Pseudomonas aureginosa Flashcards
Antibiotics that inhibit DNA gyrase
Quinolones
Eradication
early intervention can eradicate Psuedomonas for up to 2 years
Oral or inhaled therapy
Oral antibiotics
P.aureginosa
-Ciprofloxacin
5-flouroquinolone
well absorbed from GIT
primarily hepatic metabolism (which is increased in CD patients)
Dose can be therefore increased to 30mg/kg (maximum is 750mg)
-Azithromycin interferes with adherence of pathogen to epithelium modifies biofilm structure and growth 10mg/kg daily results in -improved FEV1 -fewer courses of IV antibiotics
Chronic treatment for CF patients
exacerbations
-Frequent exacerbations lead to regular IVAB therapy
3 monthly cycles of 2 weeks of therapy
3 monthly sputum samples
antimicrobial choices lead by previous sensitivities
-benefits
reduced admission to hospital (can have IVAB at home)
suppresses development of infection
Risks
resistance
on-going organ damage
colonisation with other bacteria (if done in hospital)
Antibiotics that inhibit folate synthesis
Sulfonamides
Trimethoprim
- Risk of S.aureus infection in first 2 years of life
- does isolation of patient have an impact?
- high
- no
Diagnosis and identification
- urine analysis
- FBC
- Corneal scrapings
- Sweet, fruity odour
- Florescence under UV light
- Blood culture on agar (wound/tissue, blood, sputum, discharge, stool)
Antibiotics that inhibit 50S subunit of ribosome
Macrolides Clindamycin Linezolid Chloramphenicol Streptogramins
Describe how the generations of cephalosporins differ
5 generations
Higher generations have extended spectra against aerobic gram negative bacilli
3rd generation are resistant to beta-lactamases
The two 5th generation cephalosporins are active against MRSA
Antibiotics that inhibit DNA polymerase
Rifampicin
ESBL?
Extended-spectrum beta-lactamase-producing bacteria
caused by overuse of 3rd generation cephalosporins
ESBL genes transferred by plasmid transfer
ESBLs:
-Escherischea coli
-Enterobacter cloacae
Microbiology of P.aureginosa
- Opportunistic, nosocomia pathogen (acquired in hospital)
- gram negative rod
- single polar flagellum for motility
- 0.5-3um in size
- commonly produces pyocyanin pigment
- recalcitrance (stubborn)
Aminoglycoside dose for CF patients
10kg/kg
no difference in AKI or hearing loss
Antibiotics that effect cell wall synthesis
Beta Lactams Cephalosporins Penicillins Carbapenems Monobactams
Vancomycin
Bacitracin
Cause of cystic fibrosis
-single faulty gene - CFTR
Medical conditions caused by Pseudomonas aureginosa
- respiratory tract infections
- bacteraemia/sepsis
- endocarditis
- meningitis or brain abscess
- Otitis externa or chronic otitis media
- keratitis, ocular abscess, orbital cellulitis
- osteomyletis
- enterocolitis, enteritis, diarrhoea
- Genito-urinary tract infection
- Secondary wound infection, burn wound sepsis, pustular lesions, hot tub folliculitis
Pathophysiology in CF patients especially
P.aureginosa colonises the mucous in the lower respiratory tract and then grows to cover the epithelium
- biofilms proliferation
- scarring and abscess formation
Describe Cephalosporins
- B lactam
- most widely-prescribed antibiotics
- inhibition of cell wall synthesis
- bacteriocidal
- broad spectrum
Things associated with pseudomonal colonisation
- mortality
- delayed growth
Treatment when cephalosporin resistance
Aminoglycosides -synergy with b-lactams -concentration-dependent action -Nephrotoxic (trough level dependent) -Ototoxic (peak level dependent) -Hypermetabolised in CF patients standard dose of 7mg/kg not enough for CF patients
How does resistance to cephalosporins occur on a microscopic level?
Beta-lactamases
Decreased permeability
Altered binding site
Antibiotics that target cell membrane
Polymyxins
Source
-water
-soil
-plant and animal surfaces
-part of normal human flora in some populations
-
Biofilms affect and influence what?
Biofilms represent different strains and sensitivities
affects antibiotic choices
Virulence factors
- invasive, toxigenic (exotoxin)
- Minimal nutritional requirements - shown to even grow in distilled water
- produces extracellular proteases to aid bacterial adhesion and invasion
- produces alignates to help biofilm formation
- resistant to high salt concentrations, temperature changes, weak antiseptics and many antibiotics
Emperical antibiotics for subsequent infections
-Guided by sensitivity from LAST exacerbation
Definition of infective exacerbations
Intervention
-reduction of FEV1 to <50% expected
-acute changes on X ray
-increased breathlessness or reduced exercise tolerance
Actions
-sputum sample
-IV access
-emperical antibiotics
-admit
Transmission
-variable routes
Biofilms:
-environmental sources e.g. sinks and drains
-invasive medical equipment and colonisation of moist equipment e.g. ventilators
Human transmission source
- colonisation as part of normal human flora
- limited spread by person-to-person contact
Emperical antibiotics for first infection
-Ceftazidime
3rd generation cephalosporin
particularly active against Psuedomonas
Reserved in UK for this indication
-Tobramcyin
Aminoglycoside with favourable nephrotoxicity profile
good activity against Pseudomonas
% of cystic fibrosis pathogens that are P.aureginosa
80%
Early infections
- no benefit to prophylaxis against psuedomonal infection
- rates of infection seem to be related to early viral chest infections
- newly infected patients should receive appropriate antimicrobial therapy - the goal is ERADICATION if it is a FIRST infection
Markers of it
- Positive oxidase reaction
- non-fermentative
- Aerobic respiration but will adapt to use NO3
Inhaled antibiotics
Nebuliser or inhalation solution
- Discrete and portable
- no loss of efficacy
- easy to use, covers all ages (6/12 onwards)
Antibiotics that inhibit 30S subunit of ribosome
Tetracyclines
Aminoglycosides
Cystic fibrosis symptoms
- cough
- fatty diarrhoea (steatorrhoea)
- poor weight gain
- chest infections
