Evolution Flashcards

1
Q

Methods of control of malaria

A

Vector Control: killing vector (mosquito control)
Drug: killing parasite
Decreasing contact between humans and vector

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

drug treatmetns in humans leads to

A

drug resistance in parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

why is there drug resistance in parasites

A
  1. Genetic variation in parasite sensitivity to drugs
  2. Under drug pressure less sensitiv/more resistance strains survive better and remove competitiors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

insecticide resistance

A

treatment with organophoshate between 1968-1990 because of resistance allele

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

why are antibiotics a major force of selection for bacteria

A
  • susceptible genotypes killed by antibiotics
  • resistant genotypes survive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Plasmids and Horizontal Gene Transfer

A

resistance genes can be transferred among bacterial cells via extra-chromosomal loops of DNA called plasmids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Life Cycle of HIV

A
  1. HIV is a dsRNA retrovirus
  2. infects hosts CD$ helper T cells
  3. Viral enzyme (reverse transcriptase) turns RNA into DNA
  4. Embeds genome into host DNA
  5. Viral Genes transcribed and translated by host machinary
  6. New virus buds out of host cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

AZT resistance in HIV

A
  • AZT drug binds to and inactivates HIV enzyme
  • new mutant enzyme arose with binding site that was resistant to AZT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

why does HIC evolve so fast

A
  • massive population size
  • short generation time
  • high mutation rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

solutions for drug resistance

A
  1. Higher dose
  2. earlier treatment
  3. combinations of drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

virulence

A
  • disease severity as assessed by reductions in host fitness due to infection
  • interpeted as the additional mortaility rate that a pathogen imposes on an infected individual
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Conventional Wisdom

not true

A

pathogens that harm their hosts therby harm themselves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

conventional wisom predictions

A
  • over time, the coevolution of pathogens and their host will lead to a mutualistic association
  • evolution would eventully lead to avirulance
  • instances of highly virulent pathogens are cases where host-pathogen relationship is recent**

** applies to ebola and bird flu

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

challenges to conventional wisdom

A

tuberculosis (has been around sincee 3000 BCE)
Myxoma: (rabbit disease) over time, it adapted to an intermediate vrulence which cannot be explained

  • biggest challenge
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

tradeoff hypothesis

A
  • level of virulence is consequence of pathogen replication in host => cost of replication
  • Benefit: pathogen replication is required for transmission between hosts
  • Replication rate of pathogen and virulence evolves to maximize overall tranmission and spread
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Model of virulence evolution
(equation)

A

R0=T(r) x D(r)
T(r)= # of new infections/ day (transmission rate)
D(r)= # days infection lasts (duration)
increased r (replication rate) increases transmission rate but decreases duration

pathogen cannot increase infection without decreasing duration

17
Q

optimizing virulence
most virulent=x, least virulent= y

A

most virulence= high transmission but kill host quickly
least virulent= long infections but transmit poorly
**Prediction: ** strains of intermediate virulence will increase in frequency

this prediction was upheld in myxoma

18
Q

Modes of Disease transmission

A

direct host to host transmission
Vector transmission

19
Q

direct host to host transmission

A

hosts must be mobile and functioning relatively well in order to transmit disease
prediciton low replication rate and low virulence

20
Q

vector transmission

A

host do not need to be mobile to transmit
prediction high replication and high virulence

21
Q

virulence evolution

A
  • virulance is unvaoidable consequence of parasite transmission
  • parasites need to exploit hosts to transit to new hosts
  • increase in transmission due to replication = cost of increase in virulence

transmission is the benefit, virulence is cost

22
Q

benefit-cost of parasites is maximized

A

at intermediate levels
at intermediate replication rate, marginal beneft = marginal cost

for single parasite

23
Q

at low replication rates
at high replication rates
marginal benefit vs cost

A

marginal benefit > marginal cost (selection for increasing replication
marginal benefit < marginal cost (selection for decreasing replication)

for single parasite

24
Q

Multiple infections

A

favour evolution of more virulent parasites

25
Q

tragedy of the commons

A

strains compete for same resource
more virulent strain has higher relative transmission