Amoxicillin plus temocillin as an alternative empiric therapy for the treatment of severe hospital-acquired pneumonia: results from a retrospective audit.

A formulary decision was made at a large provider of acute hospital services in Surrey to replace piperacillin/tazobactam with amoxicillin+temocillin for the empiric treatment of severe hospital-acquired pneumonia. This decision was made because the use of broad-spectrum-ß-lactam antibiotics is a known risk factor for Clostridium difficile infection (CDI) and for the selection of resistance. After the antibiotic formulary was changed, a retrospective audit was conducted to assess the effect of this change. Data from patients hospitalised between January 2011 and July 2012 for severe hospital-acquired pneumonia and treated empirically with piperacillin/tazobactam or amoxicillin+temocillin were reviewed retrospectively. Clinical characteristics of patients, data related to the episode of pneumonia, clinical success and incidence of significant diarrhoea and CDI were analysed. One hundred ninety-two episodes of severe hospital-acquired pneumonia in 188 patients were identified from hospital records. Ninety-eight patients received piperacillin/tazobactam and 94 amoxicillin+temocillin. At baseline, the two treatment groups were comparable, except that more patients with renal insufficiency were treated with piperacillin/tazobactam. Clinical success was comparable (80 versus 82 %; P = 0.86), but differences were observed between piperacillin/tazobactam and amoxicillin+temocillin for the rates of significant diarrhoea (34 versus 4 %, respectively; P < 0.0001) and for CDI (7 versus 0 %, respectively; P < 0.0028). This preliminary study suggests that the combination amoxicillin+temocillin is a viable alternative to piperacillin/tazobactam for the treatment of severe hospital-acquired pneumonia. This combination appears to be associated with fewer gastrointestinal adverse events. Further studies are needed to evaluate the place of amoxicillin+temocillin as empiric treatment of severe hospital-acquired pneumonia.

Toxic activity against alveolar macrophages of products of Pseudomonas aeruginosa isolated from respiratory and non-respiratory sites.

The toxic effect of certain products of Pseudomonas aeruginosa on guinea-pig alveolar macrophages has been studied in an attempt to account for the apparent infrequency with which certain strains of this species are associated with respiratory infection. Texts were carried out on strains derived from the respiratory tract, strains from infection at other sites, and strains from the inanimate hospital environment which were believed not to have been responsible for infection ('environmental' strains). Haemolysin, pigments, enzyme-containing fractions, slime and cell-wall fraction all exhibited toxic activity against macrophages in an in vitro system, although for any given strain of Ps. aeruginosa the haemolysin was by far the most potent factor. The activity of this factor against macrophages was directly proportional to its haemolytic activity against human erythrocytes. The haemolysin fractions of environmental strains, which have previously been found to have little activity on erythrocytes, were also less active against macrophages than haemolysin preparations from 'infective' strains. It is therefore postulated that the ability of a strain of Ps. aeruginosa to initiate respiratory infection may be related to the degree of haemolysin production. The activity of other fractions against macrophages is more variable, but they may contribute in different ways to the development of infection once entry into the lung has been achieved.

Pseudomonas aeruginosa infection in hospital: a comparison between 'infective' and 'environmental' strains.

One hundred and fifty-six infections or episodes of infection associated with Pseudomonas aeruginosa in six hospitals over 14 months were investigated. Pyocine typing and serotyping suggested that 145 distinct episodes had occurred, caused by 78 different strains. During this period 15 distinct strains were isolated from the environment at one of the hospitals; 12 of these were apparently unassociated with infection in the same ward during the period, and 4 were of types not encountered in infective processes at any hospital. There appeared to be a rather higher proportion of unclassifiable pyocine inhibition patterns among the environmental strains; in general these strains also produced smaller amounts of haemolysin. If failure to produce haemolysin in vitro is correlated with lack of virulence in vivo, this may partially explain the sporadic nature of hospital infection with Ps. aeruginosa, despite the prevalence of strains of this species in the environment.

Evaluation of commercially available antisera for serotyping of Pseudomonas aeruginosa.

Commercially available O antisera have been compared with a standard pyocine typing method in the investigation of 156 strains of Pseudomonas aeruginosa. A third of the strains belonged to serotypes 3 or 6 and 42.3% to pyocine type 1. Good differentiation of strains belonging to the predominant serotypes was achieved by pyocine typing. Although routine use of both methods provides a more complete discrimination between strains, the simplicity of serotyping renders it more suitable for use in the smaller laboratory, where only one method may be feasible. If desired, pyocine typing can be reserved for the strains which cannot be distinguished serologically.