Flashcards in Cystic Fibrosis & Antibiotic Resistance Deck (60):
What is Cystic Fibrosis?
A genetic disease caused by ~300 mutations with cause the CFTR gene to be faulty.
What are some symptoms of CF?
Poor weight gain
What percentage of children have their first pseudomonal colonisation by the age of 8?
What is pseudomonal colonisation associated with?
Delayed growth and mortality
What are the characteristics of pseudomonas bacteria?
Single polar flagellum
How big are pseudomonal bacterial?
0.5 - 3.0µm
What kind of pigment do pseudomonal bacterial produce?
A green looking pigment - pyocyanin
Where are pseudomonal bacteria found?
Water, soil, plants, humans and animal surfaces.
Can pseudomonal bacteria be present in the human flora?
Yes but not in high numbers
What can be used to mark pseudomonal bacteria?
Positive oxidase reactions
Are pseudomonal bacteria aerobes or anaerobes?
They are obligate aerobes but can grow anaerobically in the presence of NO3
What are pseudomonas bacteria's virulence factors?
- 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
How are pseudomonas bacteria transmitted?
Through various routes such as colonisation of the human flora, person to person contact.
What are biofilms?
Mechanisms of survival rather than causes of disease and they can form in environmental sources or invasive medical devices
How are pseudomonas bacterial identified?
- bacterial culture
- urine analysis
- corneal scrapings
- fluorescence under UV
- distinctive odour
Give examples of diseases caused by Pseudomonas aeruginosa
- respiratory tract infections
- genito-urinary tract infections
- wound infection
What is the pathophysiology of pseudomonas?
Colonises in the lower RT and grows to cover the epithelium through biofilm proliferations, scarring and access formations.
(different strains have different susceptibility)
How long can early intervention eradicate pseudomonas for?
2 years - this is done through oral or inhaled antibiotics which reduce the risk of recolonisation and pulmonary exacerbation
What are some advantages of inhaled antibiotics?
- discrete and portable
- no loss of efficacy
- easy to use for all ages
Give 2 examples of dry powder inhaled antibiotics?
Give 2 examples of ultrasonic nebuliser antibiotics
Which 2 oral antibiotics are used for pseudomonal infection?
Ciprofloxacin is well absorbed from...
What does ciprofloxacin do to hepatic metabolism?
Increases it in CF patients
What is the usual dose of ciprofloxacin for children?
10-20mg/kg - this can be increased to 30mg\kg
What does azithromycin do to biofilms?
Interferes with biofilm adhesion to the epithelium - modifies structure and growth
What does of azithromycin improves FEV1?
Definition of infective exacerbation (according to CF trust clinical standards)
- reduction in FEV to <50%
- acute changes on X-ray
- increased breathlessness or decreased tolerance to exercise
What actions would be taken in CF diagnosis in hospital?
- sputum sample
- IV access
- Empirical antibiotics
Give 2 examples of empirical antibiotics
- Ceftazidime: 3rd gen cephalosporin with a large MIC range
- Tobramycin: aminoglycoside with favourable nephrotoxicity
What are cephalosporins?
Beta lactam antibiotics which work in a similar to way to pencilling by blocking cell wall synthesis.
How does resistance to cephalosporins occur?
Through altered binding sites, decreased permeability and beta lactamases
Are 3rd generation cephalosporins resistant to beta lactamases?
Yes - they have a broader spectrum of activity.
Which bacteria produce "Extended spectrum beta lactase"?
E.coli and Enterbacter cloacae - the genes for resistance are transferred by plasmid DNA transfer
At what level are aminoglycosides nephrotoxic?
At trough level - 2mg/L
At what level are ahminoglycosides ototoxic?
Peak level - 8-12mg/L
When do patients have to have IVAB therapy?
If they experience frequency exacerbations
What is IVAB therapy?
3 month cycles of 2 weeks treatment and 3 monthly sputum samples. This reduces hospital admission and suppresses the development of infection.
What is MRSA?
A gram negative coccoid bacterium resistant to all beta lactic antibiotics
Which antibiotics is MRSA resistance to?
some are resistant to: macrocodes, quinolone and clindamycins.
What percentages of the population is colonised with S.aureus
~30% - most are asymptomatic
What are the usual sites of S.aureus infection?
anterior nares, axilla and perineum
How can S.aureus infection be reduced?
- screening at risk patients,
- isolating patients with MRSA
- decontaminating with skin wash, nasal ointment and mouthwash for 5
What symptoms with patients with a S.aureus infection have?
- high temp
- high white cell count
- inflammation at infection site
What is the 1st line treatment for S aureus ?
i/v vancomycin or teicoplanin for systemic infections
What is the 2nd line treatment for S aureus?
Linezolid, daptomycin and tigecycline
What are multi-resistant coliforms?
Gram negative bacilli found in the gut such as E.coli, Klebsiella pneumoniae and enterobacter.
What are multi-resistant coliforms resistant to?
Cephalosporins, quinolone and carbapenems.
What are extended spectrum beta lactamases resistant to?
Penicillins and cephalosporins
What can UTIs caused by E.coli CTX-M ESBL cause?
Where are enterococci found?
In the gut
What kind of patients are easily colonised by enterococci?
Patients who take antibiotics frequently - infections are i/v line associated.
What is the morphology of C.diff?
What percentage of C.diff is present in the gut of adults?
How can CDI be acquired?
cross infection or toxigenic strain.
What are the symptoms of CDI?
- mild diarrhoea
- bleeding from the colon
What does WCC show in CDI?
The severity of the infection.
What is mild CDI treated with?
What is severe CDI treated with?