Airborne Infections Flashcards

1
Q

What are some of the human respiratory tracts defence mechanisms?

A
Physical defences
Filtration systems
Only small particles will reach the alveoli (<5 micrometers)
Mucocilary stream
Coughing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the mucocilary system act as a defence?

A

Coats surface of respiratory tract right down to alveoli, binds any particulates as they enter the respiratory tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the alveolar macrophages?

A

Primary defence of the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the effector cells for alveolar macrophages?

A

Phagocytic

Microbicidal activities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the antigen presenting cells in alveolar macorphages?

A

Induction of acquired T-cell responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the alveolar inflammatory (innate) response?

A

Influx of neutrophils (phagocytic and microbicidal) into the alveoli (diapedesis)
In response to chemotactic factors such as complement to combat the infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the alveolar macrophages adaptive responses?

A

IgG and C- opsonins (promote phagocytosis)

Lymphoid tissue providing T and B cells for the immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the humoral defences of IgA antibodies?

A
Predominant class in the upper airways, more IgG in the lungs
Mainly dimer form, S-IgA interacts with the mucin (secreted through epithelial)
Prevents attachment of microorganisms neutralisation of toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are other factors in humoral defences?

A

Lung surfactant- may enhance bactericidal activity of macrophage and complement
Lysozyme- digests bacterial peptidoglycan (enzyme)
Transferrin and lactoferrin- bind available iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What bacterium causes diphtheria?

A

Corynebacterium diphtheriae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the structure of Corynebacterium diphtheriae?

A

Non-sporing (no spores, no dormant form of organism), aerobic Gram-positive bacillus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where does Corynebacterium diphtheriae grow?

A

Doesn’t go further than the back of the throat

Grows in upper respiratory tract (usually throat)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where does corynebacterium diphtheriae cause damage?

A

Extracellular

Does not invade the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What shape are C. diphtheria?

A

Club shaped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the steps of pathogenesis?

A

Inflammation of the pharynx
Significant inflammatory response
Pseudo-membrane and toxins associated with deaths
Largely toxin mediated disease (diphtheria toxin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the other factors in the cause of pathogenesis?

A

IgA protease- cleaves IgA
Pili for mucosal colonization
Consequence of inflammatory response- leathery pseudo-membrane of bacterial cells, dead inflammatory cells and fibrin
Cord factor (like M. tuberculosis) cell wall component
• Toxic for phagocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the diphtheria toxin responsible for?

A

Symptoms of diphtheria

18
Q

Where is the diphtheria toxin?

A

Encoded on a bacteria phage

19
Q

What carries the tox gene?

A

Lysogenic bacteriophage- destroys any cell it gets into, very potent, not a lot is required

20
Q

What is ADP ribosyltransferase for?

A

EF2 (elongation factor 2)
o Involved in protein synthesis
o Transfers ADP-ribose from NAD to EF2

21
Q

What are deaths in diphtheria due to?

A

A combination of partial suffocation and tissue-destroying effects of the toxin

22
Q

How is diphtheria treated?

A

(Horse) antitoxin- neutralises toxin
Antibiotics- must be given early
Penicillin, erythromycin

23
Q

What is the diphtheria vaccine?

A

Triple vaccine DTaP
Formalin-treated diphtheria toxin (toxoid) (D)
Ad tetanus toxoid (T) and pertussis acellular vaccine (aP)

24
Q

Why must diphtheria vaccination continue?

A

Vaccination does not prevent the carriage and the organism persists in the community

25
Q

How many deaths and infection are caused by tuberculosis?

A

9m new cases p.a. with approx. 1.7m deaths and 1/3 of population infected in some countries

26
Q

Why are there so many tuberculosis related deaths?

A

HIV african countries means they have more vulnerable immune systems
Continual antibiotic resistance to TB

27
Q

What is the bacterium that causes tuberculosis?

A

Mycobacterium tuberculosis

28
Q

What is the structure of mycobacterium tuberculosis?

A

Slow growing, non-sporing, aerobic, Gram-positive bacillus

29
Q

How is Mycobacterium tuberculosis acquired?

A

Inhalation, tubercle bacilli survive for long periods in air or dust
From milk, from cases of bovine TB (mycobacterium bovis), before pasteurisation

30
Q

What is the primary pathogenesis of TB?

A

Lung disease but may affect any organ including a cause of meningitis

31
Q

What is the damage of TB due to?

A

Not the toxin but the host immune response trying to combat this persistent organism

32
Q

What are the steps leading to pathogenesis of TB causing death?

A

Inhalation of bacteria
Bacteria reached lungs; enter macrophages
Bacteria reproduce in macrophages
Lesion begins to form (caseuous necrosis)
Lesion liquifies
Spread to blood, organs
Death

33
Q

What antibiotics are given to treat TB?

A

Prolonged treatment (6-18 months) with combinations of isoniazid, rifampicin and other drugs)

34
Q

What is the problem with antibiotics for TB?

A

Emergence of resistant strains

35
Q

What are some examples of the resistant strains of TB?

A

MDR-TB (mutli-drug resistant)
o Resistant to at least isoniazid and rifampicin, the two most powerful first-line drugs
XDR-TB (extensively drug resistant)
o As above, plus resistance to some second-line drugs

36
Q

What vaccine is used for TB?

A

Live attenuated vaccine

BCG (Bacille Calmette-Guerin)

37
Q

When was the first TB vaccine used in humans?

A

1921

38
Q

How many people have the TB vaccine?

A

3 billion to date

39
Q

What percentage of children are vaccinated for TB?

A

80%

40
Q

Why does the TB vaccine’s efficacy range from 80%-0%?

A

Vaccine batch variability
Human genetic factors
Pre-exposure to mycobacteria in environment

41
Q

Why has there been a resurgence in number of TB cases?

A

Neglect of health care programmes
Link with homelessness, drug abuse, migration of populations
Rapid international travel
Link with AIDS (HIV destroys CD4 cells)