Arms Race Flashcards
organism x environement
-> evolutionary change
components of an organism’s environment
- abiotic
- biotic
abiotic components of an organism’s environment
- temperature, humidity, water salinity, substrate colour, etc
biotic components of an organism’s environment (5)
- predators
- food/prey
- competitors (same or other species)
- partners (same or other species)
- pathogens and parasites
what can biotic interactions lead to?
- antagonistic coevolution/”arms races”
possible facets of a prey and predator relationship
better/faster:
- hiding
- mimicry, camo
- running
- size, strength
- group hunting/defense
running adaptations (3)
- running on toe tips
- longer foot bones
- tibia and fibula fusion
snail defence adaptation as prey
- proportion of snail subfamilies with thickened shells and narrowed apertures has increase through time
what are the characteristics of pathogens and parasites? (4)
- short life spans
- huge population sizes
- high mutation rates
- these traits allow pathogens to evolve as much in a day as we can in 1000 years
how can humans combat the evolutionary mismatch with pathogens?
- adaptive immunity
adaptive immune response (3)
- immune cells recognize epitopes on the surface of pathogens to mount a highly specific response against that pathogen
- jawed vertebrates only
- presence of lymphocytes (WBC): B cells (antibodies) and T cells ( helper and killer cells)
how does adaptive immunity combat rapid evolution of pathogens? (3)
- involves evolution by natural selection within the individual
- clonal selection yields cell lines that recognize and attack specific pathogens
- a memory is retained to guard against future infections by the same pathogen strains
how is variability generated in adaptive immune response?
- gene rearrangement and somatic hypermutation produces a large primary repertoire of antibody-producing B cells
innate immunity (4)
- all animals
- skin/exoskeleton
- phagocytosis by blood cells
- antimicrobial peptides
T cells
- cell-mediated response against intracellular pathogens
B cells (2)
- antibody-mediated (humoral) response against extracellular pathogens and paracites
- antigen + helper T cell simulation produces memory B cells and plasma cells (anitbodies)
adaptive immunity (3)
- somatic (within individual) evolution by natural selection
- individual protection against future infections by same strain of pathogen
- specific response not inherited by offspring
antigenic variation (2)
- continual switching of surface antigens through variable surface glycoproteins
- how the african sleeping virus escapes immune system and kills the host
how does influenza escape host defences (2)
- antigenic drift: mutation + selection (several strains can infect same species)
- antigenic shift: recombination (ability for virus to jump species)
how does the SARS-CoV2 escape host defences? (3)
- successful mutations increase transmissibility, evade immunity, or both
- rapid expansion of delta variant in India
- reduced sensitivity to neutralizing antibodies from sera following infection or vaccination
history of pandemics (6)
- spanish flu, bubonic plague, HIV, malaria, COVID-19
problem of antibiotic resistance (4)
- rapid bacterial evolution
- horizontal transfer of resistance factors
- cost of resistance can be compensated
- expression controlled by regulatory genes (adaptive resistance)
horizontal transfer of resistance factors (3)
- conjugation: bacteria to bacteria
- transduction: virus vector
- transformation: from environment
compensatory mutation
- create “fitness valleys” that prevent pathogen from reverting to sensitive type in absence of the antibiotic
fitness valleys and antibiotic resistance (4)
Relative fitness in the absence of the antibiotic
- wild type (sensitive) and uncompensated
- resistant and compensated
- resistant and uncompensated
- sensitive and compensated
disease emergence and examples (4)
- transfer of novel pathogens from animals to humans
- influenza from birds and pigs
- COVID-19 from bats
- HIV fro other primates
stages of pathogen emergence (5)
- agent in animal only (no human transmission)
- primary infection (only transmitted from animals)
- limited outbreak (from animals or few humans)
- long outbreak (from animals or many humans)
- exclusive human agent (only from humans)
R0
- mean # of secondary infections arising from one infected individual in a totally susceptible population (no interventions and all transmission routes considered)
R0 < 1
- emergence does not occur, likely a newly introduced strain
R0 > 1
- emergence occurs, most likely an evolved strain
what is characteristic of diseases with higher R0 (2)
- harder to control
- needs higher percentage of vaccination for herd immunity
virulence (3)
- reduction in lifetime reproductive success of host due to harm done by pathogen
- % mortality due to pathogen
- it is the outcome of host/pathogen coevolution
what determines equilibrium levels of virulence in pathogens? (2)
- mode of transmission
- opportunity for transmission
vertical vs horizontal mode of transmission (2)
- higher virulence in horizontal transmission because survival of host is less important
- lower virulence in vertical transmission because host must survive to spread pathogen
R0 formula
R0 = (betas)/(gammamuv)
what is beta in the R0 formula
- transmission rate: rate of contact between susceptible and infectious individuals x probability of transmission
what is S in the R0 formula
- density of susceptibles
what is gamma in the R0 formula
- rate at which an infected host clears the disease
what is mu in the R0 formula
- background mortality rate of host
what is v in the R0 formula
- mortality rate due to infection (virulence)
how does parasite increase fitness and transmission?
- increase transmission (increases beta)
- prolong the infection (decreases gamma or v)
mode of transmission (2)
- vertical vs horizontal
- direct vs vector driven
opportunity for transmission (2)
- host/vector: behaviour
- population structure and density
