Search

Human serum samples were analyzed for vancomycin concentrations by two different methods: the fluorescence polarization immunoassay and the disk plate bioassay. Each assay method offered acceptable precision. The correlation between both assay methods was excellent (correlation coefficient = 0.985). Excluding technical time, the bioassay was the least expensive method to perform but was more labor intensive than the fluorescence polarization immunoassay.

Subjecting 9-day-old quail embryos to an elevated temperature in ovo causes limb, breast, and brain tissues to shift their patterns of protein synthesis from the production of a broad spectrum of different proteins to the new and (or) enhanced synthesis of a small number of heat-shock proteins (HSPs). The HSPs synthesized by undifferentiated breast tissue in ovo (relative masses (Mrs) 88 000, 82 000, 64 000, and 25 000) are similar to those synthesized by explanted breast tissue or by primary cultures of breast myoblasts heat-shocked in culture. Heat-shocked, 120-hour-old myotube cultures synthesize HSPs similar to those detected in heat-shocked myoblasts except that myotubes also exhibit enhanced synthesis of a 55 000 dalton polypeptide and little or no synthesis of a 25 000 dalton HSP; the failure to thermally induce a 25 000 dalton polypeptide in myotubes is related to the fused nature of these cells rather than to their state of differentiation. Myoblasts, as well as myotubes, cultured in the presence of elevated amounts of arsenite, copper, or zinc also synthesize new and (or) enhanced amounts of polypeptides with isoelectric points and immunochemical properties similar to the 25 000 and 64 000 dalton HSPs. However, elevated levels of these metal ions fail to stimulate new and (or) enhanced synthesis of other HSP-like proteins. These results demonstrate that, although the protein synthetic response of myogenic cells to chemical and thermal stress may be similar in some respects, a number of the synthetic responses are clearly different.

A total of 15 Legionella pneumophilia isolated were tested against 16 antimicrobial agents used singly and in combination with clavulanic acid. When combined with clavulanic acid, 4 of the 16 antimicrobial agents produced no enhanced effect. However, the minimal inhibitory concentrations of 12 of the antimicrobial agents were reduced by one-half to one-third when in combination with clavulanic acid. These reductions reflected only a one-dilution decrease, however, in the original minimal inhibitory concentrations. Thus, clavulanic acid combinations appear to be only nominally effective beta-lactamase inhibitors against L. pneumophilia.

The susceptibility of Legionella pneumophila to a new quinolone, fleroxacin, was studied in both an extra- and an intracellular system. The activity of fleroxacin was compared with that of erythromycin, cefoxitin, and rifampicin. In the extracellular system, erythromycin inhibited while cefoxitin killed the organism. Extracellularly, fleroxacin performed similarly to cefoxitin. Rifampicin was initially bactericidal for L. pneumophila but resistant bacteria emerged at 48 h. The Horwitz monocyte model was used for studies of intracellular antimicrobial activity. At ten times the MIC, cefoxitin did not inhibit intracellular L. pneumophila. Fleroxacin was as active as erythromycin and rifampicin in inhibiting intracellular L. pneumophila. No intracellular, rifampicin-resistant L. pneumophila emerged. Addition of rifampicin to cefoxotin, erythromycin or fleroxacin provided neither synergy nor antagonism.

Recent success in overcoming rejection of transplanted organs has led to a much greater demand for organs from donors and to a reconsideration of mechanisms for increasing the availability of organs from cadavers. In the latter respect the two basic systems are "contracting-in" and "contracting-out". Each system has different benefits and harms, and it is a value judgement that should be adopted. However, both systems raise legal, ethical and practical issues that must be addressed if organs for transplantation are to become available to all who need them.

Susceptibilities of methicillin-resistant Staphylococcus aureus (MRSA, n = 32), methicillin-sensitive S. aureus (MSSA, n = 32), and S. epidermidis (SE, n = 24) were determined to fleroxacin, amifloxacin, ciprofloxacin, difloxacin, enoxacin, norfloxacin, and ofloxacin. All organisms were isolated from the blood of patients with infective endocarditis. MRSA and MSSA MIC90s were less than 1.0 mg/l of fleroxacin, ciprofloxacin, difloxacin, and ofloxacin while amifloxacin and norfloxacin produced MIC90s of less than 2.0 mg/l and enoxacin MIC90s of less than 4.0 mg/l. For S. epidermidis MIC90s were less than 1.0 mg/l of all quinolones except amifloxacin whose MIC90 was less than 2.0 mg/l. Two strains from each staphylococcal group were used in time-kill trials performed with all seven quinolones. Within 8 h, all quinolones colony counts were decreased by one log. At 24 h, most quinolones decreased MRSA, MSSA, and SE colony counts by two to four logs; however, exceptions were found with (1) difloxacin, enoxacin, and norfloxacin against MRSA, (2) ciprofloxacin and enoxacin against MSSA, and (3) ciprofloxacin against SE in which all colony counts increased one to three logs in 24 h. When quinolone time-kill trials did not show a decrease in colony counts at 24 h, the MIC's for the 24 h growth showed a four- to 250-fold increase when compared with pre-trial MICs. No selection or emergence of resistant organisms was found with fleroxacin, amifloxacin or ofloxacin.

The in-vitro susceptibility of 14 strains of Legionella pneumophila to 17 anti-microbial agents were determined. The most active antibiotics were cefoxitin, erythromycin and doxycycline while the least active were cephalothin, cefamandole and cefazolin. Subculturing, type of medium and duration of incubation did not alter the effect of the antimicrobial agents. A change in the inoculum size, from 10(4) to 10(6) cfu, increased MICs two- to sixfold. Erythromycin was not synergistic with gentamicin, tobramycin or amikacin.