Exam 3: Respiratory Viruses and Bacteria Flashcards
(158 cards)
1
Q
consists of ciliated epithelial cells, goblet cells, and dendritic cells
A
conducting airway
2
Q
- move bad things out
- synthesize antimicrobial peptides
A
ciliated epithelial cells
3
Q
produce mucus (protein called mucin with polysaccharide modification)
A
goblet cells
4
Q
- hydrophilic
- keep epithelia hydrated
- made by goblet cells
A
mucin
5
Q
what are the different types of mucin?
A
- membrane anchored mucin
- polysaccharide secreted mucin
6
Q
- intraepithelia
- carry out surveillance
A
dendritic cells
7
Q
consists of type 1 epithelial cells, type 2 epithelial cells, and macrophages
A
alveoli
8
Q
- thin for gas exchange
- provide the most coverage
A
type 1 epithelial cells
9
Q
- rounded
- produce surfactant
A
type 2 epithelial cells
10
Q
- made by type 2 epithelial cells
- protein + lipids
- attached or secreted
A
surfactant
11
Q
- carry out antigen presentation
- phagocytosis to keep airway clear
A
alveolar macrophages
12
Q
love the lipids in the airway
A
mycobacterium tuberculosis
13
Q
how do the lungs of germ free mice compare to conventional mice?
A
have less mature alveoli
14
Q
what happens if you give germ free mice Lactobacillus into the nose?
A
- develop normal lungs and normal # of alveoli
- having bacteria in lungs helps develop structure
15
Q
what happens during the flu in relation to resistance against bacterial infections?
A
decrease resistance against bacterial infections during flu
16
Q
naked virus
A
non-enveloped virus
17
Q
virus enclosed in membrane
A
enveloped virus
18
Q
naked RNA of virus
A
icosahedron
19
Q
*picornarvirus
~ssRNA
~icosahedron
A
rhinovirus
20
Q
coronavirus
A
SARS (severe acute respiratory syndrome)
21
Q
paramyxovirus
A
RSV (respiratory synctial virus)
22
Q
involves replication of genome and proteins
A
virus replication
23
Q
what are the steps of virus replication?
A
- attachment to host receptor
- entry (at least genome)
- synthesis - genome replicates and viral protein synthesis in host (in cytosol)
- assembly of stuff that was synthesized
- assembled virus particle needs to be released
24
Q
virus particle with all its parts
A
virion
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- goes from upper respiratory tract to lower tract
- icosahedral capsid
- +ssRNA
- naked
- positive sense
- cellular tropism = respiratory epithelial cells
rhinovirus
26
what are the host receptors on respiratory epithelial cells that rhinovirus binds to?
- ICAM-1 (intercellular adhesion molecule)
| - LDLR (low density lipoprotein receptor)
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increases during inflammation
ICAM-1
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viral ligands of rhinovirus that bind receptors
-capsid proteins
| ~VP 1/2/3
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- conducting airways--->alveoli
- pleomorphic
- -ssRNA
- enveloped
- tropism = ciliated epithelial cells
RSV (respiratory synctial virus)
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what is the host receptor for RSV?
CX3CR1 (chemokine receptor)
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what are the viral ligands for RSV?
-surface G & F proteins
| ~surface glycoproteins
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- in alveoli
- coronavirus
- pleomorphic/spherical
- +ssRNA
- enveloped
- tropism = pneumocytes (type 1 & 2 epithelial cells)
SARS (severe acute respiratory syndrome)
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what is the host receptor for SARS?
ACE-1 (angiotensin converting enzyme 1)
| -secretes ADH
34
what is the viral ligand for SARS?
spike protein(s)
35
what is the life cycle of rhinovirus?
1. receptor binding to viral ligand
2. receptor mediated endocytosis
3. endosome (decreased pH)
4. endosome releases +ssRNA into host
- can be used directly for protein synthesis (-RNA--> +RNA)
5. +ssRNA goes to ribosomes on rough ER
6. viral proteins and +RNA join in virus in cell
7. cell lysis to release virions
36
what is the life cycle of RSV?
1. G & F viral ligands bind with host cell receptor
2. membrane fusion
3. -ssRNA can't be used for translation directly
- makes +RNA---> -RNA
4. +RNA goes to rough ER which results in viral proteins
5. viral proteins and -RNA in capsid
6. viral proteins go to cell surface
7. budding
37
what is the life cycle of SARS?
1. ligand binds host cell receptor
2. receptor mediated endocytosis
3. endosome (decreased pH)
4. membrane fusion ---> release +RNA
- makes -RNA----> +RNA
5. +RNA goes to rough ER ---> viral proteins
6. viral proteins and +RNA join in endosome
7. exocytosis
38
where is an infection most dangerous?
alveoli because there is no cilia
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- enzyme that changes +RNA-->-RNA-->+RNA
- error prone~no proofreading
- antigenic diversity due to errors
RNA dependent RNA polymerase
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how do infected epithelial cells start the immune response?
1. induce apoptosis
2. inflammation
- type 1 interferon response
41
- gram +
- catalase -
- beta hemolysis
- found on skin
- aerotolerant
- bacitracin sensitive
- have capsule
- have pili
- have hemolysin
- M protein (surface)
Group A strep (Streptococcus pyogenes)
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what can kill Streptococcus pyogenes?
*Bacitracin (bacitracin test-->antibiotic)
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what is the capsule of Streptococcus pyogenes made of?
hyaluronic acids
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what hemolysin does Streptococcus pyogenes have?
streptolysin S and O
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- facultative anaerobe
- beta hemolysis- beta hemolysin
- bacitracin resistant
- found in intestine or vaginal tract
- have capsule
- pili
- HvgA (hyper virulent GBS adhesin)
Group B strep (Streptococcus agalactiae)
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what is the capsule of Streptococcus agalactiae made of?
sialic acid
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- alpha hemolysis
- causes pneumonia
- found in nasopharynx
- facultative anaerobe
- have capsule
- pili
- hemolysin
- phosphororylcholine teichoic acid
Streptococcus pneumoniae
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what is the capsule of Streptococcus pneumoniae made of?
* polysaccharide
| - composition gives rise to serotypes
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what is the hemolysin of Streptococcus pneumoniae?
pneumolysin
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what do capsules play a role in?
1. opsonization
| 2. phagocytosis
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what do pili play a role in?
1. attachment
| 2. adherence
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what do hemolysins produce?
pore forming toxins (proteins)
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what does the capsule of Group A strep inhibit?
* inhibits phagocytosis
| - avoids recognition by own cells
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what does streptolysin S and O of Group A strep lead to?
1. damage
2. inflammation, invasion, spread
3. strep throat or skin infection
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what does the pyrogenic exotoxin (super antigen) of Group A strep cause?
toxic shock syndrome (scarlet fever)
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what does the M protein of Group A strep result in?
1. adhesion
2. epitopes mimic our self epitopes
-autoimmune diseases
3. antibodies and T cells recognize/against M proteins
-cross reactivity with myosin, sarcolemma membrane, neuronal gangliosides
~arthritis, carditis, rheumatic fever, sydenham chorea, kidney failure
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what happens if a virulence factor of Group A strep is lost?
it may become less virulent and require more LD 50
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- a virulence factor that can be produced by certain species of Streptococcus
- help them gain entry into a host by counteracting the host's defences
- Group A strep
M protein
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what are the steps of Group B strep invasion?
1. intestines/vaginal tract
2. cross mucosal barrier
3. evade immune defenses
4. cross blood-brain barrier
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how does Group B strep cross the mucosal barrier?
1. adhesins - pili
2. paracellular translocation
- tight junctions
3. hemolysin transcellular translocation?
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How does Group B strep evade immune defenses?
- capsules
- degrade complement proteins
- bind Ig at fc
- D-ala (+) modification to teichoic acids
- inhibit AMP?
- superoxide dismutase inhibits ROS?
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what happens when Group B strep crosses the blood-brain barrier?
1. meningitis
2. beta hemolysin and HvgA (adhesin binds to host receptor)
-leads to neurotropism
~microvascular endothelium
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caused by Group B strep, Listeria monocytogenes
infant meningitis
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caused by neisseria meningitis and/or streptococcus pneumoniae
older kids/adult meningitis
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what is the path of Streptococcal pneumoniae?
1. upper respiratory tract (asymptomatic carrier)
2. lower respiratory tract
3. alveoli
4. blood
5. brain
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disease caused when streptococcal pneumoniae reaches the alveoli
pneumonia (liquid in lungs)
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disease caused when streptococcal pneumoniae reaches the brain
meningitis
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what doe streptococcal pneumoniae use to infect host?
1. neuraminidase
2. adhesins
3. pneumolysin
4. streptococcal pyruvate oxidase
5. capsule
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cleaves glycoconjugates on mucin ~ breaks mucosal barrier
neuraminidase (of Streptococcal pneumoniae)
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adhesins that streptococcal pneumoniae use to attach to epithelium
pili
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-form pores on epithelial cells
~inflammation
-inhibit mucocilliary action
pneumolysin of streptococcal pneumoniae
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synthesizes hydrogen peroxide (H2O2)
streptococcal pyruvate oxidase
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* PC-teichoic acid
| - taken up by endothelium and dump at other side?
capsule
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- aerobic
- rod-shaped
- high GC content
- Gram +
- phylogeny = actinobacterium
- very fatty bacterium
- has peptidoglycan layer and phospholipid
- mycolic acid
- slow grower
- classical intracellular pathogen
- hard to find/diagnose
mycobacterium tuberculosis
75
what percent of mycobaterium tuberculosis' genome is dedicated to fatty acid synthesis or rmetabolism?
30%
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what percent of mycobacterium tuberculosis' dry weight is lipids?
40%
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in an ideal lab condition what is the doubling time for mycobaterium tuberculosis?
15 hours
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how is mycobacterium tuberculosis treated with antibiotics?
- long term antibiotic treatment
- bacteria needs to grow for abx to work
- abx sensitivity decreases if m. tuberculosis is not growing
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what types of resistance does m. tuberculosis have?
1. phenotypic resistance
2. genetic resistance
- horizontal gene transfer is rare
- genome mutations for most part
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cellular tropism is alveolar macrophages - likes to grow in host cell
mycobacterium tuberculosis
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how does mycobacterium affect immune system?
-once infection happens, it elicits immune response
| ~disease/damage caused by immune response
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what are the common tests to diagnose mycobacterium tuberculosis?
1. TB skin test
| 2. Blood test
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involves a skin injection with tuberculin(protein extract of Mtb), which serves as an antigen
TB skin test
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what is the infection process for TB?
1.primary infection
-innate immune response
~clearance OR adaptive immne response
2. secondary infection
-adaptive immune response (t and b cells)
~clearance OR active TB (disease/infectious) OR granuloma latent infection
3. granuloma latent infection
-active TB OR clearance
85
how does granuloma latent infection trigger active TB?
* trriggers weakened immune defense
- steroids
- age
- malnutrition
- HIV~ comprimises T cell response
86
what is the result for TB test during primary infection?
negative skin test
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what is the result for TB test during secondary infection or adative immune response?
positive skin test
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- model environmental opportunistic pathogen
- very good at adapting to its environment
- 3 kinds of motility
- have capsules
- make different pigments depending on conditions
- priority 1 (critical) for WHO priority pathogen list for R+D of new antibiotics
Pseudomonas aeuroginosa
89
what are the 3 types of motility of Pseudomonas aeuroginosa?
1. swimming (flagella)
2. twitching (type 4 pili)
3. swarming (flagella + pili)
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what the capsules of Pseudomonas aeuroginosa like?
-form mucoid colonies
~polysaccharide capsule
-avoid immune recognition
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produced by Pseudomonas aeuroginosa in low phosphorus conditions
pyocyanin (green)
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produced by Pseudomonas aeuroginosa in ample phosphorus conditions and it is fluorescent
pyoverdin (green/yellow)
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what is the pathogenesis process for Pseudomonas aeuroginosa?
1. adhesion
2. damage
3. immune recognition
4. biofilm composition
5. antibiotic resistance ~ mcr-1 inhibits colistin
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what does Pseudomonas aeuroginosa use for adhesion?
-LasA protease
-elastase protease
~both proteases degrade proteins of extracellular matrix
-flagella and type 4 pili to bind to cell surface
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what does Pseudomonas aeuroginosa use to cause damage?
- pyocyanin
- ExoU
- ExoS
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-causes oxidative damage
-secretes exotoxin A
~inhibits translation
~uses type 3 secretion to get protein into cytosol of host cell
pyocyanin of Pseudomonas aeuroginosa
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phospholipase that degrades membrane
ExoU of Pseudomonas aeuroginosa
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enzyme that adds ADP to RAS that results in disruption of actin cytoskeleton
ExoS of Pseudomonas aeuroginosa
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what is involved in immune recognition of Pseudomonas aeuroginosa?
-toll like receptor 5 that recognizes flagellum
-LPS in outer membrane recognized by TLR4
~both lead to inflammation
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how is the biofilm of Pseudomonas aeuroginosa formed?
-goes from planktonic (moving) to sessile
~builds biofilm structure
-cells stick together through extracellular polysaccharides
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what are the extracellular polysaccharides that help cells stick together to form biofilm?
- Psl
- Pel
- Alginate
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what else is in biofilm that helps cells stick together?
DNA
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- helps resist antibiotics
| - creates gradient
biofilm
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what are the different sides of the gradient like formed by biofilms?
- metabolic processes occur outside the gradient
| - on the inside there is low metabolic and respiratory activity
105
how do Pseudomonas aeuroginosa resist abx?
1. modify gyrase + tophomerase to inhibit fluoroquinolones
2. enzymes degrade abx
3. eflux pump to transport abx out of cell
4. outermembrane proteins stop expression of abx or cause mutations
106
-inhibits colistin
-adds phosphoethanolamine to lipid A
~modifies charge and substrate so it can no longer bind
mcr-1
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MDR
multidrug resistance
108
HIV
human immunodeficiency virus
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- genus=lentivirus
- enveloped
- 2 copies of ssRNA
- 9 genes~18 proteins
HIV
110
how are there 9 genes but 18 proteins for HIV?
-overlapping open reading frames
| ~forms polyproteins --> cleaved by both host and viral proteases to functional proteins
111
what are the genes of HIV?
1. Gag
2. pol
3. env
4. rev
5. vif
6. Vpr
7. tat
8. Vpu
9. net
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all 3 genes together make polyprotein
- Gag
- pol
- env
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encodes core structural proteins
Gag
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encodes integrase, protease, reverse transcriptase
pol
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encode glycoproteins on envelope (gp120 & gp41)
env
116
what are the targets of HIV?
1. macrophages CD4 and CCR5
2. net protein down regulates MHC
3. super infection
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what happens if reverse transcriptase makes a mistake?
*mutations
-GP120 binds Cd4 and CXCR5 instead of CCR5
~called type switching
~new target is CD4+ T cells
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why is HIV a superinfection?
- same person can have multiple versions of HIV
| - mutation rate in HIV is much faster than adaptive immune response
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- first stage of HIV infection
| - weeks
-acute infection
120
- provirus
| - need drugs during this stage to inhibit integrase and reverse transcriptase
latent infection
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- final stage
| - 0-3 years till the end of life
AIDS
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- gram -
- Neisseria gonorrhoeae
- inner and outer membrane, lipooligosaccharides (LOS)
- facultative anaerobe
gonorrhea
123
- weak outside of host
- sensitive to environmental stresses
- humans are reservoirs
gonorrhea
124
how does gonorrhea infect a host?
-attach to vaginal or urethral epithelium
~surface proteins
~type 4 pili (twitching)
~LOS
125
how does gonorrhea evade immune defenses?
* *antigenic variation
1. gene assortment/recombination
2. phase variation
126
always modifying whats on the outside
antigenic variation of gonorrhea
127
expression of protein is sometimes on or sometimes off
phase variation
128
- caused by Treponema pallidum
- gram -
- spirochete
- no oxidative phosphorylation, no electron transport chain, no TCA cycle, no LPS
- small genome
- spread by sex
syphilis
129
what is the progression of syphilis?
sex--> primary syphilis (mild symptoms)-->secondary syphilis (treponema spreads) -->latent syphilis (3-30 yrs)-->tertiary syphilis (death)
130
serotype is a classification scheme defined by.....?
host immune response
131
true or false: all human pathogens grow best at human body temperature of 37 degrees celsius
false
132
what is the most ideal host to demonstrate rhinovirus as the causative agent of respiratory infections?
epithelial cells derived from lung tissues
133
true or false: a person with rhinovirus may still be contagious after his/her symptoms are gone
true
134
true or false: the main cause of symptoms in respiratory viral infections is immunopathological
true
135
what is the main reason why it is hard to develop a RSV vaccine?
immune immaturity of the target population
136
what specific step in viral replication does the drug Palivizumab block?
adhesion and entry
137
causes strep throat
Streptococcus pyogenes
138
causes rheumatic fever
cross-reacting antibodies
139
true or false: The LD50 for encapsulated Streptococcus pneumoniae is higher than non-capsulated Streptococcus penumoniae.
false
140
non-sporulating
Streptococcus pneumoniae
141
Beta-hemolytic
Streptococcus pyogenes
142
true or false: Mycobacterium tuberculosis had two phospholipid bilayer membranes
false
143
The host tropism of Mycobacterium tuberculosis is...
alveolar macrophages
144
does NOT exhibit rapid onset of symptoms
tuberculosis
145
- contained by cell-mediated immunity
- can be treated with antibiotics
- transmitted through respiratory route
tuberculosis
146
true or false: Tuberculosis can be effectively treated with a 2-week course of antibiotics
false
147
true or false: Mycobacterium tuberculosis without mycolic acids will have a higher LD50 value than Mycobacterium tuberculosis with mycolic acids
true
148
uses swimming, twitching and swarming motility
Pseudomonas aeruginosa
149
true or false: The only route of transmission for Pseudomonas aeruginosa is through inhalation of contaminated water droplets
false
150
- It is recognized by TLR4 on host cells
- It can facilitate interactions with CFTR on host epithelial cells
- It is a structural component of Gram negative bacteria outer membrane
LPS
151
true or false: Type three secretion system transports proteins from bacterial cytoplasm to the host cytoplasm.
true
152
Which of the following are SECRETED PROTEINS from Pseudomonas aeruginosa?
- elastase
| - phospholipase C
153
an intracellular pathogen
HIV
154
when HIV is inserted into a host chromosome, it is called a....
provirus
155
For people with a mutated version of CCR5 that doesn't bind to GP120, what would the LD50 for HIV be?
Higher than LD50 in people with wildtype copy of CCR5
156
true or false: People who die from AIDS are dying from secondary infections or cancer, not directly from HIV.
true
157
the bacterium that causes the sexually transmitted disease gonorrhea
Neisseria gonorrhoeae
158
Syphilis is caused by the bacterium.....?
Treponema (genus) pallidum (species)
