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PATH300 > infectious diseases > Flashcards

infectious diseases Flashcards

1
Q

what environmental changes increase the prevalence of infectious diseases?

A

climate change (warmer climate = disease are more prone to spread) and movement of warmer currents of water

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2
Q

what infectious disease is a big killer in Haiti?

A

cholera

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3
Q

what causes the difference in death rates of COVID-19 between countries?

A

immunization/vaccination rates

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4
Q

what is long covid?

A

long lasting illness that affects any organ system in the body.

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5
Q

balance between what and what controls the risk of infectious disease?

A

balance between host’s health (depends on lifestyle, environment, genetic background) and the pathogen’s characteristics

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6
Q

name a few things that helped to decrease gravity of infectious diseases

A

sanitation, clean water, quarantine, improved public health and nutrition, immunization

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7
Q

3 types of mutualism relationships

A
  • pathogenic: decreases the host’s fitness
  • commensal: doesn’t affect the host’s fitness
  • symbiotic: increases both parties fitness
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8
Q

how many cells vs bacterias do human have?

A

10 trillion cells for 100 trillion bacteria

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9
Q

the variable microbiome varies according to what?

A

host lifestyle, genotype, pathobiology, environment, community members, immune system, physiology

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10
Q

what other than microbes live on/in the human body?

A

viruses (virome) and gungi (mycobiome)

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11
Q

what are the sources of infection?

A

other humans, insect vectors, other species like rats, food, water

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12
Q

what are the methods of transmission for infectious diseases

A

droplets through the air, skin contact, across placenta, sexual transmission, blood-borne, insect, food, water

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13
Q

how do viruses enter and spread?

A

enter via GI, respiratory, skin, or genitourinary epithelia. reach the circulation through bloodlymphatics, inflammatory cells or nerves. spread via circulation

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14
Q

what receptor is targeted by COVID-19?

A

ACE-2 receptors

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15
Q

3 factors for a pathogen to cause an illness

A
  1. survive and multiply in a host
  2. resist host defenses
  3. cause injury
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16
Q

name the pathogen defense techniques

A
  • modulation of surface structure to avoid recognition
  • inhibition of phagocytosis
  • inhibition of antigen presentation
  • modulation of signal transduction, gene expression, cell death
  • inhibition of complement activation
  • survival in macrophages/endosomes (latency)
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17
Q

what mutations allow pathogens to hide from immune surveillance?

A

antigenic variations

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18
Q

name the 3 mechanisms of tissue damage by pathogen and give an example for each

A
  • exotoxin release: cholera
  • endotoxin release: plague
  • direct cytopathic effect: influenza
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19
Q

describe the 3 ways of cell injury by bacteria via host response

A
  • immune complexes: cause injury to body structure
  • anti-host antibody: pathogen triggers antibodies that damage the cell
  • cell-mediated immunity: destruction of the entire cell to prevent spread of the microbe
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20
Q

why are newborns so vulnerable?

A

because their immune system isn’t well developed yet and no longer receives maternal IgG (transient low level of IgG)

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21
Q

name the external host defenses

A

skin barrier, fatty acids, cilia, mucus, mucociliary blanket, acid in stomach, microbiome in intestine

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22
Q

what respiratory defenses are present in nasal cavity?

A

antibody, B cell, T cell, cytokine, complement, macrophages (10 million of them)

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23
Q

what are the first immune responses following pathogen attachment?

A

innate immunity: activation of complement and NK cells

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24
Q

which MHC class antigen presentation involves a phagolysosome?

A

MHC class II

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25
Q

4 ways how antibodies can inactivate antigens

A

leading to phagocytosis:
- neutralization: blocks viral binding sites
- agglutination: of antigen-bearing particles
- precipitation of soluble antigens
leading to cell lysis:
- complement fixation (activation)

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26
Q

what cell generates cytotoxic T lymphocytes

A

Th1

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27
Q

where can pathogens “hide” to resist defense?

A

in endosomes

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28
Q

what molecules change due to antigenic variation?

A

capsular polysaccharides at the microbe’s surface

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29
Q

what is bacteremia?

A

moderate amounts of microbes in the blood. takes longer to recover

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30
Q

4 reasons why there are more and more issues with infectious diseases?

A
  • overpopulation, poverty
  • traveling
  • overuse of antibiotics and resistance
    ignorance and misinformation (anti-vaxx)
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31
Q

what does ebola trigger?

A

release of a toxic cytokine storm that is toxic to the epithelial cell, leading to bleeding, shock, instability of epithelial cells

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32
Q

why are vaccines impractical for viruses?

A

because of rapid antigenic mutation

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33
Q

what cell adhesion molecules are recognized by rhinovirus?

A

ICAM1

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34
Q

how do viruses damage cells?

A

damage plasma membrane, cause cell lysis or fusion, deranges metabolism, neoplastic transformation

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35
Q

what is symptom of polio? is it still present?

A

crippling of the legs. still present in Afghanistan and Pakistan

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36
Q

is measle still around?

A

yes because of unvaccinated people

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37
Q

is measle still around?

A

yes because of unvaccinated people

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38
Q

name potential sites for antiviral drug action

A

cell entry, viral uncoating, nucleic acid synthesis, assembly and release of viral particles, cell exit

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39
Q

what are features of influenza?

A

virus that hijacks tracheobronchial epithelial cells when breathed in.
spread very rapidly.

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40
Q

what are the main complications of influenza? how does it happen?

A

pneumonia:
- viral = when virus reaches lower respiratory tract
- bacterial = damage caused by the virus allows bacteria to accumulate.

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41
Q

how many people die from influenza every year?

A

30-50 thousand

42
Q

how does influenza affect pregnant women?

A

it can increase risk of premature births and cause problems for the fetus and mother

43
Q

how can influenza affect immunocompromised people?

A

it can cause musculoskeletal, neurological, cardiac complications

44
Q

why is influenza more present during winter?

A

virus replicates more readily in the cold because the secretion of extracellular vesicles by nasal epithelial cells is impaired in the cold

45
Q

how do you cure influenza?

A

immune system usually clears the virus within 7-10 days

46
Q

what type of influenza virus does the influenza vaccine protect you from?

A

H3N2 viruses

47
Q

How do epithelial cells in those nose participate in defense against virus?

A

innate immunity: release extracellular vesicles with receptors capable of recognizing and capturing the virus

48
Q

on what type of receptor is influenza virus presented to T cells by DCs?

A

MHC class I

49
Q

what do CD4+ and CD8+ T cells respectively do against influenza?

A

adaptive immunity: CD4+ secretes cytokines that amplify the humoral response of B cells.
CD8+ t cells trigger cell death in the infected epithelial cells.

50
Q

when was the worst influenza pandemic?

A

1918 (50 to 100 million death)

51
Q

what viral disease has killed the most people?

A

influenza

52
Q

when were viruses discovered?

A

1930s

53
Q

how many people get infected with influenza every year?

A

1 billion

54
Q

features of RNA viruses (ex influenza)

A
  • continually mutating and has many types
  • can cross species barriers and trade genetic material
55
Q

what are structures on influenza virus and what do they do?

A

HA and NA: recognized as antigens by antibodies
- HA: determines the ability of the virus to enter a host cell depending on its affinity to polybasic cleavage sites on host cell receptor.
- NA: promotes efficient release of viral progeny from infected cells.
M2 ion channels

56
Q

Why don’t all the H and N types of influenza infect humans?

A

Not all of them are able to recognize and bind the receptors on the airway epithelial cells

57
Q

describe the 3 subtypes of influenza?

A
  • A: big killer, changes genetic makeup by antigenic drift AND shift
  • B: only mutates by genetic drift. not as dangerous as A.
  • C: 7 individual segments, doesn’t change properties, mild infection
58
Q

explain antigenic drift vs shift

A

drift = viruses accumulate small mutations and mutate over years
shift = different species of viruses exchange antigens to create a completely new virus. produces an unrecognizable virus with new HA

59
Q

is antigenic drift or shift responsible for pandemics?

A

antigenic shift

60
Q

what animal is often an intermediate for infection propagation and antigenic shift?

A

pigs

61
Q

differences between H1N1 and H5N1?

A

H1N1 = due to avian-human shift, spreads rapidly but rarely fatal, localized in the throat.
H5N1 = due to bird migration, does not spread rapidly but is often fatal, localized in the lower airways.

62
Q

stages of viral replication

A
  1. absorption of virus
  2. endocytosis of virus
  3. fusion of endosome with viral vesicle -> RNA release
  4. replication and transcription (and translation): RNA reaches nucleus
  5. assembly: newly synthesized protein and RNA form a new virus
  6. budding and release: virus buds out in ECM to infect other cells
63
Q

what drugs can interfere with virus replication and how?

A
  • amantadine: can block the fusion
  • oseltamivir and zanamivir: blocks the budding and release (NA inhibitors i think)
64
Q

more specifically how does HA (hemagglutinin) attaches to host cells?

A

by binding at the linkage between galactose and sialic acid on the tip of host cell surface receptors.

65
Q

what gives different influenza virus species their selectivity?

A

selective binding of HA depending on different linkage configurations

66
Q

what does the NA neuraminidase on virus allow for?

A

allows for viral mobility in and out of the cell by:
- removing binding between the virus and the cell so it can infect other cells &
- helping the virus to make it to the nucleus docking site in the cell.

67
Q

how can influenza become deadly?

A
  1. if there is inadequate defense
  2. severe pneumonia
  3. cytokine storm can cause lung damage
68
Q

antibodies against what part of the virus can be made?

A

against NA, HA, or M2 proteins

69
Q

how can children get Reye syndrome?

A

from taking aspirin while being infected by a viral disease

70
Q

what does it mean that influenza vaccines are trivalent or quadrivalent?

A

trivalent (protects against 2 strains of influenza A and 1 of influenza B) or
quadrivalent (2 influenza A and 2 influenza B)

71
Q

what disease might influenza be implicated in?

A

Parkinson’s.
influenza and COVID might have long term impact on neurological functions

72
Q

what do drugs that lessen the symptoms of virus target?

A
  • NA inhibitors: keep virus from leaving the infected cell
  • endonuclease inhibitors: blocks the reproduction of virus
73
Q

what are the herpes virus subfamilies?

A

alpha: HHV1, 2, 3
beta: HHV 5, 6, 7
gamma: HHV 4, 8

74
Q

name common properties amongst the 8 herpes viruses

A
  • cause cell lysis
  • latency and reactivation
  • world-wide distribution
  • difficult to control
  • triggers cell-mediated immunity
75
Q

what are herpes viruses heavily associated with?

A

cancer and tumors

76
Q

name the herpes viruses in each of the 2 categories

A
  • neurotropic: herpes simplex type 1 and type, varicella-zoster virus type 3
  • leukocyte: epstein-barr virus EBV type 4, cytomegalovirus CMV type 5, human herpes virus 6, 7 and 8
77
Q

what is HHV1? where is it located?

A

herpes simplex/cold sores: lives in neurons, gets carried via trigeminal ganglion

78
Q

what 2 molecules help transport HHV1 through nerves?

A

dynein: transports virus from periphery to cell body
kinesin: transports viral capsid to nuclei through cell body barriers

79
Q

what happens during reactivation of HHV1?

A

anterograde transport: virus gets transported from cell body to epithelial cells

80
Q

how does HHV1 lead to encephalitis?

A

Immunocompromised individuals can have spread into the rest of the brain (especially
the temporal lobe)

81
Q

how do dentists get HHV1?

A

by getting bitten by someone infected with it (doesn’t spread JUST via neurons)

82
Q

what is the most common STD? how does it travel in the body?

A

genital herpes HHV2: from genitals to dorsal root ganglia.

83
Q

what are drugs for HHV1/2?

A

acyclovir: inhibits HSV DNA polymerase. maybe an mRNA vaccine is on the way.

84
Q

what is HHV3?

A

varicella-zoster virus VZV (1st infection = varicella; reactivation = zoster)

85
Q

where can varicella (chickenpox) virus replicate?

A
  • primary viremia = regional lymphnode
  • secondary viremia = in the liver, spleen, other organs
86
Q

where does varicella stay when latent?

A

in dorsal root ganglia

87
Q

what is special ab shingles/zoster (when virus reactivates)?

A

symptoms only occur in the segment where it was latent in (dermatome) and are intense and painful.
can only be reactivated once.

88
Q

what is a complication of HHV3 reactivation (shingles)?

A

post-herpetic neuralgia: intense neural pain even when the lesion goes away

89
Q

what is disseminated presentation and who can be affected?

A

HHV3 infection can spread away from the infected dermatome, and it can kill you

90
Q

what is HHV4? what does it cause and affect? how is it spread?

A

EBV Epstein-Barr virus.
causes mononucleosis and affects oropharynx.
spreads through saliva.

91
Q

what are HHV4 symptoms?

A

swollen lymph nodes, enlarged spleen and liver during primary infection, atypical lymphocytes

92
Q

what are complications of HHV4 (EBV)?

A

can contribute to cancer (nasopharyngeal carcinoma) in immunosuppressed people.
may be linked with multiple sclerosis.

93
Q

who can be affected by HHV5?

A

immunocompromised people and fetus/neonates

94
Q

what is HHV5? what are symptoms?

A

cytomegalovirus CMV.
Causes mild to severe hearing loss, cognitive defects, impaired vision, and physical abnormalities

95
Q

hhv5 / CMV is the leading cause of what?

A

Leading cause of non-hereditary sensorineural hearing loss in children.
Leading infectious cause of brain damage in US children.

96
Q

are there drugs for HHV5?

A

yes: acyclovir, nucleoside analogs

97
Q

how does HHV4/EBV spread?

A

through saliva

98
Q

what is HHV6? how does it spread? who is it dangerous for? what disease is it associated with?

A

roseola.
spreads via saliva, dangerous for immunocompromised people, associated with multiple sclerosis.

99
Q

what is HHV7?

A

pityriasis rosea

100
Q

what is HHV8?

A

kaposi’s sarcoma (AIDS): Causes neoplastic transformation in immunocompromised patients

PATH300 (10 decks)

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