A large outbreak of Legionnaires’ disease was associated with Stafford District General Hospital. A total of 68 confirmed cases was treated in hospital and 22 of these patients died. A further 35 patients, 14 of whom were treated at home, were suspected cases of Legionnaires’ disease. All these patients had visited the hospital during April 1985. Epidemiological investigations demonstrated that there had been a high risk of acquiring the disease in the out patient department (OPD), but no risk in other parts of the hospital. The epidemic strain of Legionella pneumophila, serogroup 1, subgroup Pontiac la was isolated from the cooling water system of one of the air conditioning plants. This plant served several departments of the hospital including the OPD. The water in the cooling tower and a chiller unit which cooled the air entering the OPD were contaminated with legionellae. Bacteriological and engineering investigations showed how the chiller unit could have been contaminated and how an aerosol containing legionellae could have been generated in the U–trap below the chiller unit. These results, together with the epidemiological evidence, suggest that the chiller unit was most likely to have been the major source of the outbreak.

Nearly one third of hospital staff had legionella antibodies. These staff were likely to have worked in areas of the hospital ventilated by the contaminated air conditioning plant, but not necessarily the OPD. There was evidence that a small proportion of these staff had a mild legionellosis and that these ‘influenza–like’ illnesses had been spread over a 5–month period. A possible explanation of this finding is that small amounts of aerosol from cooling tower sources could have entered the air–intake and been distributed throughout the areas of the hospital served by this ventilation system. Legionellae, subsequently found to be of the epidemic strain, had been found in the cooling tower pond in November 1984 and thus it is possible that staff were exposed to low doses of contaminated aerosol over several months.

Control measures are described, but it was later apparent that the outbreak had ended before these interventions were introduced. The investigations revealed faults in the design of the ventilation system.

Fourteen people living in or near the city of Gloucester fell ill with Legionnaires' disease caused by Legionella pneumophila serogroup (SG) 1 between 27 August and 27 October 1986. Another patient had fallen ill on 30 May. Nine of the 15 were diagnosed retrospectively during a case finding exercise. There were three deaths. Three cases of Pontiac fever were also diagnosed.

The source was probably one or more wet cooling towers. Nineteen premises in the city with such towers were identified, and three just outside Gloucester. Samples from 11 of the 22 premises grew Legionella spp.; from nine of these L. pneumophila SG 1 (Pontiac) was isolated. The efficacy of regular addition of biocide in addition to hypochlorite added at the time of disinfection in inhibiting the growth of Legionella spp. was demonstrated.

A survey of patients' movements during their likely incubation period showed that there was no single building that all patients had visited, but there were two areas of the city which nearly all had visited or passed through by car. A case-control study demonstrated an association with one of these areas.

Cooling towers near both areas may have been sources but the evidence is insufficient to incriminate any single one. The unexpected finding of L. pneumophila SG 1 (Pontiac) in nine towers supports the hypothesis that there may have been multiple sources. Cooling towers may have been contaminated by mains water or by drift from other towers.

On 27th to 28th February 2000, a multidisciplinary workshop was convened in the USA to explore the current state of knowledge, best clinical practice, and research needs for the management of equinus gait associated with cerebral palsy (CP). The workshop began with a brief review of CP epidemiology, and an inquiry into the current understanding of the natural history of equinus. Attention then shifted to indications for and goals of intervention; a summary of interventional approaches; the criteria by which successful intervention is evaluated; and, finally, research opportunities. What follows is an overview of the workshop.

As a graduate psychology student in the early 1960s, I cameto the University of Iowa Hospital School with much energy,considerable naivety, and many questions. Do children withcerebral palsy (CP) have difficulties with psychologicaladjustment, what do their families need, can we really havean effect on their quality of life, do we know anything thatreally makes a difference in the long term? What do we meanby ‘they have to accept their disability’, what standard is thebaseline from which to best measure improvement, andwhat is ‘normal’ adjustment if a child has a physicaldisability? Over the last three decades, has practice changedfor the better for the child with CP? Have our perspectiveschanged on any of these questions?