Pseudomonas aeruginosa bacteraemia
|Publication: 18/11/2014 --|
|Last review: 23/03/2020|
|Next review: 23/03/2023|
|Approved By: Trust Clinical Guidelines Group|
|Copyright© Leeds Teaching Hospitals NHS Trust 2020|
This Clinical Guideline is intended for use by healthcare professionals within Leeds unless otherwise stated.
Department of Microbiology Bacteraemia Guideline
Pseudomonas aeruginosa bacteraemia
- About P.aeruginosa
- Antimicrobial susceptibilities
- Clinical differential diagnosis
- Antimicrobial treatment
- Supplementary investigations
Quick reference guide to the management of Pseudomonas aeruginosa bacteraemia
This document provides guidelines for doctors on the management of patients with confirmed bacteraemias (blood cultures). This document is supplementary to, and should be used in conjunction with, the antimicrobial guidelines.
The aim of this guideline is to:
- Provide education to junior microbiology registrars
- Support communication of blood culture results from microbiologists to ward doctors
- Support ward doctors in treating and investigating bacteraemic patients
The blood culture process: Timings of culture, identification, susceptibility tests and clinical liaison.
How to use this guideline: This guideline should be used to help in the management of patients with a confirmed bacteraemia. The guideline should be used to support interaction with specialist advice e.g. Microbiology.
P. aeruginosa is Gram-negative, non - fermenting aerobic bacillus.
P. aeruginosa is an environmental bacteria, it is commonly identified in the presence of water, or on moist mucosal surfaces.
P. aeruginosa carries produces an extracellular polysaccharide. It’s over production is the basis for a mucoid colony phenotype seen in Cystic Fibrosis infections. The strains isolated from the environment and nosocomial infections are typically non mucoid.
P. aeruginosa is one of the leading causes of gram negative bacteraemia and is associated with high mortality rates.
Both bacterial and host factors (See risk factors below) play a part in pathogenesis. Bacterial factors include exotoxins, endotoxins, proteases, phospholipases, exopolysaccharides, pili, flagellae, iron binding proteins, the ability to form biofilms and elaboration of pyocyanins. Because of a multitude of virulence factors coupled with increasing antibiotic resistance, P. aeruginosa continues to be amongst the top five causes of nosocomial bacteraemia.
It can colonise hospital water and plumbing systems and can cause a variety of infections, especially in immune-compromised patients and augmented care units.
Risk factors for disease:
Neutropenic/Immunocompromised hosts (Transplant patients, haematological malignancy and HIV)
Pancreato-biliary disease/Endoscopic retrograde cholangiopancreatography (ERCP) complications
Indwelling catheters (central venous/urinary), orthopaedic implants & Endotracheal tubing
Traumatic wounds contaminated with fresh water
Surgical wound infections
Genetic predisposition e.g. CF patients.
Antibiotics within last 30 days (cephalosporins, aminoglycosides, carbapenems, fluoroquinolones)
P. aeruginosa are normally only susceptible to a limited number of reliably effective antibiotics. These antibiotics are:
- Anti-pseudomonal Penicillins e.g. Piperacillin-tazobactem
- Cephalosporins with anti-pseudomonal activity e.g. Ceftazadime
- Fluoroquinolones with anti-pseudomonal activity e.g. Ciprofloxacin
- Carbapenems with anti-pseudomonal activity e.g. Meropenem
- Aminoglycosides e.g. Gentamicin
P. aeruginosa is always resistant to the following antibiotics (which often have activity against Gram negative bacteria):
Amoxicllin, Co-amoxiclav, Cefuroxime, Ceftriaxone, Cefotaxime, Cephalexin, Ertapenem.
Second line antibiotics, which have variable/sub-optimal pseudomas activity include:
Aztreonam and Levofloxacin
Acquired antibiotic resistance
P. aeruginosa is able to acquire antibiotic resistance mechanisms detected in Enterobacteriaceae (e.g. E. coli). These mechanisms e.g. extended spectrum beta lactamases, may result in resistance to ceftazidime and carbapenem resistance (meropenem).
P. aeruginosa can acquire mutations that increase the levels of efflux systems that pump out beta lactam antibiotics can result in even higher Minimum Inhibitory Concentrations (MICs) against beta lactam drugs. This results in inability to use such drugs even though they are only minimally degraded by beta lactamases.
Mutations can limit the amount of drug that enters the bacterial periplasmic space thus compromising the efficacy of drugs like Imepenem.
Evidence shows that the emergence of resistance may be driven by use of Carbapenems because there is substantial resistance to all beta lactam antibiotics whenever there is imipenem resistance.
P.aeruginosa strains also show resistance to many aminoglycosides due to impermeability and possibly efflux.
Likewise mutational events in P. aeruginosa as well as increased production of efflux pumps also result in loss of efficacy of Fluoroquinolones.
Alternative options: When resistance is present antibiotics with unpredictable efficacy may be used to treat infections, these include:
IV Colistin and Polymyxin B
Alternative aminoglycosides e.g. amikacin
- Respiratory tract infections (VAP, Bronchiectasis, Cystic Fibrosis).
- Neutropenic sepsis
- Intravascular catheters associated infections
- Intra-abdominal Infections
- Skin and soft tissue infections including burns
The table below outlines some of the common infections associated with each of the clinical syndromes. Please be aware that pseudomonas can present in unusual ways, and that this list is by no means exhaustive.
See guideline (HAP and VAP)
Intravascular catheter associated infections
See guideline & seek microbiology advice
Skin/soft tissue infections/burns
Seek microbiology advice
Consider further investigations as appropriate to source of infection, please see relevant guidelines.
|Target patient group:|
|Target professional group(s):||Secondary Care Doctors
Trust Clinical Guidelines Group
LHP version 1.0
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