Lecture 28 Flashcards

1
Q

Evolution of New Diseases

A
  • ecological changes
  • change of host
  • genetic changes
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2
Q

Evolution of Virulence

A

-change in existing disease organism

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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)
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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
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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
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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)
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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
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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
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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
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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
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11
Q

Selection: The Host Immune System

A

-variation arises from point mutations, recombination, and change of host

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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
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13
Q

Antigenic Drift

A

-drift of antigenic groups by single amino acid substitution

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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
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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
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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