Inter-strain comparison by pyrolysis mass spectrometry of Staphylococcus aureus isolates associated with nosocomial infection.

Pyrolysis mass spectrometry was used to characterise Staphylococcus aureus isolates from an outbreak of postoperative wound infections on a mixed surgical ward. The PyMS results were compared with those of phage typing. Both suggested a single strain of S. aureus, of phage type 3C, 55, 71, was responsible for six of the 13 wound infections. PyMS differentiated an isolate from a member of staff of similar phage type to the epidemic strain, which had previously been considered to be the point source for the outbreak. PyMS is a rapid and inexpensive technique for investigating nosocomial outbreaks, including those caused by S. aureus and, in this instance, was more discriminatory than phage typing.

Plasma nitrate clearance in mice: modeling of the systemic production of nitrate following the induction of nitric oxide synthesis.

Nitric oxide (NO) is produced in mammals by the enzyme NO synthase (NOS) in response to a number of agents, including the experimental antitumour agent flavone acetic acid (FAA) and the cytokine tumour necrosis factor-alpha (TNF). NO is converted rapidly in the presence of oxygen, water and haemoglobin to oxidation products, largely nitrate. To quantitate the production of nitric oxide it is necessary to know the clearance of nitrate. The concentration of nitrite and nitrate ion in the plasma of C3H and BDF1 (C57BL6 x DBA2) mice was assessed before and after injection of sodium nitrate and sodium nitrite. Nitrite was covered rapidly to nitrate and the kinetics of elimination of nitrate were determined. There was no significant difference between results obtained with different mouse strains, between levels of nitrite and nitrate, or between i.p. and i.v. administration, and the observations were therefore combined. The volume of distribution of nitrate was 0.71 +/- 0.04 l/kg and the clearance was 0.32 +/- 0.02 l/h-1/kg-1 (plasma half-life, 1.54 h). Using previously published data, we developed a pharmacokinetic-pharmacodynamic model that relates the production of TNF in response to administration of FAA, the enhancement of NOS activity in response to TNF, and the elevation of plasma nitrate in response to NO production. This information permits the prediction from observed plasma nitrate values of the amount of NOS induced in vivo.