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

Infection of the respiratory tract Flashcards

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
Q

How do you treat RSV?

A

Neutralising antibody to prevent infection (Synagis/Palivizumab a monoclonal antibody) - only used in high-risk patients because it’s too expensive

Vaccination

26
Q

What is the problem with RSV vaccines?

A

-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
Q

Which family is Influenza a member of?

A

Orthomyxoviridae
slide page 27

28
Q

What is the structure of influenza virus?

A

-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
Q

Describe the transmission of the influenza virus.

A
  • 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
Q

Describe the pathogenesis of the influenza virus.

A

-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
Q

what are the symptoms of influenza virus?

A
  • 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
Q

How does a cytokine storm cause respiratory failure?

A

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
Q

What is antigenic drift in influenza virus?

A

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
Q

What is antigenic shift in influenza virus?

A

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
Q

How does COVID-19 relate to SARS-CoV & MERS-CoV in terms of lethality & transmissibility?

A

COVID-19 is less lethal but has a higher transmissibility.

36
Q

What is the host receptor of SARS-CoV-2?

A

Host receptor is ACE2 which is present on epithelial cells, endothelial cells & macrophages.

slide 12 page 35

37
Q

What are the main target cells of SARS-CoV-2?

A

-Airway & alveolar epithelial cells
-Vascular endothelial cells
-Alveolar macrophages

38
Q

How is SARS-COV2 transmitted?

A

-Mainly through droplets and aerosols (smaller than 5um diameter which them becomes airborne)
-Direct contact
-Indirect contact

slide 12 page 36

39
Q

How is SARS-CoV-2 different to SARS-CoV?

A

Unlike SARS-CoV, SARS-CoV-2 can also infect the upper respiratory tract which boosts transmissibility

40
Q

What is the mechanism of SARS-CoV-2

A
  1. enters the airway epithelia cells leading to tissue injury.

2.excessive infiltration of inflammatory immune cells

  1. systemic cytokine storm
  2. this can lead to:
    - cell death
    - pro longed myocardial inflammation
    -fibritic lung ARDS
41
Q

What are the symptoms of COVID-19?

A

slide 13 page 38

42
Q

what is whooping cough?

A

-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
Q

What is the incubation period & 3 stages of whooping cough?

A

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
Q

What is whooping cough caused by?

A

Bordetella pertussis - aerobic, gram negative coccobacillus

(bacterial infections of the respiratory tract)

45
Q

Which family does Bordetella pertussis belong to?

A

Alcaligenaceae family

46
Q

Describe what is meant by whooping cough primarily being a toxin-mediated disease.

A
  • 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
Q

gives examples of toxins that the whooping cough bacteria releases.

A

Pertussis toxin
Adenylate Cyclase Toxin
Tracheal cytotoxin
Dermonecrotic toxin
Heat-labile toxin

48
Q

What vaccine is used against whooping cough?

A

Acellular vaccines (as opposed to the previous whole-cell vaccine that was used).

49
Q

What are potential reasons for surges in whooping cough cases?

A

-Waning immunity (loss of protective antibodies)
-Increased recognition & reporting
-Increased toxin production by infecting strains
-Antigenic differences between vaccine & infecting strains

50
Q

Give some examples of TB risk factors.

A

Being a healthcare worker, AIDS, extremes of age, malnutrition, diabetes, Hodgkin’s lymphoma, contact with active TB case

51
Q

epidemiology of tuberculosis.

A

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
Q

what is tuberculosis causes by?

A

Caused by mycobacteria tuberculosis

53
Q

what family does mycobacteria tuberculosis belong to?

A

Causative agent is a member of the Mycobacteriaceae family, genus Mycobacteria

54
Q

What is the difference between TB infection/latent TB and active TB/TB disease?

A
  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.

  1. 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
Q

How is TB treated?

A

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
Q

Describe the pathogenesis of TB.

A

-Infects via alveolar macrophages which then distribute bacteria further

-Facultative intracellular pathogen - inhibits phagasome-lysozyme fusion

57
Q

what is the host response to TB?

A
  • Host responses to M. tb are predominantly cell- mediated

-Several different key events:
infiltration
macrophages
lymphocytes
granulomas

58
Q

What is a TB granuloma?

A

-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
Q

What are the 2 responses in a TB granuloma?

A

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
Q

why are respiratiry disese dentist concern?

A

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…

HUMAN HEALTH AND DISEASE (58 decks)

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