies) and rat flea.
Adherence to surfaces depends on?
Adhesins
Types of Adhesins?
Proteins (fimbrial and Afimbrial surface proteins) and polysaccharides (part of capsules, lipo/teichoic acid)
How does E. coli adhere in UTIs?
P-pilli bind to sugar moieties (mannolose, globobiose) of glycolipids on epithelial cells lining urinary tract.
Two types of Invasion?
Extracellular and intracellular.
How is extracellular invasion achieved?
Production of enzymes that attack extracellular matrix, degrade carbohydrate-proteins complexes between cells, disrupt cell surface.
5 steps process of phagocytosis.
1: WBC encounters bacterium that binds to cell membrane.
2: Phagocyte uses cytoskeleton to push cell membrane around the bacterium creating a phagosome.
3: Phagosome seperates from cell membrane and moves into cytoplasm.
4: Lysosomes fuse with phagosome.
5: Bacterium killed and digested.
3 types of intracellular residence?
- Reside in phagolysosome.
- Reside in unfused phagosome.
- Destroy/escape phagosome and live in cytosol.
Limiting nutrient for bacteria?
Iron.
How is iron acquired?
Siderophores, these compounds (with catechol or hydroxymate group) have high affinity for iron and will compete for free or bound iron. Transport iron into cell.
How do bacteria avoid host defence?
Evade complement, resist phagocytosis, reside intracellularly, evade host antibody response.
Describe complement evasion.
Thick polysaccharide layer around cell and O-antigen (elongated O chains) prevents complement activation. LPS
Methods of resisting phagocytosis.
Prevent effective contact with phagocyte (biofilm, capsules), Affect phagocyte migration, destroy phagocytes
Describe the ‘evade host antibody response’.
Binds host proteins (S. pyogenes), surface protein which binds antibodies backwards (S. aureus) which prevents opsination (marked for elimination).
Difference between endotoxin and exotoxin?
Exotoxin is actively secreted during growth, endotoxin is part of the bacteria that is released during bacteria lysis.
Two types of transmission of exotoxins.
Ingestion of pre-formed exotonin. Colonisation followed by exotoxin production.
What do superantigens cause and lead to?
Massive non-specific inflammatory response. Leads to endothelial damage, circulatory shock and multiple-organ failure.
What does lipid A component cause?
Fever, initiates complement and clotting cascades can cause toxic shock.
Describe Quorum sensing.
Cell-cell communication. When Autoinducer (AI) concentration gets high (when there is high cell density) R protein binds to AI and activates transcription of genes for virulence factors.
