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Biology of Disease > Lecture 26 - Bacterial Pathogenicity in the Respiratory Tract > Flashcards

Lecture 26 - Bacterial Pathogenicity in the Respiratory Tract Flashcards

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1
Q

Which bacteria causes the disease diphtheria? What shape is it and is it Gram +ve or -ve?

A

The gram positive rod Cornyebacterium diphtheriae.

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2
Q

Name the bacteria that are similar to Cornybacterium diphtheriae but affect animals. Which animals do they effect?

A

C. ulcerans and C. pseudotuberculosis, cause a range of respiratory diseases in sheep, goats, cows and horses.

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3
Q

Which toxin is produced by all of C. diphtheriae, C. ulcerans and C. pseudotuberculosis?

A

Diphtheriae toxin (DTX).

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4
Q

Where is the gene for DTX carried in the bacterial genome?

A

On a bacteriophage intergrated into the bacterial chromosome.

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5
Q

What is the DTX gene controlled by?

A

Bacterial transcription factor DtxR, which represses gene expression when bound by iron (Fe) - i.e. transcription is switched on in the host where the concentration of free iron is low.

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6
Q

Where do the Cornybacteria colonise?

A

The nasopharyngeal epithelium.

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7
Q

What structure does the DTX toxin have?

A

A-B structure.

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8
Q

What result does secretion of the DTX toxin have?

A

Its secretion results in intense local inflammation and damage to mucosal cells, growth of bacteria in inflammatory exudate, and formation of a pseudomembrane which occludes the trachea.
The toxin can also lead to irregular heartbeat, coma and death.

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9
Q

Describe the stages of action of the DTX toxin.

A

1) A single A-B polypeptide binds to heparin-binding epidermal growth factor (HB-EGF) receptor via the B subunit.
2) The A-B polypeptide is ‘nicked’ by host protease furin, but A and B remain covalently connected by a disulphide bridge.
3) The DTX toxin is taken up by endocytosis.
4) Acidification of the endosome by the V-ATPase proton pump (pumps H+ ions into the endosome) triggers B-dependant translocation of A across vesicle membrane into the cytosol.
5) In the host cytosol, the disulphide bond is reduced, A is released and blocks protein synthesis by ADP-ribosylating translation elongation factor-2 (EF-2).

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10
Q

Which bacterium causes pharyngitis?

A

Streptococcus pyogenes.

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11
Q

Where does S. pyogenes colonise in the respiratory tract and by what mechanism?

A

The throat epithelium via numerous adhesins.

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12
Q

Which toxins does S. pyogenes secrete? What are their respective actions?

A

Streptolysins O and S which are pore forming toxins causing beta-haemolysis.
Pyogenic toxins - superantigens that cause toxic shock syndrome.

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13
Q

Which enzymes does S. pyogenes secrete? What are their respective actions? (4)

A

C5a peptidase which inhibits chemotaxis
Hyaluronidase which breaks down tissue
Streptokinase which lyses clots
DNAse which depolymerises DNA in pus (reduces abcess viscosity)

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14
Q

What does the surface M protein of S. pyogenes bind to? How many serotypes does it have?

A

Complement factor H.

80 serotypes.

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15
Q

Which further complications can the acute infammatory infection by S. pyogenes lead on to? (2)

A

Rheumatic fever and glomerulonephritis.

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16
Q

Describe glomerulonephritis.

A

Accumulation of Ab-Ag complexes that lodge in kidney glomeruli to cause inflammation (Type III hypersensitivity)

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17
Q

Describe rheumatic fever.

A

Heart, joint granulomas plus fever, may lead to rheumatic heart disease. Believed to involve autoimmunity, e.g. to M protein.

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18
Q

Which animal does Streptococcus equi affect, and which disease does its infection cause?

A

Horses
It leads to the highly contagious disease strangles, characterised by a purulent nasal discharge and abscesses in the lymph nodes of the head and neck.

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19
Q

What can strangles lead on to and how is it spread?

A

The systemic disease bastard strangles, with the bacteria spreading via the lymphatic system to e.g. lungs, abdomen and brain.
As with S. pyogenes, later complications can include myocarditis.

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20
Q

What is thought to be an important reservoir of infection for S. equi?

A

The carrier state in recovered horse.

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21
Q

Which Lancefield groups are S. pyogenes and S. equi respectively?

A 
Pyogenes = Lancefield group A
Equi = Lancefield group C
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22
Q

What is the percentage genome sequence identity of S equi and S pyogenes?

A

80% similarity.

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23
Q

What is equibactin?

A

An iron-binding siderophore (important for acquisition of iron by S. equi)

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24
Q

Which toxin does S. equi NOT produce that S. pyogenes does.

A

Streptolysin O

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25
Q

Describe the capsules of S pyogenes compared to S equi.

A

S pyogenes has a polysaccharide capsule.

S equi has a poorly immunogenic capsule containing hyaluronic acid

26
Q

Which bacterium in pneumonia most often caused by?

A

Streptococcus pneumoniae.

27
Q

Where does S. pneumoniae colonise and using what?

A

The nasopharynx via adhesins.

28
Q

How does S pneumoniae resist removal by mucous and ciliated cells?

A

Using pneumolysin (a pore-forming toxin) and IgA protease.

29
Q

Which host factors predispose to colonisation by S pneumoniae?

A

Alcoholism and viral respiratory infection.

30
Q

Where does S pneumoniae migrate to after colonising the nasopharynx?

A

The lower respiratory tract.

31
Q

How does S pneumoniae avoid phagocytosis by alveolar macrophages?

A

Using pneumolysin and its polysaccharide capsule.

32
Q

What is the capsule of S pneumoniae made of and why is it of importance to the survival of the bacterium?

A

It is made of polysaccharide (carbohydrate) which means that it helps prevent opsonization and therefore phagocytosis by macrophages as well as aiding survival in droplets during dissemination.

33
Q

What is the lung damage caused by in a S pneumoniae infection?

A

Pneumolysin and inflammation.

34
Q

Which bacterium causes whooping cough?

A

Bordetella pertussis.

35
Q

How many people does whooping cough kill per year in the developing world?

A

200,000 pa

36
Q

How is Bordetella pertussis transmitted?

A

Aerosol inhalation.

37
Q

What does Bordetella pertussis colonise and by what mechanism?

A

The respiratory epithelium aided by adhesins (pili, pertactin, filamentous haemagglutnin FHA)

38
Q

Where do the Bordetella pertussis bacteria multiply?

A

In the respiratory mucosa.

39
Q

What causes damage to the ciliated epithelial cells and mucosal cells in a Bordetella pertussis infection?

A

LPS lipid A (triggers acute inflammation) and exotoxins including pertussis toxin and an adenylate cyclase.

40
Q

What are the signs and symptoms of whooping cough?

A

Accumulation of mucus, inflammatory cells, dead epithelial cells and bacteria in the airway.
Fever, bronchitis.
Paroxysms of coughing (caused by above as well as toxin action on neurons).

41
Q

In what cases is whooping cough fatal?

A

In infants with underlying cardiac/pulmonary disease.

42
Q

What neurological sequelae can whooping cough lead to?

A

Encephalopathy, deafness and blindness.

43
Q

Which bacterium causes the pneumonic plague?

A

Yersinia pestis.

44
Q

How many Europeans did the pneumonic plague kill and what percentage of the English population did it kill in the 14th century?

A

25 million Europeans and a third of the English population.

45
Q

What is the difference between the bubonic and pneumonic plague?

A

The bubonic plague spread from rodents to humans, whereas the pneumonic plague spreads from human to human. Both caused by the same bacterium.

46
Q

How does the infecting Yersinia pestis spread?

A

Though lymphatic system.

47
Q

What are the large lymph nodes characteristic of the bubonic plague termed?

A

Buboes.

48
Q

What are the symptoms of the plague?

A

Haemorrhagic inflammation, spread to blood, lung infection (pneumonic plague), meningitis, septicaemia, multi-organ failure, necrotic lesions –> black death.

49
Q

What virulence factors does Yersinia pestis have?

A

Antiphagocytic capsule
Protein toxins including ‘injected’ effector proteins called Yops - including YopP and YopT - that subvert macrophages to prevent engulfment.
Additional damage caused by LPS lipid A (endotoxin).

50
Q

Which bacterium causes Tuberculosis?

A

Mycobacterium tuberculosis (and closely related M. bovis in cattle).

51
Q

How many people worldwide are infected by TB?

A

Estimated 1.8 billion. (1/4 population)

52
Q

How many a) new cases and b) deaths are there of/by TB per year?

A

9 million new cases

1.5 million deaths.

53
Q

What has been the trend in TB infection rates since the mid-1980s and why?

A

Increase in infection rates, exacerbated by co-infection with HIV.

54
Q

Where are extensively drug resistant strains (XDR) now epidemic?

A

South Africa

55
Q

Where have totally drug resistant (TDR) strains emerged and what does the term mean?

A

They have emerged in Italy, Iran and India.

56
Q

Who predominantly has TB in the UK?

A

The elderly (infected earlier), homeless, alcoholics, drug addicts and the immunosuppressed.

57
Q

How does M. bovis spread to humans?

A

It is a zoonoses and spreads to humans primarily through non-pasteurised milk.

58
Q

How has M bovis mostly been eradicated in the UK?

A

By widespread testing and slaughter of infected cattle.

59
Q

Where does bovine TB remain endemic in the UK and what is thought to be the possible reason for this?

A

The South-West of England, there may be a link to infected badgers acting as a reservoir.

60
Q

Describe Mycobacterium tuberculosis.

A

It is a non-motile obligate aerobe that grows slowly, 4-8 weeks on complex medium.
Called ‘acid-fast’ as it is difficult to destain due to a waxy impermeable cell envelope (mycolic acid) that makes the pathogen resistant to drying and disinfectants, and protects it to immune attack.

61
Q

How does the M tuberculosis spread?

A

Via small droplets

Biology of Disease (43 decks)

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