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Microbiology > M22 - Pathogens of the Resp tract 2 > Flashcards

M22 - Pathogens of the Resp tract 2 Flashcards

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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
Q

What disease can S. pneumonia cause?

A

– Pneumonia
– Ottis media
– Meningitis (rare but significant)

26
Q

Describe pneumococcal pneumonia.

A
  • 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
Q

what does pneumococcal pneumonia overcome?

A
  • Overcomes IgA through the secretion of proteases

* Overcomes mucociliary escalator by the production of cytotoxin that kills ciliated epithelial cells (& Phagocytes

28
Q

Name the virulence factors of pneumococcal pneumonia.

A

> 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
Q

what is key to phagocytic survival?

A 
•  Capsule (smooth)
–  Key to virulence
–  Complex 83 serotypes
–  Inhibits Complement &amp; Ab responses
•  Pneumolysin
–  Disrupts membranes
–  Inhibits oxidative burst
30
Q

What are symptoms of pneumonia?

A
  • 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
Q

what is the mortality rate of pneumonia?

A

5%

32
Q

what percentage of patent with pneumonia develop bacteraemia?

A

25-30%

33
Q

what is the treatment of pneumonia?

A

• Amoxycillin or Erythromycin
– Resistance is now a major problem in USA
• Cephtriaxol (chloramphenicol) for Meningitis

34
Q

what is the prevention and control of pneumonia ?

A

– 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
Q

what is legionnaires disease (Pontiac fever)?

A

Atypical, acute lobar pneumonia with multi- system symptoms

36
Q

How does legionnaires disease (Pontiac fever) occur?

A

Occurs as sporadic cases or as outbreaks

37
Q

who does legionnaires disease (Pontiac fever) affect?

A

Immuno or pulmonary compromised

38
Q

what percentage of people exposed to legionnaires disease (Pontiac fever) develop the disease?

A

1-5%

39
Q

what is the case fatality of legionnaires disease (Pontiac fever)?

A

5-30%

40
Q

how is infection caused in legionnaires disease (Pontiac fever)?

A

– Inhalation of water droplets

– No person to person spread

41
Q

How can outbreaks of legionnaires disease (Pontiac fever) occur?

A 
–  Circulating water droplets
–  Whirlpool spars &amp; warm water baths
–  Decorative fountains
–  Cooling Towers
–  Nebulisers &amp; Humidifiers
–  Potting compost in Australia
42
Q

What are the symptoms of legionnaires disease (Pontiac fever)?

A
  • 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
Q

How would you describe Pontiac fever?

A

– Non-pneumonic Legionellosis

– Dry cough, Malaise, headache, fever, GI problems – Acute illness that resolves in 2-5 days

44
Q

what are the symptoms of non-respiratory infections?

A

– Wound infections after immersion in contaminated
water
– Hematogenous spread to extra pulmonary sites

45
Q

Describe the pathogenesis of Pontiac fever.

A
  • 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
Q

Describe legionella pnemophila.

A
  • 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
Q

What stimulates growth of legionella pneumophila and can grow inside amoebae and protozoa?

A

Blue-green algae

48
Q

Describe the diagnosis of Pontiac fever/ pneumonia.

A
  • Culturing
  • direct Abody test
  • rRNA identification
49
Q

What is the treatment for pneumonia?

A
  • Erythromycin

- Azithromycin

50
Q

what is the treatment for Pontiac fever?

A

not treated

51
Q

what is the control of Pontiac fever/pneumonia?

A

– Clean water systems, hot water systems monitored

– Hot water >50 ̊C as thrive between 20 ̊C to 45 ̊C

52
Q

what is the significance of legionella?

A

Legionella spp detected in dental water supplies. (UK, Germany, USA)

53
Q

Summary slide.

A

• 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.

Microbiology (30 decks)

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