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Parasite/pathogen
Mutations and reproductive rates
Question | Answer |
---|---|
What are the pathogen groups? | - viruses ie. influenza - bacteria ie. TB - fungi ie. candida - protozoa ie. malaria - worms ie. hookworm - prions ie. kuru |
How virulent should a pathogen be? | - successful pathogens manipulate their hosts - is transmissible - needs host to survive for transmission - ideally wants host to respond to infection for transmission |
Case study: bubonic plague (Yersinia pestis) | obligate intracellular pathogen, non-motile, zoonotic, very dangerous to humans. ~100 million fatalities since 6th Cent., 90% fatality rate - infected fleas on rats bite humans - contact with infected animals - may progress to pneumonic plague |
How did the pathogen evolve? | - mutation led pathogen to better invade host tissue, so numbers boomed, going from primarily respiratory to more virulent and dangerous |
How does strain Y.pestis employ virulence factors? | - adhesions allow pathogens to be better established in host cells - structures to perforate the membrane so Yop effector proteins can be transferred to host cell to trigger apoptosis |
Case study: influenza viruses | - 4 subtypes: A,B,C,D - obligate intracellular pathogen = localised effect, zoonotic, big impact on humans not necessarily due to deaths |
Influenza A viruses | - membrane proteins H1-18 & N1-11 High mutation rates Influenza A viruses can undergo antigenic shift & antigenic drift RNA genome which lacks any proofreading mechanisms thus mutations can accumulate rapidly |
What is antigenic shift? | - rapid, big change in a subtype. Can result from a spillover event and lead to a new virus subtype. Virus combination |
What is antigenic drift? | - gradual changes in membrane proteins resulting from mutations during virus replication |
Influenza A: zoonotic origins | - All Influenza A viruses have animal reservoirs and are thus zoonotic |
What about disease X? | - the hypothetical disease coming to kill us all |
How can we put prevention methods into place? | - bridging institutional gaps, defining priority risk areas and pathogens, and emphasizing supposed risk factors for subsequent events involving emerging and re-emerging infectious disease pathogen |