Chapter 13 Background to the infectious diseases Flashcards
What happens if the multiplication threshold of a disease is reached due to a delayed immune response?
disease or death
What is the best-studied example of the appearance of a highly lethal pathogen in a host population that gradually settles down to a state of more balance pathogenicity, and what are two potential causes for this?
Myxomatosis is the best-studied example of the appearance of a highly lethal pathogen in a host population that gradually settles down to a state of more balance pathogenicity. Either the virus changes and becomes less pathogenic or the host becomes more resistant to the pathogen.
In what three main ways can pathogens invade a healthy host?
- microbial attachment/penetration mechanism
- biting arthropod
- skin wound
Invasion may also occur if the host is immunosuppressed
Who founded the ‘germ theory’ of disease, and what does this theory state?
Robert Koch’s ‘germ theory’ maintained that certain diseases were caused by a single species of microbe.
What are Koch’s postulates?
- The microbe must be present in every case of the disease.
- The microbe must be isolated from the diseased host and grown in pure culture.
- The disease must be reproduced when a pure culture is introduced into a non-disease-susceptible host.
- The microbe must be recoverable from an experimentally infected host.
Describe the ‘iceberg’ concept of infectious disease.
tip: classical disease picture
midway: less severe disease
below the surface: asymptomatic infection (individual infects others, seroconverts, resists re-infection)
What obligatory steps must a successful microorganism take?
attachment +/- entry into body
- local or general spread in the body
- multiplication
- evasion of host defenses
- shedding from body (exit)
- cause damage to host (not strictly necessary but often occurs)
How do microbes fight the mechanical host defense of being rinsed away from epithelial surface by host secretions (plus ciliary activity in respiratory tract)?`
- bind firmly to epithelial surface (surface molecule on microbe attaches to ‘receptor’ molecule on host epithelial cell
- interfere with ciliary activity (produce ciliotoxic/ciliostatic molecule)
How do microbes fight the mechanical host defense of host cell membranes as a barrier to the pathogen?
- traverse host cell membrane (fusion protein in viral envelope)
- enter cell by active penetration (microbial enzymes mediate cell penetration)
How do microbes fight the phagocytic and immediate host defense of being ingested and killed by the phagocyte?
- inhibit phagocytosis (microbial outer wall or capsule impedes phagocytosis)
- inhibit phagosome-lysosome fusion (sulphatides of M. tuerculosis inhibit fusion)
- interfere with signal transduction in macrophage (induction of SOCS protein)
- resist killing and multiply in phagocyte (exit from phagosome into cytoplasm -Listeria)
How do microbes fight the phagocytic and immediate host defense of the host molecule restricting availability of free iron needed by microbe?
microbe competes with host for iron (microbe posses avidly iron-binding siderophores)
How do microbes fight the phagocytic and immediate host defense of complement activation with antimicrobial effects?
- inactivate complement components (production of an elastase)
- interfere with complement-mediated phagocytosis (C3b receptor on microbe competes with that on phagocyte and complement access blocked)
How do microbes fight the phagocytic and immediate host defense of infected host producing interferons to inhibit virus replication?
- induce poor interferon response (core antigen of hepatitis B suppresses IFNbeta production)
- insensitive to interferons (prevent activation of IFN-induced enzymes)
What is the microbial answer to the infected host producing antibody?
- destroy antiboy (bacterium liberates IgA protease)
- display Fc receptor on microbial surface (antibody bound to microbe in upside-down position)
What is the microbial answer to infected host producing antimicrobial cell-mediated immune response?
- invade T cell, and interfere with their function or kill them (virus envelope molecule binds to CD4 on helper T-cell surface)
- induce regulatory T cells (suppress beneficial immunity)