Environmental meticillin-resistant Staphylococcus aureus (MRSA) disinfection using dry-mist-generated hydrogen peroxide.

Meticillin-resistant Staphylococcus aureus (MRSA) is a major problem in hospitals worldwide. Hand hygiene is recognised as crucial in limiting the spread of MRSA but less is known about the role of MRSA reservoirs in the inanimate hospital environment. We evaluated the effect of hydrogen peroxide vapour diffused by Sterinis((R)) against MRSA in two experimental hospital settings and in two field trials. Dipslides were used for MRSA detection and quantification before and after using the Sterinis disinfection process. In the first experimental hospital setting, four epidemic MRSA strains were placed at five locations and left for one week. All strains survived the week but not the disinfection process. In field trial one 14 upholstered chairs from a department with many MRSA positive patients were left for one month in a closed room prior to disinfection. MRSA was found on the upholstery of four of the 14 chairs. Three chairs became MRSA negative immediately after the disinfection, the fourth 24h later. The second field trial was in the private home of a MRSA positive family of four individuals. One location was found MRSA positive, remaining so after the Sterinis cycles. We found Sterinis to be effective against MRSA in the experimental hospital setting and upholstered chairs, but not in the private home of heavily colonised MRSA patients.

No difference in enterotoxin production among Staphylococcus aureus strains isolated from blood compared with strains isolated from healthy carriers.

The production of enterotoxin A, B, C and D by 196 Staphylococcus aureus strains isolated from blood cultures and 95 strains from nasal carriers was investigated. Half of the bacteraemia strains were from patients who died with or because of their infection, the other half from patients who survived. The nasal strains were selected to match the bacteraemia strains regarding phage types. Overall, 30.6% of the bacteraemia strains and 40.0% of the nasal strains produced enterotoxins; enterotoxins B and C were the toxins produced most frequently in both groups. A similar incidence and pattern of enterotoxin production was found among the bacteraemia strains of S. aureus regardless of acquisition of the infection, the portal of entry, presence or absence of endocarditis and outcome of the infection. Thus, the concept that the enterotoxins play an important role in staphylococcal infections, apart from the diseases caused by the toxins per se such as food poisoning and toxic shock syndrome, cannot be substantiated by the results of the present study.

Should probenecid be used to reduce the dicloxacillin dosage in orthopaedic infections? A study of the dicloxacillin-saving effect of probenecid.

Reduction in the dosage of dicloxacillin from 500 mg to 250 mg 3 times a day would mean lowering of costs and less side-effects in orthopaedic infections. In this cross-over study, the serum concentrations of dicloxacillin were measured in 9 patients after administration of dicloxacillin 500 mg 3 times a day (dicloxacillin 500 mg) and after co-administration of 250 mg dicloxacillin and 250 mg probenecid 3 times per day (dicloxacillin 250 mg+probenecid 250 mg). Concentrations were measured every hour after the tablet intake. The mean maximum serum concentrations of dicloxacillin were 17.1 micrograms/ml (dicloxacillin 500 mg) and 12.2 micrograms/ml (dicloxacillin 250 mg+probenecid 250 mg), respectively (P < 0.05). Serum concentrations above 3 micrograms/ml were obtained during 285 min. in both regimes, but the individual variations were biggest during in the dicloxacillin 250 mg+probenecid 250 mg treatment. Serum concentrations above 5 micrograms/ml were in mean measured during 228 min. (dicloxacillin 500 mg) and 190 min. (dicloxacillin 250 mg+probenecid 250 mg), respectively (P < 0.05). The clinical significance of these findings is being discussed. In theory, treatment with dicloxacillin 250 mg+probenecid 250 mg may be as sufficient as dicloxacillin 500 mg.

Flucloxacillin in chronic leg ulcers. Penetration of flucloxacillin into chronic leg ulcer exudate and the effect on the bacteria.

The penetration of flucloxacillin into ulcer exudate was investigated in six patients with chronic leg ulcers. The flucloxacillin dosage used was 1 g orally three times daily for three days, and the serum and exudate concentrations were measured repeatedly during a 10 h-period following the first and the seventh dose. All the ulcers were contaminated with (S. aureus) Staphylococcus aureus either in pure culture (three ulcers) or in culture mixed with Gram-negative bacteria (three ulcers). Bacterial counting in the ulcers was performed twice before and twice during the antibiotic treatment. The flucloxacillin concentrations measured in the ulcer exudate were found to be lower than the corresponding serum concentrations. However, the exudate concentrations were found to be above the minimum inhibitory concentration (MIC) for the contaminating S. aureus during an average of 7 h after each dose, and the number of S. aureus during the treatment period was reduced to less than 0.01% of the initial number. The Gram-negative bacteria were not susceptible to flucloxacillin. The number of these bacteria decreased before flucloxacillin treatment but increased again during treatment, probably owing to the changed conditions in the ulcers following the marked decrease in the number of S. aureus.

Endocarditis due to Kingella kingae.

Four cases of endocarditis due to Kingella kingae are described in compromised patients. All had primary heart disease, and two had systemic lupus erythematosis and congenital heart defect respectively, in addition. Confirmation of Kingella kingae was made in one case at autopsy. The literature on 11 cases of endocarditis, 2 bacteremia, 4 osteomyelitis, 5 septic arthritis and 1 intervertebral disc infection, all caused by Kingella kingae, is reviewed. Our findings confirm that the organism is of low pathogenicity. Children may be predisposed to infection with Kingella kingae.