Respiratory Week 2 Flashcards
1
Q
The burst duration of the phrenic nerve firing controls what aspect of quiet breathing?
A
Depth
2
Q
The inter-burst interval of the phrenic nerve firing controls what aspect of quiet breathing?
A
Rate
3
Q
For normal, quiet inspiration the phrenic nerve and the __________ motor neurons are simultaneously active
A
External intercostal motor neurons
4
Q
Where are the cell bodies of the expiratory motor neurons located?
A
In the ventral horn of the spinal cord (some thoracic, some lumbar)
5
Q
What part of the brainstem contains a respiratory neural network that is essential and sufficient for producing motor drive to respiratory muscles?
A
The medulla
6
Q
What does the dorsal respiratory group (DRG) control?
A
Inspiratory center. It contains the nucleus of the solitary tract (NTS) and is responsible for the autonomic rhythm of respiration.
Connects to the phrenic nerve which then innervates the diaphragm to control breathing
7
Q
What does the ventral respiratory group (VRG) control?
A
Expiratory center. About 2/3 inspiratory neurons, about 1/3 expiratory neurons. Contains the pre-Botzinger complex
Mostly rhythm/pattern generator.
Mediates expiration under non-rest conditions; otherwise quiet
8
Q
What are the pontine respiratory centers?
A
The pontine respiratory group (PRG) and the apneustic center
9
Q
What does the pontine respiratory groups (PRG) control?
A
Electrical stimulation in late inspiration that facilitates the termination of inspiration (not imp. for normal breathing but can influence it)
** can inhibit the apneustic center
10
Q
What does the apneustic center control?
A
Produces tonic contraction of the diaphragm (keeps the “on” switch for the inspiratory center)
11
Q
Where do afferent lung receptor inputs terminate?
A
In the NTS of the DRG
12
Q
Three types of afferent lung receptor inputs?
A
- Lung stretch receptors
- Rapidly adapting receptors
- Lung C fibers (pulmonary c-fibers/J-receptors) & bronchial c-fibers
13
Q
What do slowly adapting pulmonary stretch receptors do? Where are they located?
A
Located in the smooth muscle of the airways
Responsible for the Hering-Breuer Inflation Reflex: terminates inspiration, prolongs expiration. Important at large tidal volumes (>800ml) in adults or just normal breathing in babies
Generally insensitive to chemicals EXCEPT increasing airway CO2 will decrease their activity
14
Q
What are Rapidly Adapting Receptors? Where are they located?
A
Located in the airway epithelium and smooth muscle
Sensitive to chemical irritants (particularly histamine). Reflex responses: cough, sneeze, bronchoconstriction, hypernea
15
Q
Neural discharge of the slowly adapting pulmonary receptors is dependent on lung inflation or deflation?
A
Inflation
Increases with inflation, decreases with deflation
Continuous discharge with sustained inflation
16
Q
Neural discharge of rapidly adapting receptors is dependent on lung inflation or deflation?
A
Either
Unclear whether they function during normal breathing
17
Q
What are vagal lung c-fibers? Two types?
A
Unmyelinated, slowly-conducting fibers. Primarily chemosensitive
Two types: pulmonary and bronchial
18
Q
Where are pulmonary c-fibers/j-receptors? Function?
A
Accessible through pulmonary circulation
Respond strongly to histamine, prostaglandins and pulmonary congestion
Cause rapid, shallow breathing or sometimes apnea
19
Q
When are pulmonary c-fibers/j-receptors active?
A
In pulmonary edema
20
Q
When are bronchial c-fibers active?
A
During asthma or allergic reaction
21
Q
What are bronchial c-fibers? Where are they located?
A
Accessible through bronchial circulation
Respond strongly to histamine and prostaglandins
Stimulation causes rapid, shallow breathing, apnea, increased mucous secretion, bronchoconstriction + sometimes cough
22
Q
What links metabolism to ventilation?
A
Central and peripheral chemoreceptors
23
Q
Where are peripheral chemoreceptors located?
A
Carotid bodies and aortic arch
24
Q
Peripheral chemoreceptors located in carotid bodies have afferent neurons connecting them to what cranial nerve?
A
Glossopharyngeal (IX)
25
Peripheral chemoreceptors located in aortic bodies have afferent neurons connecting them to what cranial nerve?
Vagus (X)
26
What are peripheral chemoreceptors sensitive to?
PaO2, PaCO2, and pH of arterial blood
27
At normal PaCO2 and pH are the peripheral chemoreceptors sensitive or insensitive to PaO2?
Not very sensitive
Elevations in PaCO2 and/or a decrease in pH will change this threshold. A decreased PaCO2/increased pH will decrease the sensitivity to PaO2 whereas an increased PaCO2/decreased pH wil significantly increase the sensitivity to PaO2
28
Where are are the central chemoreceptors located?
On the ventral surface of the medulla
29
What do central chemoreceptors detect changes in?
H+ concentration
BUT: ions cannot freely diffuse the BBB so CO2 will diffuse, react with carbonic anhydrase, and create H+. Central chemoreceptors detect this change
30
Are the central chemoreceptors sensitive to PaO2 or blood pH?
Nope
31
Are the central chemoreceptors highly sensitive or relatively insensitive to small changes in PaCO2?
Highly sensitive
A 2-5 mmHg increase in PaCO2 can more than double alveolar ventilation via the central chemoreceptors
32
What is the most important regulator of ventilation in a healthy individual at rest?
PaCO2 via stimulation of the central chemoreceptors
33
How is the pH of CSF buffered?
Over time the BBB can actively transport bicarb from blood into CSF to buffer changes due to increase PaCO2
This increased buffering capacity of the CSF will reduce the sensitivity of the central chemoreceptors to changes in PaCO2
34
Why does sleep depress breathing?
Because of the reduction of inputs other than chemoreceptors
If you have central sleep apnea, then your breathing will stop (means your central chemoreceptors aren't working!)
35
What four types of viruses comprise the picornaviridae family?
Enterovirus, rhinovirus, hepatovirus, cardiovirus
36
RNA composition of picornaviruses?
(+) ssRNA
very small!
37
Four subtypes of enteroviruses?
1. Polioviruses types 1-3
2. Coxsackieviruses A1-A24 (no A23), B1-B6)
3. Echoviruses 1-34 (no 10 or 28)
4. Enteroviruses 68-71
38
Biological properties of picornaviruses (viral structure, heat/acid stability)?
Non-enveloped icosahedral capsid
heat and detergent stable
Enterovirus and Hepatovirus are acid-stable until a pH of ~3
Rhinovirus is acid-labile until pH of ~5
39
Describe picornavirus replication
ICAM-1 on host cell binds to canyon on viral cell, pulls viral cell to plasma membrane
Virion RNA acts as mRNA and is translated into a polyprotein that is then cleaved to yield structural and non-structural proteins (including RNA dependent RNA polymerase)
Occurs in the cytoplasm of the host cell
40
Where in the body does enterovirus replication occur?
In the oropharynx and intestine
41
Where does rhinovirus replication occur?
In the upper respiratory tract
42
Which picornavirus, enterovirus or rhinovirus, can lead to viremia?
Enterovirus
Certain enteroviruses have tissue tropism and can present in different tissue types (ex: coxsackie A - hand, foot & mouth disease - rash and herpangia on the skin)
43
What four virus types comprise the paramyxoviridae family?
1. Moribilivirus (measles)
2. Metapneumovirus
3. Paramyxovirus
4. Pneumovirus
44
RNA composition of paramyxoviridae viruses?
(-) ssRNA
45
Virion structure of the paramyxoviruses?
RNA genome protected by proteins
Enveloped structure with two major surface glycoproteins: Larger glycoprotein (HN, H, or g) and smaller glycoprotein (fusion, F)
46
Describe paramyxovirus family replication
(-) ssRNA --> (+) ssRNA/mRNA to make proteins and another (-) ssRNA to act as a template for viral progeny
Proteins are made in the rER, sent to the Golgi, where they're directed to the host cell membrane. The viral particles bleb off the host membrane with viral ssRNA inside
47
Parainfluenza viruses (PIV) transmission and infection
Respiratory transmission; infections limited to respiratory tract
Generally non-systemic and viremia rare
More severe in lower respiratory tract
48
What type of disease does PIV cause?
Cold-like symptoms, bronchitis, croup (laryngotracheo-bronchitis)
**Children are most at risk for more severe disease and croup; adults can be infected but with milder symptoms
49
Is there immunity to PIV?
Yes, but its short-lived. Reinfection occurs throughout life
50
How do you diagnose PIV?
Virus culture, synctia formation, hemadsorption, hemagglutination inhibition, rtPCR
51
Treatment for PIV?
Supportive care
52
What is the most fatal acute respiratory tract infections in infants and young children?
Respiratory syncytial virus (RSV)
53
75% of infants are seropositive to what virus by 1 year of age?
Respiratory syncytial virus (RSV)
54
RSV virion is easily inactivated by what?
Dryness and acid
55
What type of disease does RSV cause?
Bronchiolitis, pneumonia, common cold
56
How is RSV transmitted?
Respiratory transmission (aerosol droplets or fomites) or localized infections of the respiratory tract
**highly contagious
57
Is immunity induced by RSV?
No, reinfection occurs throughout life
Maternal antibody does not prevent infection
58
What is the treatment for RSV?
Ribavarin reduces the severity of symptoms in immunocompromised patients
Passive vaccination for high-risk infants
Palivizumab: anti-F monoclonal antibody
59
What is human metapneumovirus?
Newly discovered respiratory transmission; accounts for 15% of common colds in children
60
What disease does metapneumovirus cause?
Common cold, bronchiolitis, pneumonia, or it can just be asymptomatic
61
What picornaviridae virus has a vaccine?
Polio (Salk and Sabin)
62
Many symptoms of paramyxoviruses is due to what?
Our own immune response
Ex: rash in measles, swelling in mumps
63
Symptoms of a sinus infection?
Fever, cough, nasal discharge, fetid breath, headache, pain over sinuses, tenderness over sinuses
64
What causes acute sinusitis? Name three of these pathogens
Normal flora of the upper respiratory tract with the potential to cause disease
1. streptococcus pneumoniae
2. Non-typeable Haemophilus influenzae (gram neg. cocci)
3. Moraxella catarrhalis (gram neg diplococci)
65
What pathogens cause chronic sinusitis?
Same ones as acute sinusitis + gram-negative enterics, anaerobes
Mixed infections!
66
What physical problem enables the growth of bacteria in the sinuses?
Blockage of the sinus drainage; bacteria cannot get out and anaerobic bacteria can flourish
67
Can the pathogens responsible for sinusitis spread?
They can remain at the mucosal surface or they can cause invasive disease (bacteremia, meningitis, etc)
68
How do the bacteria responsible for sinusitis evade host defenses?
Lack of mucus drainage keeps them in the sinuses, no phagocytes, complement or antibodies are present in non-immune host
Phagocytes can appear with inflammation & sIgA can help since these pathogens are extracellular
69
How do the pathogens responsible for sinus infections multiply?
Discharge is a good breeding environment (+ blockage allows anaerobes to grow)
70
What damage do the pathogens responsible for sinusitis cause?
Inflammation and discharge leads to swelling and blockage of nasal passages and discomfort
71
What is the outcome of sinusitis? Is it transmissable?
Usually self-limiting
Can spread the bacteria via droplet/saliva but its not really "contagious" in the sense that you have an outbreak of sinusitis
72
How do you treat sinusitis?
Antibiotics, anti-inflammatory agents, decongestants, fluids
73
What type of bacteria is Streptococcus pneumoniae?
Gram + diplococci
alpha hemolytic
Has a carbohydrate capsule (what the vaccine targets)
74
What diseases does Streptococcus pneumonaie cause?
MOPS (from Sketchy!)
```
Meningitis
Otitis Media
Pneumonia
Sinusitis
Sepsis
```
75
How is Streptococcus pneumoniae encountered?
Respiratory droplet
Human only
76
How does Streptococcus pneumoniae colonize in humans?
Colonizes in the oropharynx and then is aspirated into the lungs
77
How does Streptococcus pneumoniae multiply?
it grows well in serous fluid of the alveoli space
78
How does Streptococcus pneumoniae evade host defenses?
It's an extracellular pathogen, it has an antiphagocytic capsule and it has an sIgA protease
79
What damage does Streptococcus pneumoniae cause?
Inflammation due to peptidoglycan (TLR 2!) and damage via pneumolysin (a toxin that binds to cholesterol in the host cell membrane)
80
What is the outcome of Streptococcus pneumoniae? Transmission mechanism?
Self-resolving to fatal
Transmission via droplet/saliva
81
How do you prevent Streptococcus pneumoniae?
There are two vaccines:
1. 23-valent vaccine for adults that provides IgM immunity
2. 13-valent conjugated vaccine for children (Prevnar 13) that provides IgG immunity
(Remember sketchy video with adults on the Mezzanine (IgM) and children on the ground level (IgG))
82
What are the three manifestations of otitis media?
1. Acute otitis media
2. Chronic suppurative otitis media
3. Otitis media with effusion
83
What are the symptoms of otitis media?
Fever, pain in the ear, dulled hearing
84
What pathogens are responsible for acute otitis media?
Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrhalis (same as the sinusitis pathogens!)
85
What pathogens are responsible for chronic otitis media?
Mixed infections with various URT flora
Anaerobes, enterics, and possibly viruses
86
How do we encounter the pathogens responsible for otitis media?
They are endogenous; human only
87
How do otitis media pathogens spread?
None needed; mucosal surface only
BUT infection can spread to mastoid air cells and rarely the CNS
88
How do the pathogens responsible for otitis media evade host defenses?
Impeded mucus drainage due to blockage helps them stay put and there are no phagocytes, complement, or antibodies present in a non-immune host
Phagocytes can appear (extracellular pathogens) and sIgA can help
89
How do the pathogens responsible for otitis media multiply?
The discharge is a good growth environment
90
What damage do the pathogens responsible for otitis media cause?
Inflammation and fluid exudation/edema, severe/chronic infection can lead to a damaged middle ear, and prolonged hearing impairment/learning development
91
What is the outcome of otitis media? Transmission mechanism?
Usually self-limiting, but possible severe sequelae to mastoid air cells & meningitis
Can spread to new host via droplet/saliva, BUT just like sinusitis this is just a passing of the bacteria, not an "outbreak of otitis media"
92
Treatment for otitis media?
Antibiotics
And for recurrent cases you can remove the adenoids or install myringotomy tubes
93
What type of bacteria is Haemophilus influenzae?
Gram - coccobacillus
Has a carbohydrate capsule (important for vaccine)
*Note: unencapsulated = nontypeable
94
What diseases does Haemophilus influenzae cause?
Type B --> meningitis
Nontypeable (unencapsulated) --> otitis media, sinusitis, pneumonia
95
How is Haemophilus influenzae transmitted/encountered?
Respiratory droplet; human only
Part of normal flora
96
Where does Haemophilus influenzae colonize in humans?
URT
97
Does Haemophilus influenzae spread?
Only meningitis --> blood to CNS
98
How does Haemophilus influenzae multiply?
It's fastidious; needs chocolate agar (lysed blood)
99
How does Haemophilus influenzae evade host defenses?
Type B has an antiphagocytic capsule
Nontypeable has LPS (lipopolysaccharide; highly toxic!)
Also has sIgAse
100
How does Haemophilus influenzae cause damage?
inflammation and via LPS
101
What is the outcome of Haemophilus influenzae diseases?
Meningitis: fatal, neurological sequelae
Others: usually self-limiting
102
How do you prevent Haemophilus influenzae disease?
There is a vaccine for type b (carbohydrate coupled to protein; standard infant vaccine)
103
What is acute otitis externa?
Swimmer's ear
characterized by ear pain (otalgia) and ear inflammation (otorrhea); ear is sensitive to being pulled
104
What predisposes someone to acute otitis externa?
Water in the ears, blockage
105
What is the major pathogen that causes acute otitis externa?
Pseudomonas aeurginosa
106
What causes chronic otitis externa?
Usually over-cleaning of the ear canal
Leads to itching, not pain
107
How do you treat chronic otitis externa?
topical steroids
108
What causes malignant otitis externa?
invasive pseudomonas aeurginosa
109
What type of bacteria is pseudomonas aeruginosa?
Gram negative rod; aerobic
**Key: has green pgiments pyocyanin and pyoverdin
110
What type of infections does pseudomonas aeruginosa cause?
Local infections like otitis externa, cystic fibrosis lungs, hot tub folliculitis, UTIs, etc
111
Who is at risk for pseudomonas aeruginosa infections?
Immunocompromised, burn patients, and diabetics
112
Where do we encounter pseudomonas aeruginosa?
In the environment (water, soil, air, food) --> NOT endogenous
113
How does pseudomonas aeruginosa enter the body?
Lung, intestine, wound
Forms biofilms
114
Does pseudomonas aeruginosa spread?
Yes, in immunocompromised or with burns, wounds
115
How does pseudomonas aeruginosa multiply?
Can grow on diverse substrates, even in disinfectants and cleaning materials
Does not ferment
116
How does pseudomonas aeruginosa evade defenses?
No defenses at surface & toxins can kill phagocytes
Usually held in check by neutrophils, so serious infections are usually in those that are neutropenic
117
What does mutated pseudomonas aeruginosa produce in people with cystic fibrosis?
Alginate polysaccharide, a mucoid on top of the thick mucus they already have. Double whammy.
118
What damage does pseudomonas aeruginosa cause?
Inflammation and exotoxins (exotoxin A, similar to diphtheria toxin), type 3 secreted toxin, and other numerous extracellular enzymes
119
Outcome in pseudomonas aeruginosa infections?
Self-limiting in healthy people; problematic in immunocomprised people and burn patients
Not normally transmitted between people
120
Prevention of pseudomonas aeruginosa infections?
No vaccines. Just be vigilant about infection control in the hostpital
121
Treatment of pseudomonas aeruginosa?
Antibiotics BUT p. aeuginosa is highly resistant to numerous antibiotics
122
What are the four general ways respiratory pathogens gain entry to our respiratory tract?
1. Inhalation to URT first (then aspiration to LRT or descent down mucosa)
2. Inhalation all the way down to LRT (ex: TB)
3. Hematogenous to alveoli (rare)
4. Direct penetration (rare)
123
If a respiratory pathogen does not spread, can it still cause systemic effects?
Yes, their toxin(s) can cause systemic effects even if the pathogen stays put
124
What is the main defense of a non-immune host against respiratory pathogens?
The mucociliary escalator of the URT
125
Outside of the mucociliary escalator, what other defenses must respiratory pathogens evade?
Epiglottis, larynx, and cough reflexes
Chemicals like lysozyme (degrades peptidoglycan) and lactoferrin (binds Fe)
Alveolar macrophages + complement and IgG in the lower respiratory tract
sIgA in URT
CMI - CTLs and TH1-macrophage interactions in LRT
126
General damage caused by respiratory pathogens?
Toxins (local or systemic), inflammation, adaptive immune response (TB granulation)
127
General outcome of respiratory pathogens?
Self-limiting to death
128
What are some representative URT infections?
Sinusitis, otitis media, pharyngitis, laryngitis, bronchitis, whooping cough, diphtheria
129
What causes most pharyngitis?
Virus
130
What are the bacteria responsible for pharyngitis?
Streptococcus pyogenes, Neisseria gonorrhoeae, Corynebacterium diphtheriae (in unvaccinated)
131
Basic microbiology of Strptococcus pyogenes?
Gram + cocci in chains
beta hemolytic
Has Group A carbohydrate, M protein (fibrillar layer), hyaluronic capsule, and lipoteichoic acid on its surface
132
What suppurative diseases does Streptococcus pyogenes cause?
Pharyngitis - Scarlet fever, pneumonia, skin infections (wide range), streptococcal toxic shock syndrome
133
What toxin is responsible for the "sand paper rash" seen in Scarlet Fever?
Spe toxin
134
What are the non-suppurative complications of Streptococcus pyogenes?
Rheumatic fever, glomerulonephritis, and immunologically mediated sequellae
NOTE: These complications are due to inflammation and not infection spread
135
Symptoms of pharyngitis?
Fever, exudative tonsils, lymphadenitis
NO cough, NO rhinorrhea
136
What is Scarlet Fever?
Pharyngitis + rash
Rash is a red, diffuse rash that has a "sandpaper" feel
137
What are the symptoms of Scarlet Fever?
Red, diffuse rash, strawberry tongue, red cracker lips, circumoral pallor, and red cheeks
138
How do we encounter/transmit streptococcus pyogenes?
Human only
HIGHLY contagious
139
How does streptococcus pyogenes enter?
URT, skin, adherence via M protein-fibrinogen, LTA and fibronectin binding protein
140
Does streptococcus pyogenes spread?
YES!
141
What enzymes help streptococcus pyogenes spread?
Hyalurinidase breaks down intercellular matrix
DNase B liquefies lysed neutrophil DNA so bacteria can move and not get suck in the gunk
142
How does streptococcus pyogenes multiply?
Fastidious, needs blood agar
143
How does streptococcus pyogenes evade host defenses?
M protein binds Factor H to inhibit complement opsonization
Hyaluronic acid capsule is antiphagocytic (antigenic mimicry, looks like us!)
C5a peptidase cleaves C5a to inhibit innate defenses
144
How does streptococcus pyogenes cause damage?
Inflammation
Via hemolysins (lyse host defense cells) --> streptolysin O + streptolysin S
Via pyrogenic exotoxins --> superantigens, Spe (Scarlet fever rash enzyme) and toxic shock-like syndrome
145
What is the outcome of a streptococcus pyogenes infection?
Highly variable depending upon the strain, patient circumstances, and treatment
Pneumonia can be lethal
Pharyngitis self-limiting except for rheumatic fever and glomerulonephritis
146
Microbiology of Corynebacterium diphtheriae?
Gram + non-sporeforming rod
147
Clinical manifestations of diphtheria?
sore throat, low-grade fever, dysphagia, pseuomembrane (~50%)
"bull neck" sppearance
148
What are the systemic effects of diphtheria toxin?
Carditis, neurotoxicity,renal tubular necrosis, croup & asphyxia
149
Transmission of diphtheria?
Inhalation; human only
Restricted to URT
150
How does diphtheria multiply?
Fastidious
151
How does diphtheria evade host defenses?
Not much to deal with in the URT
152
How does diphtheria cause damage?
The diphtheria toxin
153
Outcome of diphtheria?
Can be fatal if untreated
154
Diphtheria treatment?
Antibiotics + antitoxin
Can be prevented with toxoid vaccine
155
Where is the diphtheria toxin encoded?
On a bacteriophage (lysogenic conversion)
156
What type of toxin is the diphtheria toxin? What does it do?
A-B type toxin
ADP ribosylates EF-2 and inhibits protein synthesis (ultimately cytotoxic)
157
How does diphtheria toxin damage heart, nerves, kidneys, etc?
They all have a heparin-binding epidermal growth factor receptor that it can bind to.
Death from heart/nervous system damage
158
What type of bacteria is Bordetella pertussis (whooping cough)?
Gram - rod (coccobacillus)
159
What are the three clinical courses of pertussis?
Catarrhal (cough, rhinorrhea)
Paroxysmal (coughing spasms, whoop, cyanosis, vomiting, OK in between episodes)
Convalescent (decreasing but continuing symptoms)
160
What is the most contagious phase of pertussis?
Catarrhal (where you just have cough and rhinorrhea)
161
Complications of pertussis?
hospitalization, pneumonia, seizures, encephalopathy, death
162
How is pertussis transmitted?
Human only inhalation
Infected adolescents/adults are the source for infants and children
163
How does pertussis enter?
Restricted to the URT
Adheres to ciliated epithelium via filamentous hemagglutinin (FHA), pili/fimbriae, and pertactin
164
How does pertussis multiply?
Fastidious
Bordet-Gengou plates
165
How does pertussis evade host defenses?
Not much in the URT
Tracheal Cytotoxin (TCT) kills mucociliary escalator; predisposes host to other infections
166
How does pertussis cause damage?
Via the pertussis toxin
167
What type of toxin is the pertussis toxin? What does it do?
A-B toxin, like the diphtheria toxin
It's also an ADP-ribosylating toxin that binds to G protein to increase cAMP
This causes localized tissue damage and systemic toxicity (hypoglycemia, leukocytosis, neurological damage)
168
What is tracheal cytotoxin (TCT)?
It's a building block of peptidoglycan
Fragment is released and causes loss of ciliated cells & stops mucus flow
Released by bordetella pertussis
***Gulig said: "I like unique things" when talking about this****
169
Outcome of pertussis?
Usually self-limiting but can be fatal
170
How do you prevent pertussis?
Vaccine! Currently is an acellular vaccine of pertussis toxoid + FHA
171
What antibody response is used in the diagnosis of streptococcus pyogenes pharyngitis?
anti-DNaseB + Streptolysin O antibodies
172
What respiratory disease is characterized by a "barky" cough?
Whooping cough/bordetella pertussis
173
What is adenovirus? What is it responsible for?
A family of viruses that infects a wide range of vertebrate species; 51 human serotypes
Wide range of human diseases ranging from respiratory infections/pneumonia to GI and UTIs
174
Adenovirus structure and genome?
Non-enveloped icosahedral capsid
dsDNA; medium-size genome
175
How does Adenovirus transcribe its genes?
In a temporal fashion: early genes (proteins that regulate viral transcription & interfere with host cell transcription processes) and late genes (mainly structural proteins to make new virions)
176
Where are new Adenovirus virions assembled?
The cell nucleus
177
Adenovirus mode of transmission?
Fecal-oral; may establish viremia
178
Where does adenovirus replicate?
Respiratory tract, eyes, GI tract, urinary bladder
179
What virus is responsible for ARD in military recruits and children in boarding schools?
Adenovirus
| since everyone is in close proximity to each other in a stressful environment with not much sleep
180
Four hallmark symptoms of enteroviruses?
Conjunctivitis, respiratory symptoms, gastroenteritis and diarrhea, and hemorrhagic cystitis
181
How is adenovirus diagnoses?
Cell culture or viral antigen detection (ELISA)
182
Prevention of adenovirus?
A live, wild type vaccine is given to military recruits but otherwise not widely distributed
183
How does adenovirus evade host defenses?
It encodes countermeasures against MHC 1 expression and apoptosis
184
What class of viruses is the second most prevalent cause of the common cold?
Coronaviruses
185
What is SARS? What type of virus is it?
Severe Acute respiratory Syndrome
Coronavirus
186
What is MERS? What type of virus is it?
Middle East Respiratory Syndrome
Coronavirus
187
What helps coronaviruses withstand the conditions of the GI tract?
Their glycoprotein envelope
| looks like a crown
188
Coronavirus structure?
Enveloped
+ssRNA
Largest of the human RNA viruses
189
Where does coronavirus replication take place?
In the cytoplasm of the host cell
190
How are new coronaviruses released from their host cell?
Via exocytosis
191
Where does coronavirus replicate?
In the respiratory epithelium (it infects the upper respiratory tract)
192
How are coronaviruses transmitted?
droplets and aerosols
and some by the fecal-oral route
193
Coronaviruses have their highest incidence in what population(s)?
Infants and children
194
What is different about the incubation period of coronaviruses vs. rhinoviruses?
Coronaviruses have a longer incubation period (more than 3 days)
195
What does SARS cause? Symptoms of this?
Atypical pneumonia
Sx: high fever (over 38 C), chills, rigors, headache, dizziness, malaise, mylagia, difficulty breathing & cough
196
What animal transmits SARS to humans?
palm civets
197
How is SARS transmitted?
Respiratory is primary route but it also spreads via sweat, urine, and feces
198
What does MERS cause? Symptoms of this?
Atypical pneumonia
Sx: high fever (over 38 C), chills, rigors, headache, dizziness, malaise, mylagia, difficulty breathing & cough
199
How is MERS transmitted to humans?
Via camels
200
Mortality of MERS and SARS?
MERS is 40%, SARS is 10%
201
What percentage of SERS patients require mechanical ventilation?
Over 70% (during the acute phase)
202
How is MERS transmitted person-to-person?
Respiratory secretions are the main route but also present in sweat, urine, and feces
(human-to-human transmission requires very close contact!)
203
Outcome of coronaviruses?
Self-limiting
204
If you perform a lab test to diagnose SARS or MERS what would you order?
Viral RNA detecting in stool and respiratory fluids by rt-PCR
205
Different subtypes of influenza virus form through a genetic process called...?
reassortment
206
What comprises the influenza genome?
8 -ssRNA segments
207
How are influenza viruses classified?
Family: orthomyxovirus
Types: A, B, C
A more pathogenic than B. C is not a clinical problem
208
The primary reservoir of influenza A is in what animal?
Birds
Interspecies transmission can occur. It's the mixing of interspecies strains that is responsible for generating new epidemic strains by genetic reassortment of the viral genome segments
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Structural properties of influenza?
Enveloped capsid
Two surface glycoproteins (HA and NA) play an essential role in cell entry and antigenicity
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What causes the classic flu-like symptoms of influenza?
Interferon and lymphokine responses to the viral infection
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What causes the local symptoms of influenza?
Epithelial cell damage to ciliated and mucosal cells of the upper airways
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People infected with influenza are more susceptible to what?
bacterial superinfections because of the loss of natural barriers (damage to ciliated epithelial cells)
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Will influenza antibody help prevent future infections?
Only if its the same serotype
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What immune response(s) is critical for resolution of the influenza infection?
Interferon and cell-mediated immunity
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How is influenza prevented?
Vaccine
1. Killed, inactivated vaccine that is injected
2. FluMist - live, attenuated vaccine
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How is influenza treated?
If its the first 48 hours you can administer:
1. Oseltamivir (tamiflu) neurominidase inhibitor
2. Zanamivir (Relenza) neurominidase inhibitor
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Where does influenza replicate?
In the nucleus
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What drugs target the matrix of influenza cells?
Amantidine and Rimantidine
"matrix" from slides; google says these drugs target M2 proton channel after influenza virions are endocytosed into a host cell. The endosome is acidified and viral RNA is degraded.
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What is the most common cause of fatal acute respiratory tract infections in infants and young children?
Respiratory syncytial virus (RSV)
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What is bronchiolitis?
Occurs in children under 1 because of host response to RSV
Resembles asthma (wheezing, dyspnea, air trapping, hyper-expansion of lung, decreased ventilation)
Unusual in that severe infection occurs in first year in the face of maternal antibody
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Does RSV induce immunity?
No, reinfection occurs throughout life
Maternal antibodies also do not prevent infection during the first year of life for some reason
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If a question stem mentions "sudden chills episode" and "rust-colored sputum" what pathogen should you immediately think of?
Streptococcus pneumoniae
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What two categories of pneumonia are there?
1. Community-acquired
| 2. Hospital acquired (nosocomial)
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What pathogen is the most common cause of community acquired pneumonia?
Streptococcus pneumonia
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What pathogens are responsible for atypical pneumonia?
Mycoplasma pneumoniae, chlamydia pneumoniae, respiratory viruses like influenza, adenovirus, parainfluenza and RSV
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If someone has pneumonia after influenza, what pathogen is most likely responsible?
Staph aureus
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What pneumonia-causing pathogen is more common in smokers?
H. influenzae
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General characteristics of typical pneumonia (onset, sx)
Rapid onset, more severe symptoms, productive cough, purulent sputum, chest xray shows dense consolidation
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General characteristics of atypical pneumonia (onset, sx)
Subacute onset (slower), less severe symptoms ("walking pneumonia"), NONproductive cough, a little bit of white phlegm, patchy interstitial infiltrates
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On a chest xay, how can you differentiate typical vs. atypical pneumonia?
Typical has dense consolidation in the affected area whereas atypical has patchy interstitial infiltrates
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Microbiology of streptococcus pneumoniae?
Gram + diplococci
Carbohydrate capsule (imp. for vaccines)
Alpha hemolytic
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What disease does streptococcus pneumoniae cause?
MOPS!
```
Meningitis
Otitis Media
Pneumonia
Sinusitis
Sepsis
```
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What populations are predisposed to pneumococcal pneumonia (S. pneumoniae)?
Very young, elderly, asplenic, sickle cell (functionally asplenic), complement deficient
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Streptococcus pneumoniae encounter/transmission?
Transmitted via respiratory droplets; human only
Part of our normal flora!
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How does streptococcus pneumoniae enter?
Colonizes in the oropharynx and then is aspirated into the lung
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Does streptococcus pneumoniae spread?
Not necessary, but it can in the case of meningitis (blood to CNS)
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How does streptococcus pneumoniae multiply?
It grows well in serous fluid in the alveoli space
Cultured in blood agar
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How does streptococcus pneumoniae evade host defenses?
It has an antiphagocytic capsule and has an sIgA protease
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How does streptococcus pneumoniae cause damage to the host?
Peptidoglycan causes inflammation
Pneumolysin is a toxin that binds cholesterol in the host cell membrane
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What are the four stages of pneumonia?
1. Serous - mild phase; little bit of infections
2. Early consolidation - numerous bacteria, few neutrophils
3. Late consolidation - numerous neutrophils
4. Resolution - effective Ab response, macrophages clear debris
**Gulig said he loved this for an exam question**
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Outcome of streptococcus pneumoniae infection?
Self-limiting to fatal
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How is streptococcus pneumoniae prevented?
Vaccine!
23-valent for adult (IgM) and 7-valent for children (IgG)
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Microbiology of Legionella pneumophilia?
Gram - rod
Stains irregularly so a silver stain has to be used
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What disease does Legionella pneumophilia cause?
Legionnaire's disease (pneumonia of the predisposed)
Pontiac fever (flu-like in anyone)
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How is Legionella pneumophilia encountered and transmitted?
ENVIRONMENT only
Amoeba in water, natural as well in air conditioning
Has to be aerosolized for us to inhale into our lungs. Goes directly into alveoli; no URT initially
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How does Legionella pneumophilia multiply?
Fastidious
Special medium of buffered charcoal yeast extract (BCYE) is used
It replicates within amoeba in the wild and within macrophages in humans
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How does Legionella pneumophilia evade host defenses?
It's facultative intracellular of macrophages
Does this by treating them like an amoeba (how it replicates in the wild).
Uses type 4 secretion (injection), blocks phagolysosomal fusion, stimulates autophagy, creates ER-like space
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What type of immunity is required to attack Legionella pneumophilia?
Cell-mediated (because its intracellular!)
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What damage does Legionella pneumophilia cause the host?
Alveolar inflammation
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What is the outcome of a Legionella pneumophilia infection?
Can be fatal BUT treatable with antibiotics
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Is Legionella pneumophilia transmissible between humans?
Nope, it's a dead-end environmental organism
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What disease does Mycoplasma pneumoniae cause?
Tracheobronchitis/atypical (walking) pneumonia
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Microbiology of Mycoplasma pneumoniae
Wall-less (lacks peptidoglycan) and thus resistant to B-lactams and other PG-active antibiotics
Lacks definite shape and does not gram stain
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How is Mycoplasma pneumoniae encountered/transmitted?
Respiratory droplet transmission; human only
Very labile, very contagious
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How does Mycoplasma pneumoniae enter?
Inhalation and then it adheres via Terminal adhesin protein (P1)
**does not reach alveoli, P1 sticks to ciliated epithelium only
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How does Mycoplasma pneumoniae spread?
Usually restricted to URT surface (where cilia are!)
Very rarely spreads
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How does Mycoplasma pneumoniae multiply?
It needs our sterols
Takes weeks to culture in special media
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What damage does Mycoplasma pneumoniae cause the host?
Peroxide and superoxides
Community-acquired respiratory distress syndrome (CARDS) toxin. This is similar to the pertussis toxin; it breaks out mucociliary escalator
Stimulates autoimmune IgM that binds to out RBCs (cold hemagglutinin) anemia
Inflammation is monocytic as opposed to neutrophilic cellular response
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How do you treat Mycoplasma pneumoniae?
Erythromycin, doxycycline
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What is the outcome of Mycoplasma pneumoniae?
Usually self-limiting
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Microbiology of Pseudomonas aeruginosa?
Gram - rod, aerobic
Opportunistic environmental pathogen
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What disease does Pseudomonas aeruginosa cause?
Local infections: Cystic Fibrosis patient lungs, swimmer's ear, UTI
Systemic in immunocompromised and burn patients
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Why is Pseudomonas aeruginosa particularly bad in patients with Cystic Fibrosis?
P.a. can grow in mucus and causes a phenotypic conversion. Creates mucoid colonies - alginate - that is an antiphagocytic biofilm.
Basically we're taking someone who already has abnormal, thick mucus and making it more abnormal and thick. Obviously very bad.
