Pseudomonas aeruginosa is widely distributed in soil, water, sewage and plants, and is a common human intestinal bacterium. It also causes disease in humans, certain animals, insects and plants. Infection is usually restricted to hospitalised patients with predisposing conditions (it causes 14% of all nosocomial infections) but it is also associated with 5% of all community-acquired infections.

Perhaps the most commonly encountered infection outside hospitals is otitis externa ('swimmer's ear'), of which Pseudomonas aeruginosa causes 35-70%. This can usually be treated satisfactorily with aural toilet without resorting to antibiotics but, particularly in diabetics, malignant otitis externa and otitis media can occur and can be life-threatening in extreme cases, especially when extension to the cranial parameningeal deep fascial space occurs.

With the ever-increasing use of contact lenses, eye infections with P.aeruginosa are becoming more and more common. These range from purulent conjunctivitis to iridocyclitis, keratitis and iritis, corneal ulcer, and panophthalmitis, and can be sight-threatening. Refer to a previous Newsletter for details.

Wound infections are common but are frequently part of a mixed flora and often do not require specific antibiotic treatment, responding to local measures and the removal of such pathogens as Staphylococcus aureus if present. Surgical wounds and other deep or severe trauma may be exceptions.

Foot puncture wounds in children are prone to P.aeruginosa infection and can lead to septic arthritis and endocarditis. Intravenous drug abusers are even more prone to such infections, with P.aeruginosa causing 14% of endocarditis in such people.

Extensive or deep burns are also susceptible to infection with P.aeruginosa. This can usually be satisfactorily treated with a local antibiotic, such as silver sulphadiazine.

Skin infections are of two types. Pyoderma form when the organism colonises, and subsequently invades (especially when occlusive dressings are used), exfoliative lesions, venous stasis ulcers or eczema. These have a characteristic moth-eaten appearance and erythematous border. The process can be acute and invasive or chronic indolent. In the latter case, a slowly progressive, burrowing inflammation forms coalescent papulopustular lesions covered with a malodorous crust. Long term oral ciprofloxacin is usually used in treatment.

The second type is a folliculitis, consisting of discrete, maculopapular lesions a few mm in diameter, which develop a vesicle or pustule on their apices. These occur on the trunk or proximal extremities, predominately axillae and pelvis and are typically associated with spa use. A similar condition, characterised by exquisitely tender erythematous plantar nodules and labelled 'Pseudomonas hot foot syndrome' by the physicians who reported it, recently occurred as an outbreak traced to a wading pool. These conditions do not require antibiotics and are adequately treated with simple non-specific topical measures.

P.aeruginosa sinusitis is usually a result of lavage of one kind or another with contaminated water or saline. Resolution may require surgical intervention as well as antibiotic therapy.

Lower respiratory tract infections with P.aeruginosa are associated with cystic fibrosis and other chronic lung conditions and with invasive hospital procedures. Infections affecting cystic fibrosis patients are frequently due to mucoid 'strains'. It was thought that these organisms were distinct strains but research has shown that non-mucoid strains can become mucoid and vice versa and that mucoidicity is basically an indicator of long-term residence at the site. Such strains are also encountered in long-standing urinary tract infections. P.aeruginosa urinary tract infections are almost invariably the result of invasive procedures.

P.aeruginosa is also commonly isolated from sputum specimens from 'normal' patients who have been extensively treated with antibiotics. In most cases, the best response is to withdraw or withhold antibiotic treatment; these isolations usually represent colonisation and rarely proceed to frank infection. This applies to non-mucoid isolates; isolation of mucoid 'strains' may indicate that the patient is not normal and may require further investigation.

Nosocomial infections with P.aeruginosa cover the entire gamut. The organism is responsible for 5% of surgical wound infections, 8% of thrombophlebitis and is an important cause of fatal bacteremia in neutropenic patients.

Patients with granulocytopenia, defects in opsonophagocytic antibodies, local immunity or depressed or defective cell-mediated immunity or with interrupted integument are especially prone to infection with P.aeruginosa.

P.aeruginosa has natural resistance to many antibiotics, including all penicillins except ticarcillin (13% resistance in Australia) and piperacillin (9% resistance in Australia), all cephalosporins except ceftazidime (10% resistance in Australia), cefipime and cefpirome, and trimethoprim, cotrimoxazole and tetracyclines. Gentamicin (17% resistance in Australia) and tobramycin (8% resistance in Australia) remain the favoured agents for hospital use but oral norfloxacin (UTI's only) and ciprofloxacin are most widely used in outpatients. Resistance to the latter two agents is now 37-38% in the USA but 8-13% in Australia. Imipenem is occasionally used in hospitals (17% resistance in Australia). Colistin and neomycin are sometimes used topically and colistin is rarely used systemically as a drug of last resort.

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