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MS1 Spring > Respiratory Week 2 > Flashcards

Respiratory Week 2 Flashcards

1
Q

The burst duration of the phrenic nerve firing controls what aspect of quiet breathing?

A

Depth

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2
Q

The inter-burst interval of the phrenic nerve firing controls what aspect of quiet breathing?

A

Rate

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3
Q

For normal, quiet inspiration the phrenic nerve and the __________ motor neurons are simultaneously active

A

External intercostal motor neurons

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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)

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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

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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

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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

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8
Q

What are the pontine respiratory centers?

A

The pontine respiratory group (PRG) and the apneustic center

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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

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10
Q

What does the apneustic center control?

A

Produces tonic contraction of the diaphragm (keeps the “on” switch for the inspiratory center)

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11
Q

Where do afferent lung receptor inputs terminate?

A

In the NTS of the DRG

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12
Q

Three types of afferent lung receptor inputs?

A
  1. Lung stretch receptors
  2. Rapidly adapting receptors
  3. Lung C fibers (pulmonary c-fibers/J-receptors) & bronchial c-fibers
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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

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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

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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

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16
Q

Neural discharge of rapidly adapting receptors is dependent on lung inflation or deflation?

A

Either

Unclear whether they function during normal breathing

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17
Q

What are vagal lung c-fibers? Two types?

A

Unmyelinated, slowly-conducting fibers. Primarily chemosensitive

Two types: pulmonary and bronchial

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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

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19
Q

When are pulmonary c-fibers/j-receptors active?

A

In pulmonary edema

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20
Q

When are bronchial c-fibers active?

A

During asthma or allergic reaction

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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

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22
Q

What links metabolism to ventilation?

A

Central and peripheral chemoreceptors

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23
Q

Where are peripheral chemoreceptors located?

A

Carotid bodies and aortic arch

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24
Q

Peripheral chemoreceptors located in carotid bodies have afferent neurons connecting them to what cranial nerve?

A

Glossopharyngeal (IX)

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25
Q

Peripheral chemoreceptors located in aortic bodies have afferent neurons connecting them to what cranial nerve?

A

Vagus (X)

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26
Q

What are peripheral chemoreceptors sensitive to?

A

PaO2, PaCO2, and pH of arterial blood

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27
Q

At normal PaCO2 and pH are the peripheral chemoreceptors sensitive or insensitive to PaO2?

A

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

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28
Q

Where are are the central chemoreceptors located?

A

On the ventral surface of the medulla

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29
Q

What do central chemoreceptors detect changes in?

A

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

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30
Q

Are the central chemoreceptors sensitive to PaO2 or blood pH?

A

Nope

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31
Q

Are the central chemoreceptors highly sensitive or relatively insensitive to small changes in PaCO2?

A

Highly sensitive

A 2-5 mmHg increase in PaCO2 can more than double alveolar ventilation via the central chemoreceptors

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32
Q

What is the most important regulator of ventilation in a healthy individual at rest?

A

PaCO2 via stimulation of the central chemoreceptors

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33
Q

How is the pH of CSF buffered?

A

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

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34
Q

Why does sleep depress breathing?

A

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!)

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35
Q

What four types of viruses comprise the picornaviridae family?

A

Enterovirus, rhinovirus, hepatovirus, cardiovirus

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36
Q

RNA composition of picornaviruses?

A

(+) ssRNA

very small!

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37
Q

Four subtypes of enteroviruses?

A
  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
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38
Q

Biological properties of picornaviruses (viral structure, heat/acid stability)?

A

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

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39
Q

Describe picornavirus replication

A

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

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40
Q

Where in the body does enterovirus replication occur?

A

In the oropharynx and intestine

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41
Q

Where does rhinovirus replication occur?

A

In the upper respiratory tract

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42
Q

Which picornavirus, enterovirus or rhinovirus, can lead to viremia?

A

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)

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43
Q

What four virus types comprise the paramyxoviridae family?

A
  1. Moribilivirus (measles)
  2. Metapneumovirus
  3. Paramyxovirus
  4. Pneumovirus
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44
Q

RNA composition of paramyxoviridae viruses?

A

(-) ssRNA

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45
Q

Virion structure of the paramyxoviruses?

A

RNA genome protected by proteins

Enveloped structure with two major surface glycoproteins: Larger glycoprotein (HN, H, or g) and smaller glycoprotein (fusion, F)

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46
Q

Describe paramyxovirus family replication

A

(-) 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

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47
Q

Parainfluenza viruses (PIV) transmission and infection

A

Respiratory transmission; infections limited to respiratory tract

Generally non-systemic and viremia rare

More severe in lower respiratory tract

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48
Q

What type of disease does PIV cause?

A

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

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49
Q

Is there immunity to PIV?

A

Yes, but its short-lived. Reinfection occurs throughout life

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50
Q

How do you diagnose PIV?

A

Virus culture, synctia formation, hemadsorption, hemagglutination inhibition, rtPCR

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51
Q

Treatment for PIV?

A

Supportive care

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52
Q

What is the most fatal acute respiratory tract infections in infants and young children?

A

Respiratory syncytial virus (RSV)

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53
Q

75% of infants are seropositive to what virus by 1 year of age?

A

Respiratory syncytial virus (RSV)

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54
Q

RSV virion is easily inactivated by what?

A

Dryness and acid

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55
Q

What type of disease does RSV cause?

A

Bronchiolitis, pneumonia, common cold

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56
Q

How is RSV transmitted?

A

Respiratory transmission (aerosol droplets or fomites) or localized infections of the respiratory tract

**highly contagious

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57
Q

Is immunity induced by RSV?

A

No, reinfection occurs throughout life

Maternal antibody does not prevent infection

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58
Q

What is the treatment for RSV?

A

Ribavarin reduces the severity of symptoms in immunocompromised patients

Passive vaccination for high-risk infants

Palivizumab: anti-F monoclonal antibody

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59
Q

What is human metapneumovirus?

A

Newly discovered respiratory transmission; accounts for 15% of common colds in children

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60
Q

What disease does metapneumovirus cause?

A

Common cold, bronchiolitis, pneumonia, or it can just be asymptomatic

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61
Q

What picornaviridae virus has a vaccine?

A

Polio (Salk and Sabin)

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62
Q

Many symptoms of paramyxoviruses is due to what?

A

Our own immune response

Ex: rash in measles, swelling in mumps

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63
Q

Symptoms of a sinus infection?

A

Fever, cough, nasal discharge, fetid breath, headache, pain over sinuses, tenderness over sinuses

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64
Q

What causes acute sinusitis? Name three of these pathogens

A

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)
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65
Q

What pathogens cause chronic sinusitis?

A

Same ones as acute sinusitis + gram-negative enterics, anaerobes

Mixed infections!

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66
Q

What physical problem enables the growth of bacteria in the sinuses?

A

Blockage of the sinus drainage; bacteria cannot get out and anaerobic bacteria can flourish

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67
Q

Can the pathogens responsible for sinusitis spread?

A

They can remain at the mucosal surface or they can cause invasive disease (bacteremia, meningitis, etc)

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68
Q

How do the bacteria responsible for sinusitis evade host defenses?

A

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

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69
Q

How do the pathogens responsible for sinus infections multiply?

A

Discharge is a good breeding environment (+ blockage allows anaerobes to grow)

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70
Q

What damage do the pathogens responsible for sinusitis cause?

A

Inflammation and discharge leads to swelling and blockage of nasal passages and discomfort

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71
Q

What is the outcome of sinusitis? Is it transmissable?

A

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

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72
Q

How do you treat sinusitis?

A

Antibiotics, anti-inflammatory agents, decongestants, fluids

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73
Q

What type of bacteria is Streptococcus pneumoniae?

A

Gram + diplococci

alpha hemolytic

Has a carbohydrate capsule (what the vaccine targets)

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74
Q

What diseases does Streptococcus pneumonaie cause?

A

MOPS (from Sketchy!)

Meningitis
Otitis Media
Pneumonia
Sinusitis
Sepsis
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75
Q

How is Streptococcus pneumoniae encountered?

A

Respiratory droplet

Human only

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76
Q

How does Streptococcus pneumoniae colonize in humans?

A

Colonizes in the oropharynx and then is aspirated into the lungs

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77
Q

How does Streptococcus pneumoniae multiply?

A

it grows well in serous fluid of the alveoli space

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78
Q

How does Streptococcus pneumoniae evade host defenses?

A

It’s an extracellular pathogen, it has an antiphagocytic capsule and it has an sIgA protease

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79
Q

What damage does Streptococcus pneumoniae cause?

A

Inflammation due to peptidoglycan (TLR 2!) and damage via pneumolysin (a toxin that binds to cholesterol in the host cell membrane)

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80
Q

What is the outcome of Streptococcus pneumoniae? Transmission mechanism?

A

Self-resolving to fatal

Transmission via droplet/saliva

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81
Q

How do you prevent Streptococcus pneumoniae?

A

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))

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82
Q

What are the three manifestations of otitis media?

A
  1. Acute otitis media
  2. Chronic suppurative otitis media
  3. Otitis media with effusion
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83
Q

What are the symptoms of otitis media?

A

Fever, pain in the ear, dulled hearing

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84
Q

What pathogens are responsible for acute otitis media?

A

Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrhalis (same as the sinusitis pathogens!)

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85
Q

What pathogens are responsible for chronic otitis media?

A

Mixed infections with various URT flora

Anaerobes, enterics, and possibly viruses

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86
Q

How do we encounter the pathogens responsible for otitis media?

A

They are endogenous; human only

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87
Q

How do otitis media pathogens spread?

A

None needed; mucosal surface only

BUT infection can spread to mastoid air cells and rarely the CNS

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88
Q

How do the pathogens responsible for otitis media evade host defenses?

A

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

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89
Q

How do the pathogens responsible for otitis media multiply?

A

The discharge is a good growth environment

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90
Q

What damage do the pathogens responsible for otitis media cause?

A

Inflammation and fluid exudation/edema, severe/chronic infection can lead to a damaged middle ear, and prolonged hearing impairment/learning development

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91
Q

What is the outcome of otitis media? Transmission mechanism?

A

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”

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92
Q

Treatment for otitis media?

A

Antibiotics

And for recurrent cases you can remove the adenoids or install myringotomy tubes

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93
Q

What type of bacteria is Haemophilus influenzae?

A

Gram - coccobacillus

Has a carbohydrate capsule (important for vaccine)

*Note: unencapsulated = nontypeable

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94
Q

What diseases does Haemophilus influenzae cause?

A

Type B –> meningitis

Nontypeable (unencapsulated) –> otitis media, sinusitis, pneumonia

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95
Q

How is Haemophilus influenzae transmitted/encountered?

A

Respiratory droplet; human only

Part of normal flora

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96
Q

Where does Haemophilus influenzae colonize in humans?

A

URT

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97
Q

Does Haemophilus influenzae spread?

A

Only meningitis –> blood to CNS

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98
Q

How does Haemophilus influenzae multiply?

A

It’s fastidious; needs chocolate agar (lysed blood)

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99
Q

How does Haemophilus influenzae evade host defenses?

A

Type B has an antiphagocytic capsule

Nontypeable has LPS (lipopolysaccharide; highly toxic!)

Also has sIgAse

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100
Q

How does Haemophilus influenzae cause damage?

A

inflammation and via LPS

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101
Q

What is the outcome of Haemophilus influenzae diseases?

A

Meningitis: fatal, neurological sequelae

Others: usually self-limiting

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102
Q

How do you prevent Haemophilus influenzae disease?

A

There is a vaccine for type b (carbohydrate coupled to protein; standard infant vaccine)

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103
Q

What is acute otitis externa?

A

Swimmer’s ear

characterized by ear pain (otalgia) and ear inflammation (otorrhea); ear is sensitive to being pulled

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104
Q

What predisposes someone to acute otitis externa?

A

Water in the ears, blockage

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105
Q

What is the major pathogen that causes acute otitis externa?

A

Pseudomonas aeurginosa

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106
Q

What causes chronic otitis externa?

A

Usually over-cleaning of the ear canal

Leads to itching, not pain

107
Q

How do you treat chronic otitis externa?

A

topical steroids

108
Q

What causes malignant otitis externa?

A

invasive pseudomonas aeurginosa

109
Q

What type of bacteria is pseudomonas aeruginosa?

A

Gram negative rod; aerobic

**Key: has green pgiments pyocyanin and pyoverdin

110
Q

What type of infections does pseudomonas aeruginosa cause?

A

Local infections like otitis externa, cystic fibrosis lungs, hot tub folliculitis, UTIs, etc

111
Q

Who is at risk for pseudomonas aeruginosa infections?

A

Immunocompromised, burn patients, and diabetics

112
Q

Where do we encounter pseudomonas aeruginosa?

A

In the environment (water, soil, air, food) –> NOT endogenous

113
Q

How does pseudomonas aeruginosa enter the body?

A

Lung, intestine, wound

Forms biofilms

114
Q

Does pseudomonas aeruginosa spread?

A

Yes, in immunocompromised or with burns, wounds

115
Q

How does pseudomonas aeruginosa multiply?

A

Can grow on diverse substrates, even in disinfectants and cleaning materials

Does not ferment

116
Q

How does pseudomonas aeruginosa evade defenses?

A

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
Q

What does mutated pseudomonas aeruginosa produce in people with cystic fibrosis?

A

Alginate polysaccharide, a mucoid on top of the thick mucus they already have. Double whammy.

118
Q

What damage does pseudomonas aeruginosa cause?

A

Inflammation and exotoxins (exotoxin A, similar to diphtheria toxin), type 3 secreted toxin, and other numerous extracellular enzymes

119
Q

Outcome in pseudomonas aeruginosa infections?

A

Self-limiting in healthy people; problematic in immunocomprised people and burn patients

Not normally transmitted between people

120
Q

Prevention of pseudomonas aeruginosa infections?

A

No vaccines. Just be vigilant about infection control in the hostpital

121
Q

Treatment of pseudomonas aeruginosa?

A

Antibiotics BUT p. aeuginosa is highly resistant to numerous antibiotics

122
Q

What are the four general ways respiratory pathogens gain entry to our respiratory tract?

A
  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
Q

If a respiratory pathogen does not spread, can it still cause systemic effects?

A

Yes, their toxin(s) can cause systemic effects even if the pathogen stays put

124
Q

What is the main defense of a non-immune host against respiratory pathogens?

A

The mucociliary escalator of the URT

125
Q

Outside of the mucociliary escalator, what other defenses must respiratory pathogens evade?

A

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
Q

General damage caused by respiratory pathogens?

A

Toxins (local or systemic), inflammation, adaptive immune response (TB granulation)

127
Q

General outcome of respiratory pathogens?

A

Self-limiting to death

128
Q

What are some representative URT infections?

A

Sinusitis, otitis media, pharyngitis, laryngitis, bronchitis, whooping cough, diphtheria

129
Q

What causes most pharyngitis?

A

Virus

130
Q

What are the bacteria responsible for pharyngitis?

A

Streptococcus pyogenes, Neisseria gonorrhoeae, Corynebacterium diphtheriae (in unvaccinated)

131
Q

Basic microbiology of Strptococcus pyogenes?

A

Gram + cocci in chains

beta hemolytic

Has Group A carbohydrate, M protein (fibrillar layer), hyaluronic capsule, and lipoteichoic acid on its surface

132
Q

What suppurative diseases does Streptococcus pyogenes cause?

A

Pharyngitis - Scarlet fever, pneumonia, skin infections (wide range), streptococcal toxic shock syndrome

133
Q

What toxin is responsible for the “sand paper rash” seen in Scarlet Fever?

A

Spe toxin

134
Q

What are the non-suppurative complications of Streptococcus pyogenes?

A

Rheumatic fever, glomerulonephritis, and immunologically mediated sequellae

NOTE: These complications are due to inflammation and not infection spread

135
Q

Symptoms of pharyngitis?

A

Fever, exudative tonsils, lymphadenitis

NO cough, NO rhinorrhea

136
Q

What is Scarlet Fever?

A

Pharyngitis + rash

Rash is a red, diffuse rash that has a “sandpaper” feel

137
Q

What are the symptoms of Scarlet Fever?

A

Red, diffuse rash, strawberry tongue, red cracker lips, circumoral pallor, and red cheeks

138
Q

How do we encounter/transmit streptococcus pyogenes?

A

Human only

HIGHLY contagious

139
Q

How does streptococcus pyogenes enter?

A

URT, skin, adherence via M protein-fibrinogen, LTA and fibronectin binding protein

140
Q

Does streptococcus pyogenes spread?

A

YES!

141
Q

What enzymes help streptococcus pyogenes spread?

A

Hyalurinidase breaks down intercellular matrix

DNase B liquefies lysed neutrophil DNA so bacteria can move and not get suck in the gunk

142
Q

How does streptococcus pyogenes multiply?

A

Fastidious, needs blood agar

143
Q

How does streptococcus pyogenes evade host defenses?

A

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
Q

How does streptococcus pyogenes cause damage?

A

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
Q

What is the outcome of a streptococcus pyogenes infection?

A

Highly variable depending upon the strain, patient circumstances, and treatment

Pneumonia can be lethal

Pharyngitis self-limiting except for rheumatic fever and glomerulonephritis

146
Q

Microbiology of Corynebacterium diphtheriae?

A

Gram + non-sporeforming rod

147
Q

Clinical manifestations of diphtheria?

A

sore throat, low-grade fever, dysphagia, pseuomembrane (~50%)

“bull neck” sppearance

148
Q

What are the systemic effects of diphtheria toxin?

A

Carditis, neurotoxicity,renal tubular necrosis, croup & asphyxia

149
Q

Transmission of diphtheria?

A

Inhalation; human only

Restricted to URT

150
Q

How does diphtheria multiply?

A

Fastidious

151
Q

How does diphtheria evade host defenses?

A

Not much to deal with in the URT

152
Q

How does diphtheria cause damage?

A

The diphtheria toxin

153
Q

Outcome of diphtheria?

A

Can be fatal if untreated

154
Q

Diphtheria treatment?

A

Antibiotics + antitoxin

Can be prevented with toxoid vaccine

155
Q

Where is the diphtheria toxin encoded?

A

On a bacteriophage (lysogenic conversion)

156
Q

What type of toxin is the diphtheria toxin? What does it do?

A

A-B type toxin

ADP ribosylates EF-2 and inhibits protein synthesis (ultimately cytotoxic)

157
Q

How does diphtheria toxin damage heart, nerves, kidneys, etc?

A

They all have a heparin-binding epidermal growth factor receptor that it can bind to.

Death from heart/nervous system damage

158
Q

What type of bacteria is Bordetella pertussis (whooping cough)?

A

Gram - rod (coccobacillus)

159
Q

What are the three clinical courses of pertussis?

A

Catarrhal (cough, rhinorrhea)

Paroxysmal (coughing spasms, whoop, cyanosis, vomiting, OK in between episodes)

Convalescent (decreasing but continuing symptoms)

160
Q

What is the most contagious phase of pertussis?

A

Catarrhal (where you just have cough and rhinorrhea)

161
Q

Complications of pertussis?

A

hospitalization, pneumonia, seizures, encephalopathy, death

162
Q

How is pertussis transmitted?

A

Human only inhalation

Infected adolescents/adults are the source for infants and children

163
Q

How does pertussis enter?

A

Restricted to the URT

Adheres to ciliated epithelium via filamentous hemagglutinin (FHA), pili/fimbriae, and pertactin

164
Q

How does pertussis multiply?

A

Fastidious

Bordet-Gengou plates

165
Q

How does pertussis evade host defenses?

A

Not much in the URT

Tracheal Cytotoxin (TCT) kills mucociliary escalator; predisposes host to other infections

166
Q

How does pertussis cause damage?

A

Via the pertussis toxin

167
Q

What type of toxin is the pertussis toxin? What does it do?

A

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
Q

What is tracheal cytotoxin (TCT)?

A

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
Q

Outcome of pertussis?

A

Usually self-limiting but can be fatal

170
Q

How do you prevent pertussis?

A

Vaccine! Currently is an acellular vaccine of pertussis toxoid + FHA

171
Q

What antibody response is used in the diagnosis of streptococcus pyogenes pharyngitis?

A

anti-DNaseB + Streptolysin O antibodies

172
Q

What respiratory disease is characterized by a “barky” cough?

A

Whooping cough/bordetella pertussis

173
Q

What is adenovirus? What is it responsible for?

A

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
Q

Adenovirus structure and genome?

A

Non-enveloped icosahedral capsid

dsDNA; medium-size genome

175
Q

How does Adenovirus transcribe its genes?

A

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
Q

Where are new Adenovirus virions assembled?

A

The cell nucleus

177
Q

Adenovirus mode of transmission?

A

Fecal-oral; may establish viremia

178
Q

Where does adenovirus replicate?

A

Respiratory tract, eyes, GI tract, urinary bladder

179
Q

What virus is responsible for ARD in military recruits and children in boarding schools?

A

Adenovirus

since everyone is in close proximity to each other in a stressful environment with not much sleep

180
Q

Four hallmark symptoms of enteroviruses?

A

Conjunctivitis, respiratory symptoms, gastroenteritis and diarrhea, and hemorrhagic cystitis

181
Q

How is adenovirus diagnoses?

A

Cell culture or viral antigen detection (ELISA)

182
Q

Prevention of adenovirus?

A

A live, wild type vaccine is given to military recruits but otherwise not widely distributed

183
Q

How does adenovirus evade host defenses?

A

It encodes countermeasures against MHC 1 expression and apoptosis

184
Q

What class of viruses is the second most prevalent cause of the common cold?

A

Coronaviruses

185
Q

What is SARS? What type of virus is it?

A

Severe Acute respiratory Syndrome

Coronavirus

186
Q

What is MERS? What type of virus is it?

A

Middle East Respiratory Syndrome

Coronavirus

187
Q

What helps coronaviruses withstand the conditions of the GI tract?

A

Their glycoprotein envelope

looks like a crown

188
Q

Coronavirus structure?

A

Enveloped

+ssRNA

Largest of the human RNA viruses

189
Q

Where does coronavirus replication take place?

A

In the cytoplasm of the host cell

190
Q

How are new coronaviruses released from their host cell?

A

Via exocytosis

191
Q

Where does coronavirus replicate?

A

In the respiratory epithelium (it infects the upper respiratory tract)

192
Q

How are coronaviruses transmitted?

A

droplets and aerosols

and some by the fecal-oral route

193
Q

Coronaviruses have their highest incidence in what population(s)?

A

Infants and children

194
Q

What is different about the incubation period of coronaviruses vs. rhinoviruses?

A

Coronaviruses have a longer incubation period (more than 3 days)

195
Q

What does SARS cause? Symptoms of this?

A

Atypical pneumonia

Sx: high fever (over 38 C), chills, rigors, headache, dizziness, malaise, mylagia, difficulty breathing & cough

196
Q

What animal transmits SARS to humans?

A

palm civets

197
Q

How is SARS transmitted?

A

Respiratory is primary route but it also spreads via sweat, urine, and feces

198
Q

What does MERS cause? Symptoms of this?

A

Atypical pneumonia

Sx: high fever (over 38 C), chills, rigors, headache, dizziness, malaise, mylagia, difficulty breathing & cough

199
Q

How is MERS transmitted to humans?

A

Via camels

200
Q

Mortality of MERS and SARS?

A

MERS is 40%, SARS is 10%

201
Q

What percentage of SERS patients require mechanical ventilation?

A

Over 70% (during the acute phase)

202
Q

How is MERS transmitted person-to-person?

A

Respiratory secretions are the main route but also present in sweat, urine, and feces

(human-to-human transmission requires very close contact!)

203
Q

Outcome of coronaviruses?

A

Self-limiting

204
Q

If you perform a lab test to diagnose SARS or MERS what would you order?

A

Viral RNA detecting in stool and respiratory fluids by rt-PCR

205
Q

Different subtypes of influenza virus form through a genetic process called…?

A

reassortment

206
Q

What comprises the influenza genome?

A

8 -ssRNA segments

207
Q

How are influenza viruses classified?

A

Family: orthomyxovirus

Types: A, B, C

A more pathogenic than B. C is not a clinical problem

208
Q

The primary reservoir of influenza A is in what animal?

A

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

209
Q

Structural properties of influenza?

A

Enveloped capsid

Two surface glycoproteins (HA and NA) play an essential role in cell entry and antigenicity

210
Q

What causes the classic flu-like symptoms of influenza?

A

Interferon and lymphokine responses to the viral infection

211
Q

What causes the local symptoms of influenza?

A

Epithelial cell damage to ciliated and mucosal cells of the upper airways

212
Q

People infected with influenza are more susceptible to what?

A

bacterial superinfections because of the loss of natural barriers (damage to ciliated epithelial cells)

213
Q

Will influenza antibody help prevent future infections?

A

Only if its the same serotype

214
Q

What immune response(s) is critical for resolution of the influenza infection?

A

Interferon and cell-mediated immunity

215
Q

How is influenza prevented?

A

Vaccine

  1. Killed, inactivated vaccine that is injected
  2. FluMist - live, attenuated vaccine
216
Q

How is influenza treated?

A

If its the first 48 hours you can administer:

  1. Oseltamivir (tamiflu) neurominidase inhibitor
  2. Zanamivir (Relenza) neurominidase inhibitor
217
Q

Where does influenza replicate?

A

In the nucleus

218
Q

What drugs target the matrix of influenza cells?

A

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.

219
Q

What is the most common cause of fatal acute respiratory tract infections in infants and young children?

A

Respiratory syncytial virus (RSV)

220
Q

What is bronchiolitis?

A

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

221
Q

Does RSV induce immunity?

A

No, reinfection occurs throughout life

Maternal antibodies also do not prevent infection during the first year of life for some reason

222
Q

If a question stem mentions “sudden chills episode” and “rust-colored sputum” what pathogen should you immediately think of?

A

Streptococcus pneumoniae

223
Q

What two categories of pneumonia are there?

A
  1. Community-acquired

2. Hospital acquired (nosocomial)

224
Q

What pathogen is the most common cause of community acquired pneumonia?

A

Streptococcus pneumonia

225
Q

What pathogens are responsible for atypical pneumonia?

A

Mycoplasma pneumoniae, chlamydia pneumoniae, respiratory viruses like influenza, adenovirus, parainfluenza and RSV

226
Q

If someone has pneumonia after influenza, what pathogen is most likely responsible?

A

Staph aureus

227
Q

What pneumonia-causing pathogen is more common in smokers?

A

H. influenzae

228
Q

General characteristics of typical pneumonia (onset, sx)

A

Rapid onset, more severe symptoms, productive cough, purulent sputum, chest xray shows dense consolidation

229
Q

General characteristics of atypical pneumonia (onset, sx)

A

Subacute onset (slower), less severe symptoms (“walking pneumonia”), NONproductive cough, a little bit of white phlegm, patchy interstitial infiltrates

230
Q

On a chest xay, how can you differentiate typical vs. atypical pneumonia?

A

Typical has dense consolidation in the affected area whereas atypical has patchy interstitial infiltrates

231
Q

Microbiology of streptococcus pneumoniae?

A

Gram + diplococci

Carbohydrate capsule (imp. for vaccines)

Alpha hemolytic

232
Q

What disease does streptococcus pneumoniae cause?

A

MOPS!

Meningitis
Otitis Media
Pneumonia
Sinusitis
Sepsis
233
Q

What populations are predisposed to pneumococcal pneumonia (S. pneumoniae)?

A

Very young, elderly, asplenic, sickle cell (functionally asplenic), complement deficient

234
Q

Streptococcus pneumoniae encounter/transmission?

A

Transmitted via respiratory droplets; human only

Part of our normal flora!

235
Q

How does streptococcus pneumoniae enter?

A

Colonizes in the oropharynx and then is aspirated into the lung

236
Q

Does streptococcus pneumoniae spread?

A

Not necessary, but it can in the case of meningitis (blood to CNS)

237
Q

How does streptococcus pneumoniae multiply?

A

It grows well in serous fluid in the alveoli space

Cultured in blood agar

238
Q

How does streptococcus pneumoniae evade host defenses?

A

It has an antiphagocytic capsule and has an sIgA protease

239
Q

How does streptococcus pneumoniae cause damage to the host?

A

Peptidoglycan causes inflammation

Pneumolysin is a toxin that binds cholesterol in the host cell membrane

240
Q

What are the four stages of pneumonia?

A
  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

241
Q

Outcome of streptococcus pneumoniae infection?

A

Self-limiting to fatal

242
Q

How is streptococcus pneumoniae prevented?

A

Vaccine!

23-valent for adult (IgM) and 7-valent for children (IgG)

243
Q

Microbiology of Legionella pneumophilia?

A

Gram - rod

Stains irregularly so a silver stain has to be used

244
Q

What disease does Legionella pneumophilia cause?

A

Legionnaire’s disease (pneumonia of the predisposed)

Pontiac fever (flu-like in anyone)

245
Q

How is Legionella pneumophilia encountered and transmitted?

A

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

246
Q

How does Legionella pneumophilia multiply?

A

Fastidious

Special medium of buffered charcoal yeast extract (BCYE) is used

It replicates within amoeba in the wild and within macrophages in humans

247
Q

How does Legionella pneumophilia evade host defenses?

A

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

248
Q

What type of immunity is required to attack Legionella pneumophilia?

A

Cell-mediated (because its intracellular!)

249
Q

What damage does Legionella pneumophilia cause the host?

A

Alveolar inflammation

250
Q

What is the outcome of a Legionella pneumophilia infection?

A

Can be fatal BUT treatable with antibiotics

251
Q

Is Legionella pneumophilia transmissible between humans?

A

Nope, it’s a dead-end environmental organism

252
Q

What disease does Mycoplasma pneumoniae cause?

A

Tracheobronchitis/atypical (walking) pneumonia

253
Q

Microbiology of Mycoplasma pneumoniae

A

Wall-less (lacks peptidoglycan) and thus resistant to B-lactams and other PG-active antibiotics

Lacks definite shape and does not gram stain

254
Q

How is Mycoplasma pneumoniae encountered/transmitted?

A

Respiratory droplet transmission; human only

Very labile, very contagious

255
Q

How does Mycoplasma pneumoniae enter?

A

Inhalation and then it adheres via Terminal adhesin protein (P1)

**does not reach alveoli, P1 sticks to ciliated epithelium only

256
Q

How does Mycoplasma pneumoniae spread?

A

Usually restricted to URT surface (where cilia are!)

Very rarely spreads

257
Q

How does Mycoplasma pneumoniae multiply?

A

It needs our sterols

Takes weeks to culture in special media

258
Q

What damage does Mycoplasma pneumoniae cause the host?

A

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

259
Q

How do you treat Mycoplasma pneumoniae?

A

Erythromycin, doxycycline

260
Q

What is the outcome of Mycoplasma pneumoniae?

A

Usually self-limiting

261
Q

Microbiology of Pseudomonas aeruginosa?

A

Gram - rod, aerobic

Opportunistic environmental pathogen

262
Q

What disease does Pseudomonas aeruginosa cause?

A

Local infections: Cystic Fibrosis patient lungs, swimmer’s ear, UTI

Systemic in immunocompromised and burn patients

263
Q

Why is Pseudomonas aeruginosa particularly bad in patients with Cystic Fibrosis?

A

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.

MS1 Spring (10 decks)

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