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HUMAN HEALTH AND DISEASE > Infection of the respiratory tract > Flashcards

Infection of the respiratory tract Flashcards

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1
Q

Is the lung sterile?

A

-No
-it has its chracteristic microbiota that is altered in diseases e.g infections, asthma, COPD.

look slide 2 page 5

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2
Q

What is the anatomy for the upper respiratory tract?

A

slide 1 page 3

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3
Q

What is the anatomy for the lower respiratory tract?

A

slide 2 page 4

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4
Q

Which group of people are more likely to get respiratory infections?

A

Children + Elderly (65+)

-Diseases are usually more severe in these age groups

-These groups act as reservoirs and vectors of disease (more transmission)

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5
Q

What are the major respiratory pathogens in the young?

A

Major respiratory pathogens in the young: Respiratory Syncytial Virus (RSV), Bordetella pertussis, Streptococcus pneumoniae, Haemophilus influenzae b (Hib)

Malnutrition is a major underlying contributor to these deaths.

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6
Q

What are the host’s innate defense against respiratory microbes and what are their functions?

A

Mucus- trapping microbes/barrier

Mucus flow- removal of microbes

Epithelial cell tight junctions- barrier (preventing microbes penetrating between them)

Air flow- removal of microbes

Commensal microbiota- niche occupation

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7
Q

What effector molecules are produced by the host innate responses and what are their functions?

A
  1. Lysozyme - bacterial wall destruction
  2. α-defensin - microbicidal (source neutrophils)

3.β-defensin - microbicidal (source epithelial cells)

4.SLPI (Secretory Leukocyte Protease Inhibitor) - bactericidal, viricidal (blcoks viral DNA synthesis)

5.Cathelicidin/LL-37 - bactericidal and mucin secretion enhancer

6.Lactoferrin - sequesters iron

7.Complement - microbicisal, chemoattractant, opsonin

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8
Q

Why don’t epithelial cells have pathogen recognition receptors on their surface?

A

-Because there’s a commensal microbiota in the lungs.

-So you don’t want to respond to the microbes on the surface or else that will lead to hyperinflammation in the lung, causing damage.

-Instead, epithelial cells have these receptors internally

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9
Q

What is the second role of epithelial cells in mucosal immunity apart from microbial recognition?

A

Cytokine production:

-Once a pathogen is detected, one of the first things to happen is an increase in IL-8 production & you’ll see the upregulation of surface ICAM 1 & 2 expression

-ICAM 1 + 2 = chemokines which will recruit T cells, neutrophils and macrophages to respond to the microbe.

-Other chemokines will also be produced e.g. MIP1-alpha

-Pro-inflammatory cytokines will also be produced e.g. IL-1alpha, IL-1beta etc.

slide 4 page 11 and 12

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10
Q

What can epithelium infection result in?

A

-Functional impairment (epithelium cells dont function as they usually do)

-Defects in cilia action, mucus movement

-Loss of barrier function

-Mucus hyper-secretion

-Pro-inflammatory cytokine & chemokine release (could lead to cytokine storm)

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11
Q

Are different regions of the respiratory tract susceptible to different types of microbe/infection?

A

Yes, upper respiratory tract infections are mostly viral & lower respiratory tract infections are mostly bacterial

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12
Q

What are the most common respiratory tract viral infections to occur?

A

-Common cold
-Flu
-Respiratory Syncitial Virus (RSV)

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13
Q

What group of viruses causes the most colds by far and what other viruses cause colds

A

Rhinoviruses (accounts for ~60% of colds)

Coronaviruses are 2nd place, accounting for 15% of colds

Other agents include influenza viruses, RSVs & sporadically, adenoviruses

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14
Q

How many different serotypes are there of rhinoviruses and coronaviruses that cause the common cold?

A

-Over 100 different serotypes of rhinovirus

-2 serotypes of coronavirus

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15
Q

What family is rhinovirus from?

A

Picornaviridae

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16
Q

What is the biological structure of a rhinovirus?

A

Non-enveloped, single-stranded, +ve RNA genome.

look at slide 7 page 19

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17
Q

What are symptoms of the common cold caused by rhinoviruses?

A

Coughing, sneezing, hypersecretion of mucus, but rarely fever

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18
Q

Can you generate protective neutralising anti-viral antibodies against rhinoviruses

A

Yes, but there are ~150 different serotypes & within those serotypes there will be alterations & mutations, the chances of you being protected against the next virus that will infect you are very slim

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19
Q

What do the major & minor viral groups from rhinoviruses bind to?

A

-The major viral groups (RV-A & B) bind to ICAM-1 on epithelial cell

-Minor group viruses bind to low-density lipoprotein receptor (LDLR)

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20
Q

Which family is RSV (respiratory syncytial virus) a member of?

A

Paramyxoviridae

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21
Q

What is the structure of RSV?

A

Single-stranded, -ve strand RNA virus (RNA needs to be reverse-transcribed & converted into a +ve strand before it can act as mRNA)

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22
Q

How big is the genome of RSV?

A

~15,200 nucleotides
11 sub-genomic mRNAs

slide 7 page 21

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23
Q

Which groups of people are more likely to get RSV?

A
  1. Elderly
    - Often fatal, wheezing = progressive hypoxia
    -Risk factors: COPD, heart disease
  2. Infants
    -At least one RSV infection by 2 years
    -Highest risk 1-6 months
    - can lead to bronchiolitis
    -largest cause of hospitalisation in infants
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24
Q

What is RSV bronchiolitis?

A

-Infection and inflammation of bronchioles

-Buildup of mucus and swollen mucus membranes; wheezing from partial obstruction

look at slide page 24

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25
How do you treat RSV?
Neutralising antibody to prevent infection (Synagis/Palivizumab a monoclonal antibody) - only used in high-risk patients because it's too expensive Vaccination
26
What is the problem with RSV vaccines?
-Repeated infection can occur with RSV even with an adapted immune response. -Neonates and infants respond poorly to vaccines -Vaccine enhances wrong immune response, exacerbates diseases and causes pathology
27
Which family is Influenza a member of?
Orthomyxoviridae slide page 27
28
What is the structure of influenza virus?
-Enveloped, single strand, -ve RNA genome made up of 8 'chromosomes'. On the envelope, there are 2 key surface proteins: -Neuraminidase (removes virion surface glycoproteins) -Haemagglutinin (which helps bind to its target cells) slide 10 page 28
29
Describe the transmission of the influenza virus.
- Transmitted directly from person to person in aerosols caused by sneezing and coughing - Inhaled aerosol is transferred to the lower respiratory tract, although some infection occurs in the nasopharynx - Neuraminidase action liquifies mucus which may help produce aerosols for sneezing
30
Describe the pathogenesis of the influenza virus.
-Surface mucosal epithelium is destroyed, undergoing desquamation as bronchial epithelial cells are infected and killed. - Further damage is caused by host immune mediators – interferon, ISGs, endogenous pyrogens (cytokine storm)
31
what are the symptoms of influenza virus?
- Local symptoms – cough, sore throat, nasal discharge (oedema and cellular inflammation - Systemic symptoms – pyrexia (fever), aching muscles, general ill feeling. -Symptoms not due to viraemia
32
How does a cytokine storm cause respiratory failure?
Cytokine storm: Over-activation of the host immune system results in secretion of large levels pro-inflammatory cytokines (e.g. TNFα, Interferon-γ) Because of High levels of proinflammatory cytokines: -Inflammatory cell recruitment -pulmonary oedema Evetually leads to Lung damage + air way occlusion (build up of fluid due to oedema). Acute respiratory distress syndrome and Death.
33
What is antigenic drift in influenza virus?
Antigenic drift: -Minor changes from point mutations -Slow, continuous process -Some protection carried over from previous infections -Associated with epidemics (regional outbreak look at slide 11 page 31
34
What is antigenic shift in influenza virus?
Antigenic shift: -Major changes in multiple genes, RNA segments exchanged between viral strains. -Rapid/Sudden process -No protection from past infections -Associated with pandemics (worldwide) look at slide 11 page 31
35
How does COVID-19 relate to SARS-CoV & MERS-CoV in terms of lethality & transmissibility?
COVID-19 is less lethal but has a higher transmissibility.
36
What is the host receptor of SARS-CoV-2?
Host receptor is ACE2 which is present on epithelial cells, endothelial cells & macrophages. slide 12 page 35
37
What are the main target cells of SARS-CoV-2?
-Airway & alveolar epithelial cells -Vascular endothelial cells -Alveolar macrophages
38
How is SARS-COV2 transmitted?
-Mainly through droplets and aerosols (smaller than 5um diameter which them becomes airborne) -Direct contact -Indirect contact slide 12 page 36
39
How is SARS-CoV-2 different to SARS-CoV?
Unlike SARS-CoV, SARS-CoV-2 can also infect the upper respiratory tract which boosts transmissibility
40
What is the mechanism of SARS-CoV-2
1. enters the airway epithelia cells leading to tissue injury. 2.excessive infiltration of inflammatory immune cells 3. systemic cytokine storm 4. this can lead to: - cell death - pro longed myocardial inflammation -fibritic lung ARDS
41
What are the symptoms of COVID-19?
slide 13 page 38
42
what is whooping cough?
-Bacterial infection of the respiratory tract. - Once very common and potentially life-threatening in infants - Highly contagious, spread by airborne droplet aerosols - Today, whooping cough still effects 20-40 million people worldwide each year and causes between 200,000- 400,000 fatalities
43
What is the incubation period & 3 stages of whooping cough?
Incubation period: 4-21 days 1st stage: Catarrhal stage, 1-2 weeks 2nd stage: Paroxysmal stage, 1-6 weeks 3rd stage: Covalescent stage, weeks-months
44
What is whooping cough caused by?
Bordetella pertussis - aerobic, gram negative coccobacillus (bacterial infections of the respiratory tract)
45
Which family does Bordetella pertussis belong to?
Alcaligenaceae family
46
Describe what is meant by whooping cough primarily being a toxin-mediated disease.
- The bacteria itself doesn’t really cause much of the disease, its the toxins secreted that do. -Toxins secreted when bacterium adheres to ciliated epithelium of respiratory tract and colonises host, secreting toxins Toxins lead to: -Death of epithelial cells -Decrease in ciliary beating -Accumulation of mucus and cell debris, triggering coughing.
47
gives examples of toxins that the whooping cough bacteria releases.
Pertussis toxin Adenylate Cyclase Toxin Tracheal cytotoxin Dermonecrotic toxin Heat-labile toxin
48
What vaccine is used against whooping cough?
Acellular vaccines (as opposed to the previous whole-cell vaccine that was used).
49
What are potential reasons for surges in whooping cough cases?
-Waning immunity (loss of protective antibodies) -Increased recognition & reporting -Increased toxin production by infecting strains -Antigenic differences between vaccine & infecting strains
50
Give some examples of TB risk factors.
Being a healthcare worker, AIDS, extremes of age, malnutrition, diabetes, Hodgkin's lymphoma, contact with active TB case
51
epidemiology of tuberculosis.
Highly contagious disease, airbourne spread Infected/carrier individual will infect between 10-15 new people each year Although previously considered under control, mortality still runs in excess of 1.5 million each year. – This number is now increasing year on year
52
what is tuberculosis causes by?
Caused by mycobacteria tuberculosis
53
what family does mycobacteria tuberculosis belong to?
Causative agent is a member of the Mycobacteriaceae family, genus Mycobacteria
54
What is the difference between TB infection/latent TB and active TB/TB disease?
1. TB infection/Latent TB: Individual is not infectious/contagious at this point Characterised by: -Presence of M. tuberculosis in the body -Patient is asymptomatic Antibiotics can be used to prevent progression to Active TB disease. 2. Active TB/TB Disease Active TB is infectious , spread by coughing, sneezing or any exhalation of air Active TB is associated with symptoms, including: -Coughing -Weight loss -Appetite loss -Fever -Chest pains -Night sweats
55
How is TB treated?
4 standard antibiotics used simultaneously: -Isoniazid -Rifampin -Pyrazinamide -Ethambutol To be taken for 4-6 months (with nasty side effects) Problem with treatment compliance, leading to drug resistance. Strains exist that are MDR, XDR and now emerging strains that are CDR
56
Describe the pathogenesis of TB.
-Infects via alveolar macrophages which then distribute bacteria further -Facultative intracellular pathogen - inhibits phagasome-lysozyme fusion
57
what is the host response to TB?
- Host responses to M. tb are predominantly cell- mediated -Several different key events: infiltration macrophages lymphocytes granulomas
58
What is a TB granuloma?
-An organised aggregate of immune cells surrounding foci of infected cells/tissues -(so it's a chronic inflammation event) -It's a host attempt to limit the dissemination of the M. tuberculosis bacteria Depending on the prevailing cytokine microenvironment, this either works or fails slide 18 page 53
59
What are the 2 responses in a TB granuloma?
TH1 - activates M1 macrophages which keeps TB in granuloma + prevents growth + kills more rapidly TH2- Activates M2 macrophages which form giant/foam cells + bacteria can replicate and reproduce. Large amounts of bacteria is disseminated and released. BAD slide 18 page 54
60
why are respiratiry disese dentist concern?
Dentists may be the first to see the evidence of a serious infection The end of the respiratory tract is the mouth – and it points at you...

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