Lecture 28 Flashcards
1
Q
Evolution of New Diseases
A
- ecological changes
- change of host
- genetic changes
2
Q
Evolution of Virulence
A
-change in existing disease organism
3
Q
Evolution of Antibiotic Resistance in Previously Sensitive Disease Bacteria
A
- misuse of antibiotics
- selection for resistance
- roles of institutions in promoting resistance (livestock raising, hospitals)
4
Q
What makes viruses, bacteria, and protistan parasites evolve so quickly?
A
- molecular adaptations
- rapid replication
- huge population sizes
- gene transfer between species
- mutations
- strong selection
5
Q
Where do new diseases come from?
A
- changes in host from animal to human, with evolution of ability to transmit from human to human
- changes in microbes already involved with humans to produce a different and more virulent disease
6
Q
Human Factors in Promoting New Diseases
A
- land clearing/settlement and contact with new animals
- human-promoted spread of animal/insect disease hosts
- transportation and travel
- crowding in cities
- poverty
- multiple sexual contacts
- dangerous behavior (sharing syringes)
7
Q
Ebola
A
- primate virus
- breaks out in parts of Africa every year
- most serious human outbreak was in Zaire in 1970’s with a 90% fatality rate
- chills, fever, terrible joint, muscle, and throat pain hemorrhage by 4th day and vomit and excrete blood and bleed from gums
- death due to shock from fluid loss
- breaks down lining of veins which then leak fluid
- if fluid is administered it leaks into lungs and patient drowns
8
Q
Filovirus
A
- RNA virus-7 genes
- likely carrier is fruit bats which aren’t affected
- drop partly eaten fruit that’s eaten by animals which humans may eventually eat
9
Q
Problems With Eradication
A
- difficult to deal with because of contact between western medical concerns and cultural customs
- customs and poverty amplify problems with containment
- i.e. burial customs-want to kiss and wash loved ones before laying them to rest
10
Q
Lyme Disease
A
- painful chronic disease with arthritis and neurological symptoms
- tick borne
- mouse reservoir for spirochaete (reproduces in mice)
- tick rests on mouse then breeds on deer
- huge deer populations caused by deforestation and destruction of predators then deer pass ticks to humans
11
Q
Selection: The Host Immune System
A
-variation arises from point mutations, recombination, and change of host
12
Q
Influenza
A
- 1918 millions died; mostly young people
- two modes of evolution: antigenic drift and antigenic shift
- segmented genome can recombine with pig or bird viruses if replicated in the same cell to produce a novel genome
- highly dangerous and is the source of new flue viruses
13
Q
Antigenic Drift
A
-drift of antigenic groups by single amino acid substitution
14
Q
Antigenic Shift
A
- dramatic sudden large change, sudden appearance of a new version of the virus
- becomes completely unrecognizable to the antibodies in the population
15
Q
Spanish Flu (1918)
A
- evolved by drift and in humans by shift thus human flu H1N1 shifted to H2N2 and to H3N2 because humans live a long time so so do immune responses
- very different than other flues
- typically flu epidemics kill very young and very old people
- the 1918 flu produced a peak in the mid 20-30’s so the most healthy and vital people in the population were getting sick and dying
- then it disappears for a couple years
16
Q
Pigs
A
- life is a year in agriculture so pig flu evolves much more slowly
- remained H1N1
- eventually new flu might get passed to humans
17
Q
2009 Flu
A
- H1N1 similar to 1918
- recognized by same antibodies
18
Q
Why was 1918 flu so deadly to young people?
A
- probably ironically because young people are the healthiest
- cytokine stimulated death response genes are highly activated in infected mice
- younger patients might have mounted a stronger cytokine response to flu pneumonia than younger and older patients
19
Q
Controversial Research Project
A
-dug up flu victims and reconstructed flu virus using the fragments of virus RNA-highly virulent and mice died rapidly
20
Q
Darwinian Evolution at Work
A
- selection in evolution of antibiotic resistance by pathogenic bacteria
- components: bacteria and selection–>try to kill those bacteria by exposing them to antibiotics lethal to most bacterial cells and heritable variation among bacterial cells in resistance to antibiotic
21
Q
Antibiotic Resistance Genes
A
- lots of mutations available in large bacterial population
- antibiotic use produced great drop in US infectious diseases
- medicine ignored evolution-no thought about ability of bacteria to evolve-despite early warnings that bacterial strains resistant to antibiotics were turning up in hospitals
- all microbes evolve rapidly
22
Q
How Antibiotic Resistance Spreads
A
- misapplication of antibiotics in agriculture not to treat disease but to promote growth
- three mechanisms: inactivation of antibiotic by modification or destruction
- blocking access of antibiotic to target
- alteration of antibiotic target site
- there has been an emergence of clinically important antibiotic resistance
23
Q
Resistance Transfer Factors on Bacterial Plasmid
A
- bacterial cell with chromosomal DNA and plasmid DNA
- plasmid DNA much smaller than bacterial chromosome and is capable of transfer to other bacteria, and capable of recombination with other plasmids
24
Q
Why do antibiotics and antibiotic resistance methods exist in nature?
A
- both are part of arms race between microbes that supplies selective pressures-tough competition
- number of bacteria and fungi produce antibiotics-that’s how discovered and produced
25
Q
Resistance Mechanisms
A
- organism that makes antibiotic evolves self-protection
- target organism is under selection
- bacteria readily share genes for resistance across species
- when exposed to low doses of antibiotics they grow better
26
Q
What do bacteria do with antibiotics and resistance in their lives in nature?
A
- original idea: inhibit growth of competition
- play roles at non therapeutic levels
- modulation of interactions within bacterial communities
- intermicrobial signaling
27
Q
Where does antibiotic resistance come from?
A
- huge numbers of antibiotic resistance genes in environment
- self protection from own antibiotics suggested by universal multidrug resistance efflux pumps
- antibiotic resistance genes may have arisen as general environmental detoxifiers
28
Q
Big Evolutionary Shift
A
- use of antibodies in clinical settings at very high levels
- resistance genes switch in control from fine tuned to constitutive under strong promoters
- easier transfer to plasmids
