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Infectious Disease > Prelim 2 > Flashcards

Prelim 2 Flashcards

1
Q

Fungal diseases in humans

A
  • Only about 300 fungal species are known to make people sick
  • Fungal diseases are often caused by fungi common in the environment
  • Most fungi are not dangerous, but some are serious
  • Cause 1.5 million mortalities per year
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2
Q

Categories of human fungal diseases

A
  • Common but generally not serious
  • Endemic (affect people in certain areas, but not widespread)
  • Affecting people with weakened immune system
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3
Q

Common fungal diseases

A
  • Fungal nail infections
  • Ringworm
  • Candida infections of the mouth, throat, or esophagus; vaginal Candida infections (yeast infections)
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4
Q

Endemic Fungal diseases

A
  • Caused by fungal species that occur in specific regions
  • Can cause serious disease, particularly in people with weakened immune systems
  • Can be a concern if taking immunosuppressants
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5
Q

Blastomycosis

A
  • Blastomyces dermatitidis
  • Common in moist, decomposing, organic matter
  • Infection occurs after inhaling spores, only in some people
  • Lung infection with flu-like symptoms can be serious if not treated
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6
Q

Valley Fever (Coccidioidomycosis)

A
  • Coccidiotis immitis
  • Flu-like systems
  • Common in the southwestern United States, recently found in washington
  • People who get sick, will get better on their own within weeks to months, some people will need antifungal medication
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7
Q

Opportunistic fungal diseases

A
  • Aspergillus
  • Common molds, we are always exposed to these spores
  • In immunocompromised individuals - flu like and upper respiratory symptoms
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8
Q

Why are fungal pathogens problematic?

A
  • They are eukaryotes, drugs used against them must not target our cells
  • Fungi produces spores, which are environmentally persistent and hard to get rid of
  • In a susceptible host, fungal pathogens are often highly virulentA
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9
Q

Antifungal drugs

A

Fungal molecular targets that can be exploited for drug development without the risk of cross-target toxicity are limited
- chitin ( cell wall)
- ergosterol biosynthesis and function (cell membrane component)

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10
Q

Why are fungi good at dispersing?

A
  • Fungal spores last a long time in the environment and are easily dispersed by wind or water

Therefore, fungal pathogens can evolve very high virulence in hosts

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11
Q

Virulence evolution theory

A
  • Transmission of a pathogen can be limited by high virulence
  • This is sometimes called the “virulence-trasmission trade off”

More virulent –> less transmissible

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12
Q

Virulence evolution theory in relation to fungi

A
  • Fungi are often good at transmitting bc they grow fast, make durable spores, and live in multiple host
  • Since their transmission is so great they don’t need to afford to lose anything for the tradeoff. They can be both highly transmissible and virulent which is dangerous
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13
Q

Emerging Candida auris Infections

A
  • Yeast, common in human microbiomes
  • Causes infection in immunocompromised individuals
  • 1/3 people who develop bloodstream infections will die
  • Recently multidrug resistant strains have been spreading
  • Particularly in hospitals and care facilities
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14
Q

The Baltimore System

A
  • Viruses are categorized in 7 different classes
    1: ds DNA
    2: ss DNA
    3: ds RNA
    4: ss RNA (+)
    5. ss RNA (-)
    6. RNA (RT)
    7. ds DNA in cytoplasm (RT)
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15
Q

DNA vs RNA

A
  • RNA viruses may use a DNA intermediate which can insert into the host chromosome, this has consequences for both the host and virus
  • RNA is more error prone, RNA polymerases often lack proofreading
  • High mutation rates can increase viral genetic diversity
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16
Q

Some types of virus

A
  • Icosahedral
  • Filamentous
  • Head-tail
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17
Q

Does HIV have a DNA intermediate?

A

Yes

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18
Q

Lytic phage (is specific for viruses that attack bacteria) cycle

A

This is how a phage injects its genetic mateiral into a host cell
1. Attachment. The phage attaches to the surface of the host
2. Penetration. The viral DNA enters the host cell
3. Biosynthesis. Phage DNA replicate and phage proteins are made
4. Maturation. New phage particles are assembled
5. Lysis. The cell lyses releasing the newly made phages

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19
Q

How do viruses attack animal cells?

A
  • Some viruses fuse with the host cell membrane. New viruses bud of the host with parts of the cell membrane
    1. Fusion of HIV to host cell surface (vesicles)
    2. HIV RNA, reverse transcriptase, integrase, and other viral proteins enter the cell
    3. Viral DNA is formed by reverse transcription (intermediate)
    4. Viral DNA is transported across the nucleus and integrates into the host DNA
    5. New viral RNA is used as genomic RNA and to make viral proteins
    6. New viral RNA and proteins move to the cell surface, and a new, immature HIV forms
    7. Virus is released, viral protease cleaves new polyproteins to create mature infectious virus
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20
Q

How do viruses fuse to the animal cell?

A
  • Viruses may trick the host cell into engulfing them (endocytosis)
  • They may localize viral proteins into the cell membrane to form the viral envelope
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21
Q

What are the parts of the flu that help it?

A
  • Flu is mainly caused by Influenza A
  • Uses the HA to bind to host cells
  • NA (neuraminidase
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22
Q

Who is the natural reservoir of influenza viruses

A

Birds, especially water birds, are considered natural reservoirs of influenza viruses

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23
Q

How does HA bind to host cells exactly

A

Host cells have sialic acid terminal ends that bind HA. These transmembrane glycoprotein are especially common in the respiratory tract.

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24
Q

What are the types of sialic acid?

A

a-2,3
a-2,6
birds and pigs have a lot of a-2,3
pigs and humans have a lot of a-2,6

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25
Q

Antigenic shift

A
  • Reassortment of genetic segments
  • Requires coinfection of genetically different viruses in a coinfected host

ex. avian influenza and human influenza could be in pigs, who can be infected by both. allowing for anitgenic shift and a creation of a new virus

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26
Q

Who had the worst response to the spanish flu?

A

Young, healthy adults aged 20-20 were more lilely to have severe cases. THey may have been exposed to H3 strains, not H1 strains
- Mya have mounted a strong immune response leading to tissue damage, cytokine storm

H1N1 subsequently mutated to be less virulent and replaced the seasonal flu strains

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27
Q

Antigenic drift can occur

A

at a high rate of replication and high population size of virus. requires the need for a new vaccine every year

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28
Q

How can you determine if new strains are circulating

A

Phylogenetic trees (researchers do extensive research do determine what the dominant flu strain could be that season to make a vaccine against that)

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29
Q

What are influenza phylogenies based on?

A

HA or NA sequences to demonstrate antigenic drift

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30
Q

How do you determine if the genetic changes due to antigenic drift matter?

A

Use hemagglutination inhibition (HI) assays to test if antibodies recognize new HA
- without virus, red blood cells sink to the bottom of the well
- with virus, cells form diffuse lattice
- without antibodies, agglutination of virus to RBC
- antibodies bind viruses, preventing agglutination

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31
Q

A strain might be a good candidate for the vaccine if

A
  • It shows antigenic drift and has diverged from other lineages
  • It is spreading quickly in the lead up to the flu season
  • It’s HI assay results show that antibodies to currently circulating strain don’t bind the virus
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32
Q

What are the two different types of flu vaccine?

A
  • Trivalent vaccine
    2 Influenza A strains, H1N1 and H3N2
    and 1 Influenza B strain
  • Quadrivalent vaccine
    2 straisn of each (best for older ppl)
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33
Q

Vaccine Production

A
  • Take the circulating strain, the strain you think it gonna be the dominant one, and a master high-growth strain that isn’t pathogenic but can infect eggs
  • Put the two of them in an egg
  • Let the recombination of genes occur
  • Amplify by having this done in a lot of eggs
  • Take the amniotic fluid and in there will be your inactive influenza vaccine
34
Q

Newly Emerged

A

Recorded in human history for the first tume
ex. HIV, SARS, Swine flu (any pandemic flu rlly)

35
Q

Reemerging

A

Previously found in humans, newly virulent, in new locations, or reappearing after elimination
ex. dengue and west nile virus (both spread to new locations because of human movement)
MRSA: pathogen evolution makes treatment infective

36
Q

What factors may lead to disease emergence?

A
  • Antibiotic resistance
  • Climate change and changes in biodiversity
  • Human encroachment on wildlife - increased contact
  • Poor biosecurity with livestock
  • Poverty and poor sanitation
  • Lacking of monitoring and public preparedness
  • Globalization and movement of diseases/vectors
37
Q

Why was the columbian exchange uneven?

A
  • Differences in the types of diseases that were prevalent in European versus American populations
  • Europe had a higher prevalence of “crowd epidemic” diseases
  • Higher prevalence of zoonotic disease from agricultural animals
38
Q

Crowd epidemic diseases

A
  • Acute diseases that effectively transmit between individuals and lead to long lasting immunity
  • Such pathogens require large or highly interconnected populations because they will quickly “burn through” susceptible individuals (meaning they can only survive in Europe and the Americas were not populated enough which isn’t true btw)
  • This covers many of the pathogens introduced to the Americas by the Europeans: smallpox, influenza, measles, diphtheria, pertussis
39
Q

Population Structure

A

You’d rather have a continuous population rather than a patchy or non-equilibrium if you’re a virus and you would like to spread because you prefer more populated areas.

40
Q

Smallpox

A
  • Caused by variola virus
  • Causes fever and distinctive rash/sores
  • In recent times, documented with a 30% mortality rate
  • Relatively high transmission rate, but requires direct contact with an infected individual or fomite (blanket)
41
Q

Smallpox Vaccines

A
  • Edward Jenner is credited with developing the first vaccine in 1796
  • Protective exposure to pox viruses to immunize children was used in Asia and Africa before Jenner
  • This process was called variolation
    • Inoculating susceptible individuals with pus from people with small pox
  • Was somewhat protective, death reate was 10 instead of 50.
42
Q

Variolation in the American Revolution

A
  • George Washington “variolated” American revolutionary war soldiers at Valley Forge because ppl in the americas weren’t as prepared for small pox as the british soldiers, putting them at a disadvantage
43
Q

How did Jenner Vaccinate ppl? (not the same way Africans and Asians did)

A
  • He discovered that milkmaids who had cowpox dont get small pox
  • he used cowpox to successfully vaccinate people
  • Named vaccines for the latin for “cow”
44
Q

Is smallpox eradicated?

A

Smallpox is the only human pathogen to be successfully eradicated globally

45
Q

Why was eradication successful?

A
  • It involved a worldwide effort for vaccination and used a strategy called “ring vaccination”. Containment vaccination of contacts and communities of infected individuals
  • Long latent period (initial infection and actual signs of sickness), but individuals are only contagious when rash/sores appear
  • The live virus vaccine is effective even if you have already been exposed
  • No asymptomatic carriers or reservoirs
46
Q

1616-1619 Wampanoag Epidemic

A
  • Relatively brief and acute, killed an estimated 30-90% of the population, including the entire village of Patuxet near Plymouth Harbor
  • This severity suggests a new outbreak with no existing immunity
  • Timing coincides with interaction with Europeans from the north coast
47
Q

Symptoms of 1616-1619 Wampanoag epidemic

A

Symptoms included jaundice and fever, yellowing being the most distinctive and consistent trait mentioned in accounts

48
Q

Leptosprirosis

A

Comes from rats and was given to humans

49
Q

Zoonotic diseases

A
  • Animals are a common source of spillover events, and are common reservoirs of disease
  • Domestic or peridomestic animals increase these risks because of their closeness to humans
  • European, African and Asian populations tended to have more numbers and species of domestic animals
50
Q

Introduction of animals to the Americas

A
  • Animals were introduced both purposefully (livestock like pigs) and coincidentally (black rats, brown rats)
  • They brought diseases with them, and both the animals and their associated microbes could then become endemic
51
Q

Hernando de Soto

A
  • De Soto’s group brough 200 pigs wth them, these established th efirst feral pig population in the southeast US
  • In the next 100 years, the thriving indigenous population dropped by an estimated 90%
52
Q

Apicomplexan parasites

A

Use apical complex for infecting host cells. Apicomplexans infect humans and other animals

53
Q

Examples of Apicomplexan parasites

A
  • Cryptosporidiosis - infects humans and other mammals
  • Toxoplasmosis - Toxoplasma gondii infects cats and humans
  • Gregarines - infect arthropods
  • Malaria - plasmodium
54
Q

Malaria association with primates is ancient

A
  • Plasmodium infecting humans probably evolved from species infecting other apes
55
Q

Where is the malaria burden the highest?

A

In Africa

56
Q

Anopheles mosquitoes

A

Lots of diversity, primary carriers of malaria

57
Q

Malaria infections can be severe or deadly

A

Asymptomatic infection –> fever –> severe malaria (RBCs affected in the brain) –> death

58
Q

Immunity to malaria…

A

develops over time

59
Q

Most common plasmodium species

A

Plasmodium falciparum

60
Q

Plasmodium life cycle

A
  • Plasmodium reproduces in a mosquito
  • Mosquito bites a host, sporozoites are released into the host
  • Sporozoites go into liver where they becom eMerozoites and infect RBCsWh
61
Q

What does Plasmodium secrete?

A

PfEMP1 is secreted by P.falciparum to th esurface of the RBC

62
Q

Rossetting

A

When infected rbcs bind to uninfected ones to hide themselves

63
Q

Cost and benefits of Pfemp1

A
  • Plasmodium uses this protein to cause RBCs to stick together and hide within the body, preventing them from being cleared
    but
  • The protein also exposes an infected cell to the immune system
64
Q
  • What are things plasmodium does to escape the immune system?
A
  • Hides in tissues with less immune function
  • Avoiding clearance as blood cells are passed through the spleen
  • Rosetting hides the infected RBCs behind healthy ones
  • Variation in var genes expression avoids an immune response
65
Q

Variation of PfEMP1

A
  • Variation coded by 60 different var genes
  • Ternminal position of DB1a
  • Other anitgenically active regions determine affinities to different receptors
66
Q

Antigenic variation in P.falciparum

A
  • Different lineages of Plasmodium can have different var genes, this genetic diversity can make it hard for a host to develop immunity (becasue even if you’ve had it before, the body recognizes it as a complete new thing)
  • P. falciparum can also swtich var gene expression within a host, which makes it hard for the host to track the parasite within the body. Antigenic variation.
67
Q

Antigenic variation

A

Active - parasites express one var gene (monoallelic expression) variant of PfEMP1 when initially growing within the RBC
- Silent but Poised, when growth is nearly done, the parasites stop expression of teh var gene epigentically, but expression can start again on the next cycle
- Switch - a portion of the parasite population switches to a new var gene

68
Q

Why is malaria difficult to control

A
  • Biology of the pathogen (use of var genes and evading the immune system)
  • Biology of the vector (mosquitos are super common and good at spreading)
  • Most common in areas with high poverty
  • Cultural feelings about malaria
69
Q

Malaria control options

A
  • Antimalarial drugs: drug resistance is common, may not be accessible where malaria is prevalent
  • Control of vector: kill mosquitos, destroy mosquitos habitat
  • Prevent transmission: sleep under mosquito netting, use netting treated with insecticides
70
Q

Future for Malaria vaccine

A

Using CRSPr or a bacteria symbiont that limits the mosquitos ability to transmit viruses.

71
Q

RTS targets CSP the dominant protein on sporozoites

A
72
Q

Sars is single stranded RNA

A
73
Q

Alpha beta coronaviruses in bats and sometimes rodents

A

Gamma delta coronaviruses found in birds

74
Q

Host shifts

A

Coronavirus shift species for host quite often

75
Q

SARS CoV-2 has a low mutation rate

A

RNA polymerase for SARs COv2 is very good at catching errors so there is a low mutation rate there. This means vaccines could last longer BUT it could mean a slower loss of virulence

76
Q

What does SARS-CoV 2 bind to on host cells

A

ACE2 receptors

77
Q

ACE2

A

Angiotensin converting enzyme 2
An enzyme that causes vasoconstriction to regulate blood
pressure, a drug target for cardiovascular diseas

78
Q

Over Response to SARS-CoV-2

A

cytokine storm
bradykine storm (regulate blood pressure and inflammation)

bradykinin storms could explain the diversity in symptoms

79
Q

SARS-CoV-2 unique spike protein

A

This spike protein cleaves from the host cell very efficiently

80
Q
A

Infectious Disease (3 decks)

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