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
2
Q
what infectious disease is a big killer in Haiti?
A
cholera
3
Q
what causes the difference in death rates of COVID-19 between countries?
A
immunization/vaccination rates
4
Q
what is long covid?
A
long lasting illness that affects any organ system in the body.
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
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
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
8
Q
how many cells vs bacterias do human have?
A
10 trillion cells for 100 trillion bacteria
9
Q
the variable microbiome varies according to what?
A
host lifestyle, genotype, pathobiology, environment, community members, immune system, physiology
10
Q
what other than microbes live on/in the human body?
A
viruses (virome) and gungi (mycobiome)
11
Q
what are the sources of infection?
A
other humans, insect vectors, other species like rats, food, water
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
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
14
Q
what receptor is targeted by COVID-19?
A
ACE-2 receptors
15
Q
3 factors for a pathogen to cause an illness
A
- survive and multiply in a host
- resist host defenses
- cause injury
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)
17
Q
what mutations allow pathogens to hide from immune surveillance?
A
antigenic variations
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
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
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)
21
Q
name the external host defenses
A
skin barrier, fatty acids, cilia, mucus, mucociliary blanket, acid in stomach, microbiome in intestine
22
Q
what respiratory defenses are present in nasal cavity?
A
antibody, B cell, T cell, cytokine, complement, macrophages (10 million of them)
23
Q
what are the first immune responses following pathogen attachment?
A
innate immunity: activation of complement and NK cells
24
Q
which MHC class antigen presentation involves a phagolysosome?
A
MHC class II
25
4 ways how antibodies can inactivate antigens
leading to phagocytosis:
- neutralization: blocks viral binding sites
- agglutination: of antigen-bearing particles
- precipitation of soluble antigens
leading to cell lysis:
- complement fixation (activation)
26
what cell generates cytotoxic T lymphocytes
Th1
27
where can pathogens "hide" to resist defense?
in endosomes
28
what molecules change due to antigenic variation?
capsular polysaccharides at the microbe's surface
29
what is bacteremia?
moderate amounts of microbes in the blood. takes longer to recover
30
4 reasons why there are more and more issues with infectious diseases?
- overpopulation, poverty
- traveling
- overuse of antibiotics and resistance
ignorance and misinformation (anti-vaxx)
31
what does ebola trigger?
release of a toxic cytokine storm that is toxic to the epithelial cell, leading to bleeding, shock, instability of epithelial cells
32
why are vaccines impractical for viruses?
because of rapid antigenic mutation
33
what cell adhesion molecules are recognized by rhinovirus?
ICAM1
34
how do viruses damage cells?
damage plasma membrane, cause cell lysis or fusion, deranges metabolism, neoplastic transformation
35
what is symptom of polio? is it still present?
crippling of the legs. still present in Afghanistan and Pakistan
36
is measle still around?
yes because of unvaccinated people
37
is measle still around?
yes because of unvaccinated people
38
name potential sites for antiviral drug action
cell entry, viral uncoating, nucleic acid synthesis, assembly and release of viral particles, cell exit
39
what are features of influenza?
virus that hijacks tracheobronchial epithelial cells when breathed in.
spread very rapidly.
40
what are the main complications of influenza? how does it happen?
pneumonia:
- viral = when virus reaches lower respiratory tract
- bacterial = damage caused by the virus allows bacteria to accumulate.
41
how many people die from influenza every year?
30-50 thousand
42
how does influenza affect pregnant women?
it can increase risk of premature births and cause problems for the fetus and mother
43
how can influenza affect immunocompromised people?
it can cause musculoskeletal, neurological, cardiac complications
44
why is influenza more present during winter?
virus replicates more readily in the cold because the secretion of extracellular vesicles by nasal epithelial cells is impaired in the cold
45
how do you cure influenza?
immune system usually clears the virus within 7-10 days
46
what type of influenza virus does the influenza vaccine protect you from?
H3N2 viruses
47
How do epithelial cells in those nose participate in defense against virus?
innate immunity: release extracellular vesicles with receptors capable of recognizing and capturing the virus
48
on what type of receptor is influenza virus presented to T cells by DCs?
MHC class I
49
what do CD4+ and CD8+ T cells respectively do against influenza?
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
when was the worst influenza pandemic?
1918 (50 to 100 million death)
51
what viral disease has killed the most people?
influenza
52
when were viruses discovered?
1930s
53
how many people get infected with influenza every year?
1 billion
54
features of RNA viruses (ex influenza)
- continually mutating and has many types
- can cross species barriers and trade genetic material
55
what are structures on influenza virus and what do they do?
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
Why don’t all the H and N types of influenza infect humans?
Not all of them are able to recognize and bind the receptors on the airway epithelial cells
57
describe the 3 subtypes of influenza?
- 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
explain antigenic drift vs shift
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
is antigenic drift or shift responsible for pandemics?
antigenic shift
60
what animal is often an intermediate for infection propagation and antigenic shift?
pigs
61
differences between H1N1 and H5N1?
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
stages of viral replication
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
what drugs can interfere with virus replication and how?
- amantadine: can block the fusion
- oseltamivir and zanamivir: blocks the budding and release (NA inhibitors i think)
64
more specifically how does HA (hemagglutinin) attaches to host cells?
by binding at the linkage between galactose and sialic acid on the tip of host cell surface receptors.
65
what gives different influenza virus species their selectivity?
selective binding of HA depending on different linkage configurations
66
what does the NA neuraminidase on virus allow for?
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
how can influenza become deadly?
1. if there is inadequate defense
2. severe pneumonia
3. cytokine storm can cause lung damage
68
antibodies against what part of the virus can be made?
against NA, HA, or M2 proteins
69
how can children get Reye syndrome?
from taking aspirin while being infected by a viral disease
70
what does it mean that influenza vaccines are trivalent or quadrivalent?
trivalent (protects against 2 strains of influenza A and 1 of influenza B) or
quadrivalent (2 influenza A and 2 influenza B)
71
what disease might influenza be implicated in?
Parkinson's.
influenza and COVID might have long term impact on neurological functions
72
what do drugs that lessen the symptoms of virus target?
- NA inhibitors: keep virus from leaving the infected cell
- endonuclease inhibitors: blocks the reproduction of virus
73
what are the herpes virus subfamilies?
alpha: HHV1, 2, 3
beta: HHV 5, 6, 7
gamma: HHV 4, 8
74
name common properties amongst the 8 herpes viruses
- cause cell lysis
- latency and reactivation
- world-wide distribution
- difficult to control
- triggers cell-mediated immunity
75
what are herpes viruses heavily associated with?
cancer and tumors
76
name the herpes viruses in each of the 2 categories
- 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
what is HHV1? where is it located?
herpes simplex/cold sores: lives in neurons, gets carried via trigeminal ganglion
78
what 2 molecules help transport HHV1 through nerves?
dynein: transports virus from periphery to cell body
kinesin: transports viral capsid to nuclei through cell body barriers
79
what happens during reactivation of HHV1?
anterograde transport: virus gets transported from cell body to epithelial cells
80
how does HHV1 lead to encephalitis?
Immunocompromised individuals can have spread into the rest of the brain (especially
the temporal lobe)
81
how do dentists get HHV1?
by getting bitten by someone infected with it (doesn't spread JUST via neurons)
82
what is the most common STD? how does it travel in the body?
genital herpes HHV2: from genitals to dorsal root ganglia.
83
what are drugs for HHV1/2?
acyclovir: inhibits HSV DNA polymerase. maybe an mRNA vaccine is on the way.
84
what is HHV3?
varicella-zoster virus VZV (1st infection = varicella; reactivation = zoster)
85
where can varicella (chickenpox) virus replicate?
- primary viremia = regional lymphnode
- secondary viremia = in the liver, spleen, other organs
86
where does varicella stay when latent?
in dorsal root ganglia
87
what is special ab shingles/zoster (when virus reactivates)?
symptoms only occur in the segment where it was latent in (dermatome) and are intense and painful.
can only be reactivated once.
88
what is a complication of HHV3 reactivation (shingles)?
post-herpetic neuralgia: intense neural pain even when the lesion goes away
89
what is disseminated presentation and who can be affected?
HHV3 infection can spread away from the infected dermatome, and it can kill you
90
what is HHV4? what does it cause and affect? how is it spread?
EBV Epstein-Barr virus.
causes mononucleosis and affects oropharynx.
spreads through saliva.
91
what are HHV4 symptoms?
swollen lymph nodes, enlarged spleen and liver during primary infection, atypical lymphocytes
92
what are complications of HHV4 (EBV)?
can contribute to cancer (nasopharyngeal carcinoma) in immunosuppressed people.
may be linked with multiple sclerosis.
93
who can be affected by HHV5?
immunocompromised people and fetus/neonates
94
what is HHV5? what are symptoms?
cytomegalovirus CMV.
Causes mild to severe hearing loss, cognitive defects, impaired vision, and physical abnormalities
95
hhv5 / CMV is the leading cause of what?
Leading cause of non-hereditary sensorineural hearing loss in children.
Leading infectious cause of brain damage in US children.
96
are there drugs for HHV5?
yes: acyclovir, nucleoside analogs
97
how does HHV4/EBV spread?
through saliva
98
what is HHV6? how does it spread? who is it dangerous for? what disease is it associated with?
roseola.
spreads via saliva, dangerous for immunocompromised people, associated with multiple sclerosis.
99
what is HHV7?
pityriasis rosea
100
what is HHV8?
kaposi's sarcoma (AIDS): Causes neoplastic transformation in immunocompromised patients
