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SUMMARY C reactive protein (CRP) was measured serially in 29 patients with infective endocarditis. Twenty one patients were initially treated with antimicrobial drugs. In 13, serial measurement ofCRP concentrations showed a progressive return to normal (less than 10 mg/l), which correlaWd with a satisfactory recovery. Of the remainder (eight patients), five had persistently high concentrations of CRP, indicating a failure to respond to antimicrobial treatment alone. Two of these five patients died and three underwent valve replacement. Of 11 patients treated with antibiotics and valve replacement, CRP concentrations returned to normal in nine. Two patients had infective complications and the CRP concentration did not return to normal. A transient rise in CRP concentration during an otherwise uneventful fall to normal was a sign of allergic reaction in two and of intercurrent infection in three more patients. Serial measurements of CRP concentrations in patients with infective endocarditis may be useful to monitor treatment and also to detect other infections and complications.

The bacteriological investigation of an outbreak of Legionnaires' disease in Glasgow Royal Infirmary affecting 16 patients is described. Most of the patients had been treated in high-dependency areas on two floors of the hospital supplied by the same two air-conditioned ventilation systems. The source of infection was traced to contamination of a cooling tower from which a plume of spray discharged into the intake vents of the two ventilation systems. Rubber grommets within the cooling tower probably provided a nidus of infection there. The control and management of the outbreak are discussed: a policy of frankness about the course and progress of the investigations was adopted and helped to allay anxiety on the part of both staff and media.

Experiments were carried out to determine whether immunization of female rabbits with highly purified staphylococcal alphaor beta-toxins would protect them against intramammary challenge with staphylococci. High circulating anti-alpha-toxin titers reduced the lethal hemorrhagic edematous form of the disease ("blue-breast") produced by strains BB and Compton 201 to a localized chronic abscess form. No such protection was afforded by high anti-beta-toxin titers. Immunization with alphaor beta-toxins produced no change in the clinical picture of the disease produced by CN.6708, a strain of Staphylococcus responsible for a natural outbreak of abscess-type rabbit mastitis. From these experiments it would appear that alpha-toxin is a key antigen in the blue-breast form of rabbit mastitis. Since the abscess form of the disease was not prevented by immunization with either alphaor beta-toxin, other virulence factors must be acting to produce this more localized disease.