M22 - Pathogens of the Resp tract 2 Flashcards

(53 cards)

1
Q

What bacteria are involved in upper respiratory tract infections?

A

– Streptococcus pyogenes
– Corynebacterium diptheria
– Bordetella pertusis
– Haemophilus influenza

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2
Q

What bacteria are involved in lower respiratory tract infections?

A

– Haemophilus influenza

– Streptococcus pneumoniae

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3
Q

What range of disease does haemophilia influenza cause?

A
–  Epiglotitis
–  Bacteremia
–  Sinusitis
–  Tracheobronchitis
–  Pneumoniae
–  Cellulitis
–  Meningitis
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4
Q

Describe some features of haemophilus influenza.

A
•  Exclusive human parasite
–  Difficult to observe,
–  Small, pleomorphic, Gram-ve bacilli 
–  non-motile
–  Specific growth requirements
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5
Q

Describe the non-invasive H.influenza (75% carriage).

A

– H. influenzae non-encapsulated strains
– Opportunistic infection of ear, sinuses, or eye
– Secondary invaders of damaged tissue e.g. virus, smoking, mucocilliary escalator impaired
– Bronchopneumonia & chronic bronchitis

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6
Q

Describe the invasive H.influenza (2-3% carriage).

A

– Capsulate strain causes acute primary infections
– Sore throat with fever, may obstruct airway
– Pneumonia, Bacteremia, Purulent Arthritis, Meningitis

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7
Q

Describe how an individual is infected with H.influenza.

A

– Infection from respiratory droplet or direct contact with patient
– Bacteria attach to epithelial cells
– Organism penetrates to submucosa (nasopharynx)
– Causes local inflammation & swelling
– 50% of cases present as headache, fever & stiff neck
– Usually confined to epiglottis, facial & neck tissue
– Spreads from initial site to infect bones, joints, CNS

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8
Q

Describe features of meningitis.

A

• Winter disease (commonest)
• Children 2 months to 2 years
– (gap between maternal Antibody & raising of Antibody to capsule)
• 6% Mortality, 20% of survivors have permanent damage, e.g. hearing loss

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9
Q

Describe encapsulated and non-encapsulated forms of H.influenza.

A

– Polysaccharide capsule (a,b,c,d,e,f, serotypes)
– Serotype B originally responsible for 95% of invasive infections, largely pediatric (<5 years).
– Haemophilus influenza type B i.e Hib

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10
Q

what is the virulence related to capsule formation.

A

– PRP (polyribosyl ribotol phosphate) Capsule
– Protects bacteria from phagocytosis
– Reduces susceptibility to antibacterial role of serum

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11
Q

what is the target for P2 and other outer membrane proteins?

A

Sialic acid oligosaccharides

in mucin

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12
Q

what is the target for fimbriae/pili?

A

mucosal cells of nasopharynx

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13
Q

what is the target for non-pillus adhesins?

A

mucosal cells of nasopharynx

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14
Q

Describe the tissue invasion of H.influenza.

A

• H. influenza can be isolated from sub- epithelial layers without damaging epithelium.
– Passes between cell junctions Paracytosis
– Adheres & enters non-ciliated epithelium cells
– Viable bacteria detected in macrophage cells

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15
Q

what are the antibiotic treatments for H.influenza diseases?

A
  • Bronchitis- amoxycillin or erythromycin
  • Pneumonia - flucloxacillin and amoxycillin
  • meningitis - cephtriaxone
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16
Q

What is the immunisation for H.influenza diseases?

A

– Hib (capsule type B) vaccine given at 2,3 & 4 months

Cell wall LPS also important for immunity

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17
Q

What is pneumonia?

A

An acute inflammation of the lungs, often caused by inhaled pneumococci of the species Streptococcus pneumoniae. The alveoli and bronchiles of the lung become plugged with a fibrous exudate

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18
Q

what are the 2 main cause of pneumonia?

A
  • community-acquired pneumonias - (Streptococcus pneumoniae)

- Hospital -aquired pneumonias (Star aureus, gram negative bacilli)

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19
Q

Describe the structure of strep pneumoniae.

A
•  Encapsulated Gm+ve cocci
•  Oval or lancet shaped
•  Arranged in pairs (diplococci)
•  Colonies α-heamolytic
–  Encapsulated strains large
•  Round &amp; mucoid
–  Non encapsulated small
•  Flat
•  Fastidious (prefers 5% CO2)
–  Grows on media enriched with blood products, Catalase negative * requires catalase in the media to prevent build up of H2O2
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20
Q

How do you identify S.pneumoniae?

A
  • Deoxycholate (bile) sensitivity
  • Optochin sensitivity
  • Diplococci
  • Gm +ve staining α-heamolytic (aerobic)
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21
Q

what is S.pneumoniae a commensal of?

A

oropharynx

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22
Q

what population does S.pneumoniae affect the most?

A

– Age related decrease in carriage – Peak 10 year olds (55%)

23
Q

How does S.pneumoniae bind?

A

Bound to surface carbohydrates :

  • N-acetyl-glycosamine
  • Neuraminidase A
24
Q

How is S. pneumoniae transferred?

A

horizontal transfer from resistant to susceptible

25
What disease can S. pneumonia cause?
– Pneumonia – Ottis media – Meningitis (rare but significant)
26
Describe pneumococcal pneumonia.
* Invasion of lower respiratory tract by aerosol * Normally bypass ciliated epithelial * Progress to alveolus, & cell wall promotes binding to cells expressing the Platelet Activating Factor receptor. * Teichoicacidsare exposed on cell surface & present in the cell wall
27
what does pneumococcal pneumonia overcome?
* Overcomes IgA through the secretion of proteases | * Overcomes mucociliary escalator by the production of cytotoxin that kills ciliated epithelial cells (& Phagocytes
28
Name the virulence factors of pneumococcal pneumonia.
> Cellwallinitiates inflammation – Teichoic acid & PG • Activate C5a • Alternative complement pathway ``` > Pneumolysin, pore forming (typeII) toxin > Hydrogen Peroxide > Phosphorycholine – Present on cell wall – Binds to PAF receptor – Induces receptor mediated endocytosis ```
29
what is key to phagocytic survival?
``` • Capsule (smooth) – Key to virulence – Complex 83 serotypes – Inhibits Complement & Ab responses • Pneumolysin – Disrupts membranes – Inhibits oxidative burst ```
30
What are symptoms of pneumonia?
* Normally preceded by 1-3 days of viral respiratory infection. * Abrupt onset * Severe shaking chill, sustained fever 39 ̊ to 41 ̊C * Productive cough with blood-tinged sputum * Chest pain (pleurisy) * Lobar pneumoniae confined to lower alveolar lobes
31
what is the mortality rate of pneumonia?
5%
32
what percentage of patent with pneumonia develop bacteraemia?
25-30%
33
what is the treatment of pneumonia?
• Amoxycillin or Erythromycin – Resistance is now a major problem in USA • Cephtriaxol (chloramphenicol) for Meningitis
34
what is the prevention and control of pneumonia ?
– PCV7, 7 surface antigens better for young children some limitations (racial). – Pneumococcal Vaccine 2, 4, 13 months – Anti-capsular vaccine consisting of 23 capsular polysaccharides covers 94% of all strains
35
what is legionnaires disease (Pontiac fever)?
Atypical, acute lobar pneumonia with multi- system symptoms
36
How does legionnaires disease (Pontiac fever) occur?
Occurs as sporadic cases or as outbreaks
37
who does legionnaires disease (Pontiac fever) affect?
Immuno or pulmonary compromised
38
what percentage of people exposed to legionnaires disease (Pontiac fever) develop the disease?
1-5%
39
what is the case fatality of legionnaires disease (Pontiac fever)?
5-30%
40
how is infection caused in legionnaires disease (Pontiac fever)?
– Inhalation of water droplets | – No person to person spread
41
How can outbreaks of legionnaires disease (Pontiac fever) occur?
``` – Circulating water droplets – Whirlpool spars & warm water baths – Decorative fountains – Cooling Towers – Nebulisers & Humidifiers – Potting compost in Australia ```
42
What are the symptoms of legionnaires disease (Pontiac fever)?
* Incubation period 2-10 days * Cough, fever, sweats, loss of appetite, headache, general pains. * Rapidly degenerates, yellow/green sputum can be stained with blood, tight chest, breathless, a sharp pain in the side of the chest * Confusion & diarrhea are possible symptoms * Complications include heart, brain & kidneys
43
How would you describe Pontiac fever?
– Non-pneumonic Legionellosis | – Dry cough, Malaise, headache, fever, GI problems – Acute illness that resolves in 2-5 days
44
what are the symptoms of non-respiratory infections?
– Wound infections after immersion in contaminated water – Hematogenous spread to extra pulmonary sites
45
Describe the pathogenesis of Pontiac fever.
* Failure to clear inhaled organism (conc, virulence) * Contact with alveolar macrophages * Phagocytose bacteria, but phagosome fails to mature * L. pneumophila multiply within infected phagocyte * Lyse phagocyte and re-infect * Spread through lymph & blood
46
Describe legionella pnemophila.
* Facultative intracellular parasite * Slender unencapsulated rods * Appear coccobacilliary in clinical material * Gm-ve but stain poorly with carbol fuchsin (Gimenez staining instead) * Strict aerobes * Fastidious
47
What stimulates growth of legionella pneumophila and can grow inside amoebae and protozoa?
Blue-green algae
48
Describe the diagnosis of Pontiac fever/ pneumonia.
- Culturing - direct Abody test - rRNA identification
49
What is the treatment for pneumonia?
- Erythromycin | - Azithromycin
50
what is the treatment for Pontiac fever?
not treated
51
what is the control of Pontiac fever/pneumonia?
– Clean water systems, hot water systems monitored | – Hot water >50 ̊C as thrive between 20 ̊C to 45 ̊C
52
what is the significance of legionella?
Legionella spp detected in dental water supplies. (UK, Germany, USA)
53
Summary slide.
• Upper & Lower Respiratory tract infections • Haemophilus infleunza : – Gram-negative – Upper respiratory associated infectionto pneumonia – Capsular type & Hib vaccination • Streptococcus pneumonia – Usually follows viral infection – Single,doubly pneumonia &meningitis – Relatively recent control through vaccine but antibiotic resistance a problem • Legionella – Environmental source,grows within single celled eukaryotes, water lines, air conditioning etc.