Cystic Fibrosis & Antibiotic Resistance Flashcards

1
Q

What is Cystic Fibrosis?

A

A genetic disease caused by ~300 mutations with cause the CFTR gene to be faulty.

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2
Q

What are some symptoms of CF?

A

Cough
Chest infections
Steatorrhoea
Poor weight gain

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3
Q

What percentage of children have their first pseudomonal colonisation by the age of 8?

A

~50%

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4
Q

What is pseudomonal colonisation associated with?

A

Delayed growth and mortality

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5
Q

What are the characteristics of pseudomonas bacteria?

A

Opportunistic
Narocomial
Gram negative
Single polar flagellum

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6
Q

How big are pseudomonal bacterial?

A

0.5 - 3.0µm

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7
Q

What kind of pigment do pseudomonal bacterial produce?

A

A green looking pigment - pyocyanin

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8
Q

Where are pseudomonal bacteria found?

A

Water, soil, plants, humans and animal surfaces.

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9
Q

Can pseudomonal bacteria be present in the human flora?

A

Yes but not in high numbers

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10
Q

What can be used to mark pseudomonal bacteria?

A

Positive oxidase reactions

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11
Q

Are pseudomonal bacteria aerobes or anaerobes?

A

They are obligate aerobes but can grow anaerobically in the presence of NO3

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12
Q

What are pseudomonas bacteria’s virulence factors?

A
  • Invasive
  • Toxigenic
  • Minimal nutritional requirements
  • Produce proteases to assist adhesion and invasion
  • Produce alginates to aid in biofilm formation
  • Can resist body temp, high salt concentrations, weak antiseptics and many antibiotics
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13
Q

How are pseudomonas bacteria transmitted?

A

Through various routes such as colonisation of the human flora, person to person contact.

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14
Q

What are biofilms?

A

Mechanisms of survival rather than causes of disease and they can form in environmental sources or invasive medical devices

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15
Q

How are pseudomonas bacterial identified?

A
  • bacterial culture
  • urine analysis
  • FBC
  • corneal scrapings
  • fluorescence under UV
  • distinctive odour
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16
Q

Give examples of diseases caused by Pseudomonas aeruginosa

A
  • respiratory tract infections
  • bacteraemia
  • keratitis
  • genito-urinary tract infections
  • wound infection
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17
Q

What is the pathophysiology of pseudomonas?

A

Colonises in the lower RT and grows to cover the epithelium through biofilm proliferations, scarring and access formations.
(different strains have different susceptibility)

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18
Q

How long can early intervention eradicate pseudomonas for?

A

2 years - this is done through oral or inhaled antibiotics which reduce the risk of recolonisation and pulmonary exacerbation

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19
Q

What are some advantages of inhaled antibiotics?

A
  • discrete and portable
  • no loss of efficacy
  • easy to use for all ages
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20
Q

Give 2 examples of dry powder inhaled antibiotics?

A
  • tobramycin
  • amikacin
    (aminoglycosides)
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21
Q

Give 2 examples of ultrasonic nebuliser antibiotics

A
  • Colistin

- Tobramycin

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22
Q

Which 2 oral antibiotics are used for pseudomonal infection?

A
  • Ciprofloxacin

- Azithromycin

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23
Q

Ciprofloxacin is well absorbed from…

A

GIT

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24
Q

What does ciprofloxacin do to hepatic metabolism?

A

Increases it in CF patients

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25
Q

What is the usual dose of ciprofloxacin for children?

A

10-20mg/kg - this can be increased to 30mg\kg

26
Q

What does azithromycin do to biofilms?

A

Interferes with biofilm adhesion to the epithelium - modifies structure and growth

27
Q

What does of azithromycin improves FEV1?

A

100mg/kg

28
Q

Definition of infective exacerbation (according to CF trust clinical standards)

A
  • reduction in FEV to <50%
  • acute changes on X-ray
  • increased breathlessness or decreased tolerance to exercise
29
Q

What actions would be taken in CF diagnosis in hospital?

A
  • sputum sample
  • IV access
  • admission
  • Empirical antibiotics
30
Q

Give 2 examples of empirical antibiotics

A
  • Ceftazidime: 3rd gen cephalosporin with a large MIC range

- Tobramycin: aminoglycoside with favourable nephrotoxicity

31
Q

What are cephalosporins?

A

Beta lactam antibiotics which work in a similar to way to pencilling by blocking cell wall synthesis.

32
Q

How does resistance to cephalosporins occur?

A

Through altered binding sites, decreased permeability and beta lactamases

33
Q

Are 3rd generation cephalosporins resistant to beta lactamases?

A

Yes - they have a broader spectrum of activity.

34
Q

Which bacteria produce “Extended spectrum beta lactase”?

A

E.coli and Enterbacter cloacae - the genes for resistance are transferred by plasmid DNA transfer

35
Q

At what level are aminoglycosides nephrotoxic?

A

At trough level - 2mg/L

36
Q

At what level are ahminoglycosides ototoxic?

A

Peak level - 8-12mg/L

37
Q

When do patients have to have IVAB therapy?

A

If they experience frequency exacerbations

38
Q

What is IVAB therapy?

A

3 month cycles of 2 weeks treatment and 3 monthly sputum samples. This reduces hospital admission and suppresses the development of infection.

39
Q

What is MRSA?

A

A gram negative coccoid bacterium resistant to all beta lactic antibiotics

40
Q

Which antibiotics is MRSA resistance to?

A
  • penicillins
  • cephalosporins
  • carbapenems

some are resistant to: macrocodes, quinolone and clindamycins.

41
Q

What percentages of the population is colonised with S.aureus

A

~30% - most are asymptomatic

42
Q

What are the usual sites of S.aureus infection?

A

anterior nares, axilla and perineum

43
Q

How can S.aureus infection be reduced?

A
  • screening at risk patients,
  • isolating patients with MRSA
  • decontaminating with skin wash, nasal ointment and mouthwash for 5
44
Q

What symptoms with patients with a S.aureus infection have?

A
  • high temp
  • high white cell count
  • inflammation at infection site
45
Q

What is the 1st line treatment for S aureus ?

A

i/v vancomycin or teicoplanin for systemic infections

46
Q

What is the 2nd line treatment for S aureus?

A

Linezolid, daptomycin and tigecycline

47
Q

What are multi-resistant coliforms?

A

Gram negative bacilli found in the gut such as E.coli, Klebsiella pneumoniae and enterobacter.

48
Q

What are multi-resistant coliforms resistant to?

A

Cephalosporins, quinolone and carbapenems.

49
Q

What are extended spectrum beta lactamases resistant to?

A

Penicillins and cephalosporins

50
Q

What can UTIs caused by E.coli CTX-M ESBL cause?

A

Septicaemia

51
Q

Where are enterococci found?

A

In the gut

52
Q

What kind of patients are easily colonised by enterococci?

A

Patients who take antibiotics frequently - infections are i/v line associated.

53
Q

What is the morphology of C.diff?

A

Gram negative

anaerobic

54
Q

What percentage of C.diff is present in the gut of adults?

A

<5%

55
Q

How can CDI be acquired?

A

cross infection or toxigenic strain.

56
Q

What are the symptoms of CDI?

A
  • mild diarrhoea
  • ulceration
  • bleeding from the colon
57
Q

What does WCC show in CDI?

A

The severity of the infection.

58
Q

What is mild CDI treated with?

A

Metronidazole

59
Q

What is severe CDI treated with?

A

Vancomycin

60
Q

Which antibiotics should be avoided in CDI?

A

fluoroquinolone, cephalosporins and clindamycin